Neuroscience Exam 1: Odyssey Of The Mind

Front 1

CNS components

Back 1

a. Brain
b. Brain stem (medulla, pons, midbrain)
c. Spinal cord (SC)

Front 2

PNS components

Back 2

a. 31 pairs of spinal nerves
i. 8 cervical
ii. 12 thoracic
iii. 5 lumbar
iv. 5 sacral
v. 1 coccygeal
b. 12 pairs of cranial nerves

Front 3

Nerves of ANS

Back 3

a. Sympathetic output (i.e., splanchnic nerves)
b. Parasympathetic output (i.e., pelvic nerves, etc)

Front 4

What does the Nervous System Do for an Organism?

Back 4

a. Reception of sensory information (environmental awareness, internal or external info)
b. Analysis of stimuli (information) – interpret, coordinate, integrate, modulate
c. Transmission of the motor response to the analyzed information (response goes out through the PNS)
d. Initiation of an effector response (effector because its leaving the CNS; if tear glands produce tears= effector response, if muscles contract = effector response, fear due to scary thought process = effector resonse)

Front 5

2 types of reception of stimuli characteristics

Back 5

i. Internal (thought processes, things within the body)
1. Physiologic
ii. External/environment (proprioception, auditory, etc., processed by PNS)

Front 6

Analysis of information characteristics

Back 6

a. Gets into CNS by PNS (99% of analyzing occurs in CNS)
b. CNS can coordinate stimuli that it receives and interpret it to make sense
c. Reflex activity is the simplest form of analysis of information
d. Modulation- ex. decreasing pain

Front 7

Transmission of analyzed information characteristics

Back 7

a. Takes place in PNS upon leaving CNS

b. CNS pathways may transmit to other places (travel up SC to brain, etc.)

Front 8

Initiation of an effector response characteristics

Back 8

i. Afferent: information coming into CNS
ii. Efferent: information going away from CNS
iii. Afferent information is ALWAYS sensory
iv. Efferent information is ALWAYS motor
v. SAME (Sensory afferent, motor efferent), DAVE (Dorsal afferent, ventral efferent)

Front 9

Examples of effector responses:

Back 9

i. Muscle contraction
ii. Reflexively swat someone after they pinch you
iii. Gland secretion
iv. Behavior patterns

Front 10

# neurons in brain

Back 10

Brain has 100 billion neurons and we have different kinds of glial cells

Front 11

4 characteristics of neurons

Back 11

1. Neurons can produce an action potential (AP) to transmit information from point A to point B.
2. Neurons are sensitive to O2 deprivation.
3. There is limited ability for neurons to mitose after birth
4. Different kinds of neurons differentiate into different forms and functions

Front 12

sensitivity of neurons of O2 deprivation characteristics

Back 12

a. under normal conditions, NS uses 40% of the O2 carried in the blood by RBCs
b. decreased amounts of O2 will have serious consequences

Front 13

limited ability for neurons to mitose after birth characteristics

Back 13

a. research shows that there are some areas of the brain in which mitosis may take place
i. It DOES occur in hippocampus (memory area of temporal lobe), reincephalon (smell perception)
b. most of the neurons you are born with are in place for life when you are born.
c. You cannot re-grow neurons once they are dead (amitotic)

Front 14

Topographical (somatotopic) representation in the brain characteristics

Back 14

1. Specific part of brain controls specific part of the body
2. Somatosensory strip – post central gyrus
3. Motor strip – pre-central gyrus

Front 15

NS cannot work alone. it is influenced by other systems. Examples:

Back 15

i. CV system influences NS via blood flow (decrease in O2, metabolites, etc)
ii. Endocrine system- hormones, insulin is needed in every cell (decrease will effect NS)
iii. Immune system – autoimmune like MS
iv. Body relies on digestive and CV systems to get glucose to the brain – glucose is the only molecular form that neurons need

Front 16

synonyms for sensory neurons (Just FYI)

Back 16

Primary Muscle Spindle/Golgi Tendon Organ
Type I, Type Ia
Afferent Sensory Neuron
1st order Sensory Neuron
Sensory Fiber
Mechanoreceptor
Proprioreceptor
Rod and Cones
Pseudounipolar (T-Cell)
Other terms

Front 17

synonyms for motor neurons (Just FYI)

Back 17

1. Motor neurons
2. Efferent neurons/fibers
3. Alpha motor
4. Gamma motor
5. Upper motor neuron (UMN)/Lower motor neuron (LMN)
6. Multipolar neuron
7. Pyramidal cells {neurons}

Front 18

3 categories of NS cells

Back 18

a. Nonneuroglia: non impulse transmitting (i.e., no AP)
b. Neuroglia (Glia): non impulse transmitting (i.e., no AP)
c. Neurons: conduct impulse in the form of AP

Front 19

4 types of glial cells

Back 19

astrocytes (macroglia)
oligodendrocytes (macroglia)
Schwann cells (macroglia)
migroglia

Front 20

nonneuroglia cells characterisitcs (no AP)

Back 20

i. Non-supporting cells (unlike glial cells), they do not add structural support to the brain.
ii. Small cell bodies
iii. Embryonically form from ectoderm
iv. Collectively called the ependymal (constitutes the coroid plexus)
1. Located in the roofs of the ventricular system of the brain
2. Function to produce cerebrospinal fluid (CSF)

Front 21

neuroglial cells (no AP) characteristics

Back 21

i. Occur in CNS and PNS
ii. More abundant than neurons (5-50x) – depending on the area of the brain you’re in
iii. Located in spaces not occupied by blood vessels and neurons
iv. NOT involved with impulse transmission/ action potentials
v. Functions (on other slide)
vi. Are mitotic (glial cells can undergo mitosis to reproduce whereas neurons can not)

Front 22

fxns of neuroglial cells

Back 22

1. Acts as “connective tissue” for the brain by providing structural support
2. Add nutrients to the neurons
3. Clean cellular debris after damage/infection
4. Myelinate/Insulates neurons – help separate the neurons
5. Provides chemical signals that influence neurons (neurodevelopment) and how they function
6. Involved in synapse formation
7. Involved in blood-brain barrier
8. Gliosis process: scar tissue formation

Front 23

astrocytes structure and types

Back 23

star-shaped cells with long cellular processes

1. fibrous astrocytes- in white matter

2. protoplasmic astrocytes- in grey matter

Front 24

fibrous astrocytes characteristics

Back 24

i. Cellular processes are fewer, longer, and straighter than protoplasmic astrocytes.
ii. Main supporting cells of the CNS
iii. Involved w/ gliosis (scar formation in the brain)
iv. Limited involvement in phagocytosis
v. Involved with metabolic support to neurons by influencing the ionic concentration of the neuronal environment. (via end feet)
vi. Inhibit/promote the outgrowth of nueronal cellular processes during development (gestational) by synthesizing and releasing trophic and adhesion molecules (allowing NS to grow).
vii. Release chemicals involved in the destruction of synapses
viii. Form transient (temporary) scaffolding to developing neurons during gestation (enabling neurons to migrate)
ix. form blood brain barrier (BBB): links between capillaries of the brain and the neurons of the brain

Front 25

blood brain barrier (BBB) definition

Back 25

Specialized barrier formed by endothelial cells and astrocytes which prevents large proteins and charged molecules from entering CNS (a metabolic & anatomical barrier)

Front 26

BBB capillaries characteristics

Back 26

2. Endothelial cells line capillaries and mediate diffusion of substances from blood directly into interstitial fluid (brain tissue between cells).
a. Capillaries are once cell thick & hooked together; as blood goes through the capillary, O2 leaves as well as glucose & enzymes.

Front 27

End feet of astrocytes fxn in BBB

Back 27

-influence passage of substances between capillaries and neurons of the brain.

-Allows certain things to enter and exit the BBB; protects the brain

Front 28

What can go through BBB?

Back 28

a. glucose, O2, electrolytes
b. Meth, alcohol

Front 29

What can’t go through BBB?

Back 29

Large molecules
a. serum proteins (i.e., albumin which causes brain to swell)
b. penicillin (cannot use to treat brain infection)

Front 30

Protoplasmic astrocytes characteristics

Back 30

i. Processes are more numerous, thicker, more branched and shorter than fibrous astrocytes

ii. Function: Isolate receptive surfaces of neurons:
1. Separating/insulating neurons
2. Reduces random flow of neuronal activity

Front 31

oligodendrocytes characteristics

Back 31

-macroglia, smaller than astrocytes (small, rounded cell body)
a. Most numerous cell in CNS
b. small number of cellular processes
c. Located in white matter of CNS (brain & spinal cord)

Front 32

oligodendrocytes fxns

Back 32

myelinates cellular processes of the neurons in CNS, providing insulation
i. Must produce myelin (a phospholipid---that is what is responsible for the white color; fatty substance)
ii. Forms concentric layers of myelin (laminated)
iii. CAN myelinate more than one axon of a neuron

Front 33

schwann cells characteristics

Back 33

similar to oligodendrocytes (small round cell bodies), but found in PNS
a. Myelinate cellular processes of neurons in PNS
b. Basically function like oligodendrocytes to laminate neurons for insulation.

Front 34

microglia cells characteristics

Back 34

very small, constitute 10% of glial cells
a. Normally live in CNS and are inactive during normal brain functioning.
i. Maintain integrity of synapses, provide proper nutrition, and structural support
b. In a diseased brain/infection/inflammatory condition, they take on an immune function
i. Act like white blood cells and undergo phagocytosis process to kill bacteria via enzymatic digestion
c. DO NOT occur in PNS, only in CNS
d. Involved w the following disease processes: generalize dementia, Alzheimer’s disease, Parkinson’s, schizophrenia, neuropathic pain following PNS damage
e. Come from mesoderm (only glial cell that comes from mesoderm, others come from ectoderm)

Front 35

cell body of neurons characteristics

Back 35

1. Fairly larger
2. Shape varies
3. Contents are similar to that of other cells in the body
a. most obvious structure is the nucleus (large & spherical, generally in the center of the cell body)

Front 36

Characteristics of cell body/neuronal cell:

Back 36

1. Nucleus: middle of cell body (if not in the middle, the cell is considered pathological)
a. Large, spherical
b. A double layered nuclear membrane (also known as nuclear envelope)
c. Has nuclear pores in the nuclear membrane that allow for passage of large macromolecules coming from cytoplasm {cytosol} or leaving from the nucleus.
d. Contains 46 chromosomes and DNA wrapped in chromosomes
e. Protein Synthesis:
f. Nucleolus (w/in nucleus): large inclusion within the nucleus where ribosomal RNA is synthesized and produced.
1. rRNA involves w/ protein synthesis at the ribosomes

Front 37

protein sythesis in neuronal cell

Back 37

i. Transcription: nucleus
ii. Translation (put together a protein molecule; gene sequence): rough endoplasmic reticulum in cytosol (cytoplasm)
iii. Protein Synthesis: rough endoplasmic reticulum in cytosol (cytoplasm)
1. Outer membrane is continuous with endoplasmic reticulum (ER)

Front 38

mitochondria characteristics

Back 38

scattered throughout cell body, involved with cellular respiration; energy production (ADP -> ATP).
1. neurons can only use glucose or glucose products for energy (Can’t use fatty acids or amino acids)
2. They also require O2
3. Neurons CANNOT store glucose, unlike skeletal muscle. Once their energy supply is gone, there is no more energy (unconsciousness). Can only use what the blood is bringing

Front 39

lysosomes charcteristics

Back 39

double membrane-bound vesicles that contain hydrolytic enzymes
1. Function of enzymes: autolytic digestion (self breakdown) of substances that originating in and out of the cell – breakdown the cell that they are in.
2. If cells are to die, lysosomes pick up the trash
3. Ways for cells to die via lysosomes:
a. Necrosis: lysosomes rupture and digest the contents of the cell
b. Apoptosis: Genetically determined cellular self-destruction process. Cells programmed to die off.

Front 40

Rough ER characteristics

Back 40

contains Nissl Substance - ribosomes
1. Found in: cell body, dendrites
2. Not found in: axon, axon hillock
3. flattened {lamella}, double-layer membrane lined with ribosomes {Nissl bodies} which makes it “rough”
4. Site of protein synthesis

Front 41

protein sythesis in rough ER characteristics

Back 41

a. translation & synthesis of proteins take place here
i. General proteins – enzymes carry out catalytic reactions
1. Enzymes, actin, tubulin, microfilaments, neurofilaments
ii. Plasma membrane proteins
iii. Neurosecretory proteins – neurotransmitters, neuromodulators

Front 42

smooth ER characteristics

Back 42

1. Continuation of RER, but contains no ribosomes/Nissl bodies
2. Functions to channel proteins produced in the RER to the Golgi apparatus
3. No synthesis taking place.

Front 43

golgi apparatus characteristics

Back 43

complex of double-membranes, has layers to it that look like flattened sacs
1. Receive protein molecules from the smooth ER
a. Here they are modified & sorted into specific membrane-enclosed vesicles
b. Sends the vesicles to various regions

Front 44

golgi apparatus send vesicles to

Back 44

i. Cell membrane regions
ii. Lysosomes
iii. Neurotubules
iv. Etc.
vi. Nucleus (DNA) ->Cytosol (Cytoplasm) -> Rough ER -> Smooth ER -> Golgi apparatus (body) -> see places above

Front 45

Cytoskeleton/Fibrillar protein characteristics

Back 45

NOT AN ORGANELLE!!!!
1. Found w/in cytoplasm & axon & extend into the dendrites
2. Gives shape and support to neuron through fibrillar proteins

Front 46

3 types of fibrillar proteins

Back 46

microfilaments
microtubules {Neurotubules}
Neurofilaments {Neurofibrils}

Front 47

microfilaments characteristics

Back 47

i. primarily made up of actin (protein molecule)
1. smallest in diameter.
2. Involved in actoplasm
ii. Actin molecules are in constant flux
iii. A lot of actin is found near the cell membrane and at the growth cone
iv. Actin molecules are involved w/ Growth cone production - as dendrites grow throughout development, so neuron can get from point a -> b
1. growth cone helps the axon keep its shape while it’s growing

Front 48

microtubules (neurotubules) characteristics

Back 48

long tubular structures that form tracts to transport metabolites, vesicles, and ions
i. “Axonal transport system”
ii. Tubulin molecule proteins- largest of the three proteins (Actin is smallest)
iii. Found: cytoplasm, axon, dendrites

Front 49

Neurofilaments {Neurofibrils}

Back 49

most abundant of fibrillar proteins
i. Found in cytoplasm
ii. In the axon- Neurofilament molecule protein (Most abundant of the three proteins (Actin smallest, Tubulin is largest, Neurofilament is most abundant)
iii. Add strength (resiliency) and diameter {caliber} to axon
iv. Oriented along the length of the axon (run parallel)
v. Are defective in Alzheimer’s patients. Seen as neurofibullary tangles which results in death of neurons

Front 50

axonal transport characteristics

Back 50

related to neurotubules
1. Transport of substances from cell body to cellular processes and conversely using microtubules

Front 51

2 directions of axonal transport

Back 51

a. anterograde/orthograde: away from cell body to cellular processes{efferent}
b. retrograde: towards cell body from cellular processes {afferent}

Front 52

2 rates of axonal transport

Back 52

a. fast: 200-400 mm per day ; both anterograde & retrograde
b. slow: 1-5 mm per day; anterograde

Front 53

Movement direction/speed options of axonal transport

Back 53

a. Fast anterograde
b. Fast retrograde
c. Slow anterograde
d. There is no Slow Retrograde

Front 54

fast anterograde structures

Back 54

-Plasma membrane components
-Smooth ER
-Synaptic vesicles containing neurotransmitter
-Mitochondria

Front 55

fast retrograde structures

Back 55

-Mitochondria
-Degenerated structures: these get back into the system this way
-Vesicles and molecules: nerve growth factor and other trophic molecules that need to get back into the cytoplasm and ultimately into the nucleus

Front 56

slow anterograde structures

Back 56

-Soluble enzymes
-Proteins for regeneration
-Proteins to renew cytoskeleton and plasma membranes

Front 57

Force-generating Motor Proteins- 2 categories

Back 57

a. Kinesin: motor protein molecule for anterograde movement
b. Dynein: motor protein molecule for retrograde movement

Front 58

energy for vesicle movement during axonal transport characteristics

Back 58

Energy for motion comes from ATP; molecules bind to microtubule and vesicle and work their way through tubules. The molecules follow the vesicle in order to stay on track.

Front 59

3 options for movement of vesicles

Back 59

a) Can pass another vesicle moving in the same direction on the same neurotubule; (ie. Cross to the other side of the street to pass)
b) Two vesicles can move bi-directional (opposite directions) on the same neurotubule; (like 2 way road)
c) Vesicles can shift between adjacent neurotubules; (can switch tracts and bypass other vesicles)

Front 60

axon characteristics

Back 60

a. ALWAYS EFFERENT in nature (conduct action potential away from cell body)
b. There is only one axon per cell body
c. Originates at axon hillock
d. No ribosomes/Nissl Bodies -> No protein synthesis
e. Smaller in diameter than dendrites
f. Smooth, uniform in length - dendrites’ diameter changes down their lengths
g. Axons are Much longer than dendrites, varies btw .01mm to 1 M in length
h. Do not have spines like dendrites do
i. Distal end enlarges and starts to branch forming telodendria (treelike
j. Axons contain cellular organelles as well: mitochondria, neurotubules, etc.

Front 61

telodendria definition

Back 61

specialized structures that facilitate transmission of AP to adjacent neurons

Front 62

buton characteristics

Back 62

-small rounded swelling on the ends of the branches of the telodendria; which enhances synapse formation
-contain presynaptic membrane that forms a synapse with a postsynaptic membrane

Front 63

A synapse with a postsynaptic membrane can be (4 options)

Back 63

a. axodendritic: axon of one neuron synapsing w/ the dendrites of another
b. axoaxonic: axon of one neuron and the axon of another
c. axosomatic: axon of one neuron and the cell body (soma) of another
d. dendodendritic: dendrite of one neuron and dendrite of another

Front 64

Myelination of an axon characteristics

Back 64

a. Insulating axons with myelin, but not the dendrites
b. Myelin is a phospholipid (fat)
c. Most neurons are myelinated
i. Not myelinated: post ganglionic, C pain fibers
d. Begins in the 4th month of gestation
e. CNS: myelination occurs via oligodendrocytes
f. PNS: myelination occurs via Schwann cells
g. Non-myelinated axons are slower because they have to depolarize down the whole axon instead of jumping from Node of Ranvier to Node of Ranvier

Front 65

myelination in CNS characteristics

Back 65

myelination occurs via oligodendrocytes
i. Can myelinate more than one axon
ii. There are nodes of Ranvier, but not as many as neurons in the PNS

Front 66

myelination in PNS characteristics

Back 66

myelination occurs via Schwann cells
i. Schwann cells wrap around a segment of the axon, internodes (insulated segments of myelination in the axon that are difficult to depolarize)

Front 67

nodes of ranvier characteristics

Back 67

occur between internodes, not myelinated
a. Saltatory conduction: when AP comes down the axon, the AP can “leap-frog” from node to node, speeding up the AP
b. Not all axons in PNS are myelinated, but Schwann cells are still involved
i. These axons do not have saltatory conduction, so the AP is slower.

Front 68

dendrites characteristics

Back 68

a. ALWAYS AFFERENT
b. Short, numerous, highly branched, not myelinated
c. Thicker at their origin and not uniform in length
d. Comes off of cell body
e. Covered in dendritic spines that increase surface area and increases efficiency of synapse formation
f. Contain microtubules, microfilaments, and neurofilaments (fibiliar components)
g. Contain ribosomes/Nisil bodies (substance), so protein synthesis does occur
h. Contain elongated mitochondria
i. Conduct AP towards the cell body (afferent)

Front 69

sensory neuron characteristics

Back 69

Morphology is different than a motor neuron; when usually talking about neurons then we assume we are talking about motor neurons.
a. Instead of axon and dendrite, you have distal (peripheral) and proximal process (Central)
b. Dorsal root ganglion: location of cell body in a sensory neuron
c. Myelination occurs the same as a motor neuron

Front 70

structure of cell membrane

Back 70

1. Double layered structure
a. It is composed of 2 layers of phospholipid molecules
i. Phosphate groups are on the outside
ii. In the middle there are two layers of lipid molecules (triglycerides); between the two phosphate layers
b. This flexible membrane surrounds the soma and all processes

Front 71

permeability of cell membrane

Back 71

a. Permeable to molecules such as fat, steroids, and gases (CO2 and O2)
i. lipid soluble molecules
ii. water insoluble molecules; these are also referred to as hydrophobic.

Front 72

impermeability of cell membrane

Back 72

a. Impermeable to sugars and amino acids, as well as ions.
i. water soluble molecules (hydrophilic)

Front 73

Proteins and CHO that are imbedded randomly throughout the cell membrane characteristics

Back 73

a. Protein molecules
i. Receptor Sites
ii. Channels/Pores
iii. Metabolic pumps (ie. Na/K+)
iv. Transporter molecules
b. Lipids
i. Cholesterol
c. Carbs
i. Glycoprotein

Front 74

anatomy of a peripheral nerve

Back 74

1. products of dorsal and ventral rami of spinal nn. cranial nn. are also classified as peripheral nn.
2. held together by connective tissue
3. may contain both motor and sensory nerves, or just one or the other
4. grossly appear white due to myelin. Note that all peripheral nn. are not myelinated

Front 75

microanatomy of a peripheral nerve

Back 75

a. entire n. is surrounded by epineurium
b. within each nerve are bundles of neurons called fascicles
c. each fascicle is surrounded by perineurium (barrier to passage of material in/out of fascicle)
d. each neuron in the fascicle is surrounded by the endonerium

Front 76

fertilization steps

Back 76

Egg + Sperm = zygote -> 2 cells -> 4 cells -> 8 cells -> ball of cells -> blastula

Front 77

initial embryonic stages

Back 77

o Cleavage due to mitosis (due to mitosis, stops around 64 cells and morula starts)
o Morula- solid ball of cells
o Balstula – hollow ball of cells
o Gastrula – ball of cells that are hollowed out start to develop germ cells

Front 78

gastrual stage- 3 germ cells formed

Back 78

• Mesoderm- muscles, bone, blood, connective tissue
• Endoderm- lining of vessels, heart, GI tract
• Ectoderm- NS, integument

Front 79

Primitive streak (becomes the human) characteristics

Back 79

o At 2 weeks, you are a primitive streak
o There is an ectodermal layer, a neuroectoderm, and notochord (intervertebral disc)
o The ectoderm thickens and forms the neuroectoderm, which forms the neural plate.
o The neural plate becomes the NS

Front 80

neural plate becomes NS at 18 days characteristics

Back 80

AT 18 days, neural plate begins invaginating along central axis forms (beginning of neural tube)
-Neural groove
-2 neural folds
o Neural folds begin moving toward midline to close and completely close into neural tube at 23 days
o Neural folds close in this order to make neural tube:
-> Middle, Superior, Inferior
o Improper closing of neural tube: Spina bifida (failure to close inferior)
-Some of the neuroectodermal cells are left over and do not incorporate into tube and are left on the outside of neural tube – Forms Neural crest

Front 81

neural tube becomes

Back 81

CNS

Front 82

neural crest becomes

Back 82

PNS (w/ some exceptions)

Front 83

Neural Tube/ CNS formation characteristics

Back 83

o Lateral walls of neural tube thicken to form a small lumen called central canal (contains CSF)
-> Becomes ventricular system of the brain
-> Runs full length of spinal cord
o Middle indentations become sulus limitans
-> Forms dorsal alar plate: become dorsal horns of spinal cord, sensory
-> Forms ventral basal plate: become ventral horns of spinal cord, motor

Front 84

3 layers of the CNS

Back 84

Ventricular/ Ependymal layer: 1st layers, innermost
Marginal layer: 2nd layer, outermost
Mantle: 3rd layer, middle of the three

Front 85

Ventricular/ Ependymal layer of CNS characteristics

Back 85

1st layers, innermost
• Surrounds central canal
• Produces neurons, forms glial cells (astrocytes, oligodendrocytes, etc)

Front 86

Marginal layer of CNS characteristics

Back 86

2nd layer, outermost
• Formed when ventricular layer differentiates and cellular processes displace laterally
• Becomes white matter of SC (due to cellular processes)

Front 87

Mantle layer of CNS characteristics

Back 87

3rd layer, middle of the three
• Due to proliferation of neuroblasts (immature neurons
o Means they migrate from ventricular layer to mantle layer
o Then they will help form gray matter (dorsal and ventral horns)
-> Gray matter = cell bodies

Front 88

3 meninges of spinal cord

Back 88

Dura mater : from mesoderm; outermost
Arachnoid mater: from neural crest from ectoderm; middle
Pia mater: From neural crest from ectoderm; innermost

Front 89

myelination in embryo characteristics

Back 89

o Insulates axons – phospholipid, concentric layers
o 4.5 mo gestation through 1st post natal year in spinal cord
o At birth, brain myelination is limited to only a few areas of the brain
o In CNS, Fiber tracts become functional about the same time myelination is complete.

Front 90

brain myelination at birth characteristics

Back 90

-> Brain neurons: myelinates posterior to anterior with frontal lobe being myelinated last
• Explains teenagers- frontal lobe (decision making) not fully matured/myelinated
-> Brain doesn’t complete myelination until 25 y/o
-> Also starts inferiorly and works its way superiorly

Front 91

brain embryonic development 28 days characteristics

Back 91

o 28 days
-> Neural tube forms
• Prosencephalon = forebrain
• Mesencephalon = midbrain
• Rhombencephalong = hindbrain
o Rostral/Ventral (towards front of brain), Caudal/posterior (towards back of brain)
o The neural tube bends ventrally/rostrally to form:
- Midbrain flexure (cephalic flexure): between forebrain and midbrain
- Pontine flexure: between pons and medulla
- Cervical flexure: transition btw hindbrain and SC

Front 92

brain embryonic development 35 days characteristics

Back 92

- Forebrain and hindbrain separate and form 2 vesicles each
- 5 vesicles
• Prosencephalon/Forebrain (2)
o Telencephalon (endbrain) – cerebral hemisphere
o Diencephalon (interbrain) – thalamus structures
• Mesencephalon/Midbrain (1)
• Rhombencephalon/Hindbrain (2)
o Metencephalon (cerebellum and pons)
o Myelencephalon (medualla oblongata)

Front 93

Majority of PNS comes from neural crest except:

Back 93

lower motor neurons of PNS are in ventral horn of SC which is from neural tube

Front 94

neural crest forms

Back 94

- All sensory neurons of PNS (spinal nerves and cranial nerves w cell bodies outside the neural tube!)
- Schwann Cells – myelinate cellular processes in the PNS
- Autonomic NS ganglia

Front 95

All sensory neurons of PNS from neural crest characteristics

Back 95

• Spinal NN and sensory neuron cell bodies are located in dorsal root ganglia
• Sensory neurons associated w cranial nerves cell bodies located in ganglia in the head and neck
o V, VII, VIII, IX, X
o II, VII, IX, X: parasympathetic, pre from tube and post from crest
o Olfactory (I) and optic (II) nerves are outgrowths of brain and not truly nerves  Products of neural tube

Front 96

Autonomic NS ganglia from neural crest characteristics

Back 96

• Pre ganglionic and postganglionic neurons synapse – both sympathetic and parasympathetic of ANS
• Postganglionic fibers -> from neural crest (efferent motor neurons); cell bodies in ganglia outside CNS
• Preganglionic fibers -> from neural tube ; cell bodies in CNS

Front 97

All motor neurons of peripheral NN have their cell bodies located ( ) and are a product of ( )

Back 97

ventral horns of spinal cord

neural tube

Front 98

General Growth and Development of nervous system

Back 98

1. Once the neurons leave the neural tube/crest (developed), they lose their mitotic ability; some exceptions
2. During neurodevelopment/gestation, excess neurons are formed
3. 2,500 neurons are produced each minute during gestation -> 1,263,600,000,000 (trillion) -> When born, 100 billion neurons in the mature adult brain (Go from trillions of neurons to billions)
a. Overproduction during development
b. Where did they all go?
^Excess production ensures that the NS has the potential to do all that it needs to do.

Front 99

ADHD neural development characteristics

Back 99

In ADHD children the thickening process is delayed in the frontal lobe (based on PET studies)

Front 100

How do cells differentiate into various types of neurons & glial cells?

Back 100

i. Begin as neuroblasts (come from stem cells) – immature neurons that haven’t decided what to do; can differentiate into all kinds of neurons
ii. Differentiation depends on a series of chemical signals that control gene transcription (i.e., protein synthesis)
1. something tells the neuroblast at the DNA level to synthesize specific protein molecules

Front 101

What regulates the signals for neuron and glial cell differentiation?

Back 101

1. genotype: factors inherited by cells
a. no control over these factors
2. phenotype: factors provided by other cells & chemicals in the local embryonic environment
a. how genotype is expressed

Front 102

b. Examples of Environmental Influences on cell differentiation

Back 102

i. Cell to cell interaction: adjacent cells produce , which influence transcription (Up regulation of genes) such as signaling molecules, growth factor, neurotrophic chemicals, hormones, etc.
ii. Mesodermal cells influence ectodermal cells of the neural plate
iii. Using tissue grown experimentally in culture, it is possible to influence differentiation by changing the environment (i.e., signaling molecules, hormones, and growth factors)

Front 103

b. How do neurons reach target areas?.( there are 6 layers of cells in the cerebral cortex that communicate with each other. All the cells of the cerebral cortex come from the neural tube. How do the neurons get to the right layer? It isn’t a random organization!) 2 mechanisms of guidance

Back 103

1. radial glial cells: - located in the cerebral cortex - act like scaffolding to guide a migrating axon to its target (mechanical type of guidance system)
2. guidance cues: at the distal end of axon, there is a growth cone; Has feet like structures that are collectively called filopoda

Front 104

guidance cues for neurons characteristics

Back 104

a. terminal ends of filapoda are always moving (extending/retracting to check out environment and looking for chemical cues as to where it needs to go)
b. receptor protein molecules that are embedded with in the cell/plasma membrane of filopoda
c. Guidance cues comes from the extracellular matrix (space around the neuron)
i. Cues come from fibroblast (immature connective tissue cells), target structures (like skeletal muscle cells) and glial cells in the extracellular matrix
d. 2 categories of guidance cues: (NCAMS & Neurotrophic factors (neurotrophins))

Front 105

NCAMS ( neural cell adhesion molecules) characteristics

Back 105

): found on surface of neighboring cells & in extracellular matrix
1. glycoprotein molecules: stabilize the axon as it grows so that past position is not lost; stabilize the growth
a. binds to NCAM cells & stays permanent to that point so you wont lose what you have gained

Front 106

Neurotrophic factors (neurotrophins) characteristics

Back 106

released by target structures which attract the growth cone (chemotaxis type of event; attractance)
1. 3 types: NGF (nerve growth factor, neurotrophins), BDNF (brain derived neurotrophic factor), NT-3 (neurotrophin 3);
2. All are protein molecules
3. Provide chemical cues to attract axon to get it to go where they want
4. Not all are attractants, some repel the axon
5. Also can indicate which way the axon needs to turn

Front 107

What happens to excess neurons?

Back 107

i. APOPTOSIS is the process that gets rid of the excess neurons (read process on pg. 25 in syllabus)
ii. Programmed cell death, no inflammatory process
iii. Have to make a distinction between apoptosis & normal necrosis
iv. Small vesicles of debris are developed, these are then broken down w/out the inflammatory process
1. orderly breaking down of cells
2. genetically controlled

Front 108

Clinical Relevance of NS Development Processes

Back 108

1. There is a genetic predisposition for the NS to be “hardwired” due to the evolutionary process.
2. In order for “hardwired” pathways to be working right, adequate stimulation from the environment must take place during embryonic & postnatal development using guidance cues.

Front 109

adequate stimulation from the environment must take place during embryonic & postnatal development using guidance cues characteristics

Back 109

a. Genotype: genetic makeup of the organism (totally of DNA)
b. Phenotype: physical or chemical expression of the genotype
c. Use it or lose it! – if not stimulated by the environment then we will lose it

Front 110

Use it or lose it embryonic & postnatal development - characteristics

Back 110

i. Environment is important
ii. Pathways will never be established if not exposed.
iii. 1st 3 years are critical for developing pathways
1. Increasing synapses
2. The better the environment the better their pathways will be
iv. NS is developed by about age 12, but myelination and synapses are still forming up to age 25.

Front 111

Clinical Relevance of NS Development Processes
Examples

Back 111

a. Children who have not been exposed to any type of auditory language cannot develop significant language skills after age 12.
b. Lack of visual stimulation at birth will cause neurons in the cortex in occipital lobe to die or be averted to other functions
c. The synapses on dendrites of mentally handicapped children are different than those on a healthy child.
d. Criminals- brains could possibly lack the moral decision making hardwiring due to lack of nurturing as a child.
e. Animals (mice & rats) raised in enriched environments histologically 25% more synapses than animals raised in empty cages
f. Enriched environment:
g. Information embedded in an emotional context seems to stimulate neural circuitry more than information alone
h. Use it or lose it also applies to elderly:

Front 112

Use it or lose it for the elderly characteristics

Back 112

i. Synaptic contacts in elderly who read/participate in activities are better (more dendrites) = enriched environment
ii. More synapses in older adults that are w/in an enriched environment as compared to an environment that does not have much intereaction.
iii. Active vocalization & exercise also contributes to more dendrites.
iv. Neuroplasticity:
1. Adults need competent functional synaptic levels to maintain.
2. The older you get, the less neural plasticity you have.

Front 113

simple diffusion characteristics

Back 113

i. the movement of ions (K+, Na+, Cl-) from high concentration to low concentration, establishing a resting membrane potential and action potential
ii. This Diffusion referred to as conductance
1. gradient: passive movement of ions
2. molecules want to go where there is less energy to reach equilibrium
iii. May occur in 3 types of channels embedded in the membrane {ionophores, pores}
-The same ion can go through each type of channel, it just depends on the circumstances.

Front 114

what kinds of ions and molecules need to enter and exit a neuron?

Back 114

Ions
a. Glucose, Growth hormones, thyroxin, etc. have to get through the plasma membrane for health and development of the cell
i. Glucose and its derivatives involved with ATP production
ii. Growth hormone/regular hormones to produce protein (insulin for metabolic rate, thyroxin)
iii. Gases (CO2, O2)

Front 115

simple diffusion- Non-gated channels characteristics

Back 115

a. Ions can always go through
b. Chemical nature of protein molecule controls what ion can go through (i.e., Na+ channel only allows Na+ to go through)
i. Ex: non-gated channel for Na+, non-gated channel for K+, etc.

Front 116

simple diffusion- voltage-gated channels

Back 116

always closed in resting membrane; open in response to change in voltage (aka: potential difference) across cell membrane
a. Used in AP
b. Protein molecules must undergo conformational change (change in shape) in response to voltage change; makes it conducive to allow ions to go through

Front 117

simple diffusion- Ligand-gated channels

Back 117

normally closed; undergo conformational change by interacting with ligand (chemical)
a. Ligands are chemicals that attach to a receptor site on the protein pore and cause a conformational change to open channel
b. Neurotransmitters or neuromodulators behave this way

Front 118

osmosis characteristics

Back 118

-movement of only water through semipermeable membrane
-Tendency of water to move outside the cell to area of high concentration; water moves with concentration gradient to try and achieve equilibrium. Solutes, such as Glucose, do not move since they are too large

Front 119

facilitated diffusion characteristics

Back 119

movement of ions (or macromolecules) from high concentration to low concentration, but faster than simple diffusion, is due to carrier molecules
i. PASSIVE process
ii. Utilizes carrier molecules
1. protein molecules are imbedded in the cell membrane
2. movement is bi-directional
iii. Requires energy from the concentration ( [ ] ) gradient

Front 120

Active transport characteristics

Back 120

movement of ions/molecules against concentration gradient (uphill/backwards) – from low concentration to high concentration
i. Requires a lot of energy expenditure that comes from hydrolysis of ATP
ii. Use transporter molecules imbedded in cell membrane (protein molecules)
iii. Under certain conditions, active transport can maintain concentration gradient within cells.

Front 121

active transport can maintain concentration gradient within cells examples

Back 121

1. Helps maintain ionic differences between intracellular and extracellular fluids
2. Interstitial (outside) – high sodium, low potassium
3. inside – high potassium, low sodium

Front 122

primary ions used in active transport

Back 122

-Potassium, sodium, chloride ions, etc. are the primary ions used in active transport.
-Are different kinds depending on what it is transporting (ie. Sodium Potassium pump)

Front 123

biological fluid (water) compartments

Back 123

Intracellular: Within the confines of a cell membrane
Extracellular: Fluid outside a cell membrane
-Intravascular: Within the confines of a vessel
-Interstitial (tissue fluid): Outside vessels but between cells

Front 124

exocytosis characteristics

Back 124

neuron releases macromolecules (Neurotransmitters & neuromodulators) by diffusion of vesicles within plasma membrane
i. Vesicles from golgi apparatus bind to the plasma membrane forming a fusion pore complex
ii. When Ca++ influx, pores open & release chemicals into synaptic cleft.
iii. Chemicals function as NTM/neuromodulators

Front 125

endocytosis characteristics

Back 125

engulfment of material in a vesicle by the plasma membrane (plasma membrane surrounds and engulfs something)
i. Preserves some of NTM dumped into synaptic cleft to recycle them;
ii. Do not have to continually process NTM

Front 126

Resting membrane potential (RMP) characteristics

Back 126

neurons are charged, but are not conducting AP
a. Caused by a potential electrical difference (voltage) which exists across a cell membrane, causing excitability in the neuron. (muscle cells and neurons are the only cells that have the ability to get excited)
i. Positive charge on outside, Negative charge on inside

Front 127

what accounts for electric potential difference in neurons?

Back 127

i. Physiological factors: diffusion of ions through cell membrane through non-gated pores
ii. Biological factors : membrane’s relative permeability to certain ions (based on nature of cell membrane)

Front 128

Na, Cl, and K [ ] at RMP

Back 128

-Na + is 10x more concentrated in extracellular fluid; -Cl- is 14x more concentrated in extracellular fluid
-K+ is 30x more concentrated in intracellular fluid.
Anions are negatively charged proteins that are too big to cross the membrane, but stay intracellular

Front 129

Membrane at rest is more permeable to:

Back 129

Membrane at rest is not conducting an AP, so it is 50-100x more permeable to K+ than Na+

Front 130

Migration of K when membrane is at rest characteristics

Back 130

ii. As K+ diffuses outside of cell, excessive (-) ions are left inside the cell, maintaining negativity due to loss of (+) ions (K+).
iii. Migration of K+ continues until excess of (-) inside and additional K+ outside of cell restrains continued K+ diffusion.
1. i.e., K+ ion reaches equilibrium.
2. there is a limited diffusion of Na+ into cell because the membrane is not very permeable to it.
3. Na+ does not play a major role in determining RMP, since the membrane is more permeable to K+ than Na+
4. Left with a positive charge on the outside and a negative charge on the inside

Front 131

Nernst equation characteristics

Back 131

used to calculate equilibrium potential for ions.
i. Takes into account:
1. Charge of ion in question
2. Temperature
3. Ratio of internal/external [ion concentration]

Front 132

Equilibrium potential for K+

Back 132

-80 mV

Front 133

equilibrium potential for Na+

Back 133

+60 mV (see syllabus, p. 30)

Front 134

RMP for normal human neuron

Back 134

-70mv (big player in determining this is K+)

Front 135

If conductance of ions naturally takes place through non-gated pores, why is there a need for concentration gradient?

Back 135

due to active transport
ii. Na+/K+ pump is active transport that occurs against the concentration gradient
1. Requires energy = ATP
2. For each ATP: 3Na+ out, 2K+ in cell to maintain concentration gradient to have a charged cell.
a. Causes Na+ to be 10x higher outside of the cell and K+ to be 30x higher inside of the cell
3. No active transport for Cl- : it just passively diffuses

Front 136

RMP Review

Back 136

i. Requires semipermeable membrane
ii. Certain ions passively conduct along a concentration gradient in non-gated channels. (Na+, K+, & Cl-)
iii. K+ is principle ion due to permeability as compared to Na+ and Cl-
iv. Presence of Na+/K+ pump maintains the concentration gradient of Na+/K+.
1. Everything would reach zero equilibrium w/out this & there would be no charge
v. Nernst equation calculates the equilibrium potential for each ion.
1. Sum of equilibrium potentials = RMP (-70mV).
vi. When a neuron reaches a resting, charged state, it is polarized

Front 137

excitable neuron definition

Back 137

a. If a neuron is charged, it is excitable
b. It can communicate between 2 points.
i. Electrochemical signal is needed for communication

Front 138

action potential definition

Back 138

an electrical signal based on depolarization of a neuron, which travels its full length, based on the flow of ions into and out of the cell.

Front 139

where does AP begin?

Back 139

i. Depends on location in NS
1. Sensory neuron: begins at 1st Node of Ranvier on the distal process of the sensory neuron. (node is not myelinated)
2. Lower Motor neuron: begins at axon hillock.
3. Projection neuron: (projects from one point to another in brain) begins at axon hillock.

Front 140

threshold of activation level definition

Back 140

critical level of depolarization of neuron’s membrane at which the cell can actively generate an AP. (-60 mV) – above 60 mV then it will not fire; it has to reach 60 mV

Front 141

threshold of activation basic characteristics

Back 141

i. All or None = when it hits 60 then the whole neuron will fire, not just part of it. It will fire at the same intensity every time
ii. Always travels the same velocity
iii. After the threshold has been met a change in cell membrane to make it permeable to Na+ occurs; 6x more permeable
iv. Na+ conducts to high concentration & passes through voltage-gated channel; extracellular to intracelluar
v. Within milliseconds, Na+ equilibrium is reached and Na channels close.
vi. During depolarization, K+ voltage gated channels open and let K+ out of cell.
vii. Repeated AP over time results in an excess of Na+ and K+, causing an imbalance

Front 142

KEY TO AP

Back 142

influx of Na+ due to stimulation ( mechanical)

Front 143

Na+ conducts to high concentration & passes through voltage-gated channel; extracellular to intracelluar causing

Back 143

1. Changing the shape of the membrane will also change the voltage.
a. Extracellular is more negative and intracellular is more positive
2. Depolarization is a function of the sodium through the voltage gated channels
a. Na+ is the most important ion for depolarization
b. As Na influx happens, there is a change in polarity where it is more + inside

Front 144

repolarization occurs due to

Back 144

: occurs as a result of flux of K+, reestablishing RMP.
a. ONLY takes a FEW Na+ ions to cause depolarization (AP)
b. ONLY takes a FEW K+ ions to cause repolarization (RMP)

Front 145

Repeated AP over time results in an excess of Na+ and K+, causing an imbalance causing

Back 145

1. This will cause the balance to get messed up w/excess ions
2. This excess is taken up by Na+/K+ pump, maintaining concentration gradient.

Front 146

2 methods of AP conduction

Back 146

saltatory conduction

continuous conduction

Front 147

saltatory conduction characteristics

Back 147

involves myelinated neurons
1. Much more rapid than non-myelinated neurons
2. 120-30 m/sec
3. AP jumps from one node of Ranvier to another (leap frog)
4. Ex: lower motor neurons, proprioceptors (type I)

Front 148

continuous conduction characteristics

Back 148

– involves non-myelinated neurons
1. Slower than myelinated neurons (does not leap frog)
2. 3-0.5 M/sec
3. Ex: Type III (A-delta; painful info) & Type IV (C-fibers; also painful info

Front 149

d. What are the 2 variables that determine the velocity of AP?

Back 149

i. Myelination or not (Myelinated is faster)
ii. Diameter of cellular process (axon or dendrite) of neuron
1. Large diameter, the less the resistance, the quicker the velocity
2. Smaller diameter = more resistance, slower velocity

Front 150

hyperpolarization state characteristics

Back 150

post AP
a. Occurs during repolarization, ending up with an excessive (-) charge intracellularly.
b. Reason for this: brief increase in membrane potential occurs b/c K+ channel that opened during the latter phase of AP closed milliseconds after RMP has been reached. (stay open for milliseconds after AP)
i. Membrane potential becomes further from threshold of activation
ii. concentration gradient becomes greater

Front 151

absolute refractory period definition

Back 151

i. Immediately follows AP
ii. A period of time where no matter what the stimulation, the cell cannot create an AP

Front 152

relative refractory period definition

Back 152

i. Follows the absolute refractory period
ii. Possible to trigger an AP, but stimulation must be stronger than normal.
iii. If increase stimulation, you can fire neuron. Relative b/c you have to increase the stimulus

Front 153

refractory periods due to:

Back 153

Both periods are due to the residual inactivation of Na+ channels and the opening of K+ channels.

Front 154

graded potentials characteristics (local potential)

Back 154

transition between RMP and AP; does not travel the distance of the neuron (meaning it is not propagating; hasn’t reached threshold = no AP; depolarizing, but not much)
a. Has no threshold or refractory period
b. Slower than AP
c. 1000s of localized depolarization might be enough to generate an AP
i. Graded potentials must have an additive effect to reach threshold.

Front 155

receptor potential characteristics

Back 155

“rare”, and are associated w/ the inner ear - cells are modified neurons located on the distal end of a sensory neuron
1. Hair cells move and cause partial depolarization of cell membrane & release NTM.
2. NTM then influence the receptor structure on the sensory neuron (CN 8 – vestibulocochlear)
3. They release NTM onto receptor organs
4. Cell needs to partially depolarize (making it a graded potential) to release NTM

Front 156

Generator potential characteristics

Back 156

1. Responds to all types of sensation (chemical, mechanical, nociceptor – pain, etc.)
2. Mediated/activated by voltage/ligand gated channels
3. Voltage-gated channels respond to voltage stimulation
a. Allows Na+ voltage gated channels to open.
4. Ligand-gated channels respond to chemical stimulation
5. Deformation of the cell membrane (by mechanically touching the skin) causes localized depolarization to occur by opening Na+ voltage-gated channels, allowing Na+ in, however it is not enough to generate an AP (less than threshold = Graded potential)
a. Graded potentials can not produce an AP
6. Do not abide by all-or-none law; their amplitude and duration vary and threshold is not reached. You could have hundreds of these and never reach threshold, where as when you have an AP you always reach the threshold
7. Generator potentials occur a lot which is additive.
8. An AP is generated at the first Node of Ranvier by the additive effects of many generator potentials (requires many of these for an AP)

Front 157

synaptic potential definition

Back 157

occurs where one neuron approximates another neuron (comes very close but does not touch it) via synapse (axoaxonic, axodendritic, etc.); Have to be in CNS

Front 158

presynaptic membrane fxns

Back 158

a. Presynaptic membrane: always belongs to neuron that GENERATES AP.
i. Releases NTM into synaptic cleft
1. AP descends the axon triggering Ca++ voltage-gated channels to open and allow an influx of Ca++ (into the presynaptic membrane region of the neuron)
2. The influx of Ca++ causes a fusion pore complex of the vesicles to form and NTM is released via exocytosis
3. NTM diffuses across synaptic cleft and binds to a receptor on ligand-gated channels on the postsynaptic membrane

Front 159

If the NT is excitatory, an ( ) will be generated

Back 159

EPSP (Excitatory post synaptic potential) will be generated resulting in a small amount of depolarization
1. Utilizes ligand gated Na+ channels
2. Increases positivity inside cell = closer to threshold = partial depolarization

Front 160

if the NT is inhibitory, an ( ) will be generated

Back 160

IPSP (inhibitory post synaptic potential) will be generated resulting in a small amount of hyperpolarization
1. Increases negativity = further from threshold = harder for AP to be produced (Inhibitory)
2. Utilizes ligand gated Cl- channels (More Cl- = more negative ions = hyperpolarization)

Front 161

Will a neuron be excited or inhibited?

Back 161

a. It is a function of the algebraic addition of input at any point in time on the postsynaptic membrane
b. If excitatory->input exceeds inhibitory=fire (AP)
c. If inhibitory->input exceeds excitatory=does not fire (no AP), still charged but no AP

Front 162

How do neurons know when to fire?

Back 162

spatial and temporal summation
c. In reality, both types of summation are occurring simultaneously.
i. Therefore, to get the proper algebraic calculation you have to add up the spatial & temporal summation to determine if it does/does not fire

Front 163

spatial summation definition

Back 163

the adding together of the effects of many presynaptic neurons acting at different sites on the postsynaptic cell
i. Getting all input from multiple sites at the same time

Front 164

temporal summation definition

Back 164

the process by which consecutive synapses at the same site are added together in the postsynaptic cell.
i. One site & getting input one after another

Front 165

Neuromuscular Junction (NMJ) definition

Back 165

where a motor neuron innervates a skeletal muscle cells at the NMJ or motor endplate

Associated with motor units

Front 166

where does neuromuscular jxn (NMJ) occur?

Back 166

Occurs at the distal end of the motor neuron, within the muscles where a LMN innervates a skeletal muscle cell.

Front 167

motor unit definition

Back 167

ratio of one lower motor neuron and how many skeletal muscle cells it innervates

Front 168

low/high motor unit ratio characteristics

Back 168

i. Lower ratio=increased dexterity, fine movements (i.e., 1:10 flexor pollicis, facial muscles, etc.)
ii. Higher ratio=decreased dexterity, larger movements (i.e., 1:500 gluteal mm cells);

Front 169

process of activation at NMJ

Back 169

AP -> Ca++ -> Ach -> MEP (nicotinic rec.) -> Na/K+ Channels -> EPP -> AP -> Ca++ -> SFT

Front 170

AP arrives at distal end of a lower motor neuron causing

Back 170

b. Change in voltage causes voltage-gated Ca++ channels to open up = an influx of Ca++ = initiating exocytosis (vesicles fusion to presynaptic membrane and NT release)
i. Each vesicle contains 5-10,000 molecules of Ach (NTM)
ii. ACh in the synaptic cleft increases 100,000 fold after release.
c. NTM released into synaptic cleft (ACh is NTM for skeletal mm)
d. ACh diffuses across synaptic cleft and binds to receptors on the motor end plate (MEP)

Front 171

Motor end plate location

Back 171

MEP located on postsynaptic membrane of sarcolemma (cell membrane of skeletal mm) – where ACh binds to

Front 172

receptors on MEP are:

Back 172

are ligand-gated channels
1. Nicotinic receptors: NMJ’s and other cells; binds to ACh
2. Muscarinic receptors: located on on autonomic parasympathetic postganglion neurons and cardiac tissue; also binds to Ach

Front 173

what happens at MEP receptors and after:

Back 173

i. Binds to ACh after an AP
ii. Use ligand-gated channels which causes a change of protein molecule, influx of sodium, & will allow potassium to go back out
iii. Binding causes a endplate potential (EPP) = depolarization of motor endplate; due to influx of Na+
1. EPP will only generate a graded potential (partial depolarization)
iv. EPP=~ -70mV (similar to EPSP)
v. EPP will cause an AP (unlike an EPSP which is a graded potential which can not be enough to cause an AP; only need one EPP to cause AP)
1. EPP = partial depolarization of a skeletal muscle cell
2. EPSP = partial depolarization of a neuron
vi. The partial depolarization continues to depolarize the length of the sarcolemma, using voltage-gated Na+ channels to continue AP.. (Note: Started with ligand gated channels and continued w voltage gated channels)
vii. This depolarization also then opens voltage gated Ca++ channels
viii. The presence of excess Ca++ causes skeletal muscle proteins (actin and myosin) to slide (sliding filament theory)

Front 174

To avoid rigidity or continuous depolarization at one site (If Ach remained bound, rigidity would happen)

Back 174

Within milliseconds, the Ach is then released from the receptors back to the synaptic cleft
1. Ach-esterase enzyme present in synaptic cleft breaks down Ach
a. AChesterase enzyme is a naturally occurring enzyme
b. Released and binds to motor endplate
2. ACh is broken down into an inactive form and cannot facilitate depolarization
a. Acetyl and choline molecules
3. Endocytosis process of presynaptic neuron begins
a. Neuron that released ACh takes up the inactive molecules once broken down back into the presynaptic membrane region of the neuron
b. Molecules are put back together and placed in vesicles & are now packaged and ready to be used again

Front 175

hyperkalemia definition

Back 175

a. Increased levels of K+ in blood

Front 176

hyperkalemia caused by

Back 176

b. Caused by renal failure (i.e., kidneys did not clear K+)
i. K+ leaves the blood and goes into the interstitial fluid due to high concentrations of K+ in the blood stream to reach equilibrium = higher levels of K+ in the interstitial fluid

Front 177

hyperkalemia effects on RMP

Back 177

c. Changes in the ratio of intracellular:extracellular K+
i. Ratio is now not as great since K+ moves from blood to interstitial fluid; extracellular gets more like the intracellular
d. RMP is less (it is primarily based on K+ levels), meaning less negativity = closer to the threshold of activation
e. RMP is closer to threshold, so it is easier to generate AP (i.e., overinnervation) less than – 70mV
i. Easier to fire the neuron (takes less stimulation)
ii. Prone to excessive firing of AP

Front 178

hyperkalemia symptoms

Back 178

i. Loss of effective cardiac output (constant contraction/quivering of myocardium)  Can lead to cardiac failure
ii. Causes excessive contractions of smooth muscle
1. Cramping of GI tract (esophagus, small/large intestines, etc.)

Front 179

hypokalemia definition

Back 179

a. Decreased level of K+ in blood

Front 180

hypokalemia caused by

Back 180

b. Caused by excessive dehydration, vomiting, diarrhea, etc. (Fluid loss)

Front 181

hypokalemia effects on RMP

Back 181

c. Migration of K+ from interstitial to intracellular
i. b/c K+ is leaving the extracellular to go into the blood
d. Ratio increases causing hyperpolarization
i. Meaning more negativity for the RMP = harder to reach threshold
e. RMP is farther from threshold, so it is harder to cause an AP (i.e., under-innervation) - higher than -70mV

Front 182

hypokalemia symptoms

Back 182

i. Causes a decrease in the activity of smooth & skeletal muscle (i.e., bradycardia, decreased peristalsis, and constipation)

Front 183

lidocaine is

Back 183

a local anesthetic

Antagonistic type drug

Used for pain, nerve blocks, etc.

Front 184

lidocaine's effects on voltage gated channels

Back 184

a. Binds to voltage gated channels on the receptor organs and axons of passage
i. Prevents voltage gated channel from working = prevents the passage of Na++
b. Closes Na+ voltage-gated channels
i. Na+ cannot pass through channel
ii. Depolarization cannot occur
iii. Therefore “dead” area and no AP

Front 185

curare definition

Back 185

naturally occurring plant compound that binds to nicotinic receptor sites

Front 186

curare's mechanism

Back 186

a. Competes with ACh for receptor site, so it acts as an antagonist to Ach
b. Decreases the polarization of the MEP = preventing sodium from polarizing. If receptor sites are filled with curare there is no where for ACh to bind
c. If injected, it competes for nicotinic receptors associated with MEP, and skeletal mm cannot contract (paralyzed)

Front 187

curare's uses in surgery

Back 187

i. Normally you would get all kinds of reactions from skeletal muscles when you are cutting into them; use this to keep them relaxed
ii. Pancuronium – drug that acts this way

Front 188

Succinylcholine definition

Back 188

similar to curare

NMJ blocker, antagonist, prevents AP in skeletal mm

Front 189

Succinylcholine mechanism and uses

Back 189

b. Binds to nicotinic ACh receptors as well
c. Anesthetic to paralyze the patient during surgery
d. To reverse anesthesia, pts are given succinylcholinesterase – function like AChase
i. Reversal is the same for curare
e. Anticholinesterase drugs get rid of succinylcholine

Front 190

Anticholinesterase drugs (i.e., Neostigmine & physostigmine)

Back 190

a. Prevent the action of ACh-esterase (the enzyme that naturally breaks down ACh)
b. Result: increases the volume of ACh in NMJ; in synaptic cleft, it increases the AP, increasing the skeletal mm contractions = excessive prolonged contraction
c. Often poisonous chemicals
d. Prolongs mm contractions:
i. Leads to convulsions and respiratory distress
1. Respiratory arrest
ii. Suffocation will result if diaphragm involved
e. Used primarily as antidote for chemical warfare agents and poisons that deplete ACh

Front 191

Myasthenia Gravis definition

Back 191

debilitating muscular disease
Weakness and fatigue of frequently used muscles
Progressive, autoimmune disease (immunoglobulin G)
more fatigued in the p.m. than the a.m.

Front 192

myasthenia gravis mechanism

Back 192

c. Destruction of ACh receptors (nicotinic receptors) on the postsynaptic membrane at MEP.
i. The body itself perceives these receptors are foreign structures and activates an immune response and destroys the nicotinic receptors.
ii. ACh cannot bind and AP cannot occur of the skeletal muscle cell
d. Basic lesion is found on skeletal mm

Front 193

treatment myasthenia gravis

Back 193

drug that can inhibit AChase, prolonging levels of ACh (Anticholinesterase drugs)
i. Higher levels of ACh=enhanced contraction
ii. Over time you keep getting destruction & it continues to get worse, but this drug will slow it down

Front 194

Botulinum toxin produced by

Back 194

a. Produced by the clostridium botulinum bacteria
i. Produces a toxin as a byproduct
b. Commonly known to cause food poisoning

Front 195

botulinum toxin causes

Back 195

c. Toxin also affects neurons
d. Prevents release of ACh at NMJ by blocking the voltage-gated Ca++ channel on presynaptic membrane
i. No influx of Ca++ = no fusion pore complex = no Ach released = No AP = no mm contraction
f. Can result in death via suffocation since it effects the respiratory muscles too

Front 196

botulinum toxin use in plastic surgery

Back 196

i. botox – keeps facial muscles from contraction and causing creases in the skin
ii. De-innervating something with a chemical instead of cutting the nerve

Front 197

nerve gases characteristics

Back 197

a. Inhibitor of AChase = elevated level of ACh
b. You will have a repetitive firing of AP which gives you constant muscle contractions/convulsions
c. Antidote = atripeine
i. Ach Antagonistic drug & reduces the effect of the nerve gas
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nerve gases symptoms

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Over activation of skeletal muscle, excessive salivation, excessive tearing, rapid heart rate

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prozac characteristics

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specific to NT serotonin
a. Blocks reuptake of serotonin after being released by the receptors
i. End up with elevated levels of serotonin & stay bound to the receptors
ii. Reuptake usually occurs via endocytosis
b. Even though works as an anti-depressant for depression, it may also cause side effects elsewhere.
i. It takes a few days/weeks to get a level of serotonin that is therapeutic

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aspirin comes from

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willow trees

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aspirin causes

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b. Useful in pain reduction through the breakdown of prostaglandin (which is a chemical released during inflammation)
i. Prostaglandin typically binds to ligand gated receptors on the receptor organ – initiating an influx of Na++ -- causing a graded potential & eventually an AP
ii. If broken down, Cannot stimulate neurons to convey pain to NS
iii. Not as good as lodocaine b/c not as effective

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when a skeletal muscle gets de-innervated it

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-it gets highly concentrated w/ receptors anticipating an AP w/ACh
a. Axons will regenerate and re-innervate the muscle cells & excess receptors start to disappear b/c you don’t need them anymore (This is Neural plasticity )

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Transmitter Substances (TS) definition

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w/in neurotrasmitters
1. General term which implies that they are involved with transmission of AP from one neuron to the next or to muscle cell or gland cell (Neurotransmitters – NT, Neuromodulators – NM)

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neurotransmitters (NT) definition

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substance which is released from presynaptic neuron & affects the postsynaptic membrane (neuron, muscle cell, gland cell) in a specific manner in milliseconds

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NT characteristics

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a. May be involved w/ excitatory OR inhibitory effects
i. Chemical nature of the receptor determines whether the NT is excitatory or inhibitory
b. Same NT may have opposite effects on different kinds of postsynaptic membranes of neurons
c. Same neuron has different receptors for different NT
d. NTs have subtypes (different forms of the same NT); can bind to different types of receptors

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criteria to be a NT

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i. Must be synthesized in neuron & become localized in presynaptic membrane
ii. Must be released into synaptic cleft
iii. Need to bind to receptors of postsynaptic membrane
1. Receptors are ligand gated channels
2. Control conductance of ions (hyper or hypopolarization)
iv. Need to be removed from receptor by specific mechanisms

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ACh characteristics

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: binds to nicotinic and muscarinic receptors
1. Causes EPP to cause skeletal muscle contraction
2. Typically excitatory NT
3. found in:
a. NMJ
b. All pre and post ganglionic parasympathetic neurons
c. Preganglionic sympathetic neurons

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dopamine characteristics

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1. Has 5 sub-types (D1, D2, etc)
2. Inhibitory
3. Produced in substantia nigra
4. Ends up in basal ganglia to control muscle activity
a. Parkinsons: substantia nigra degenerates, dopamine not released, resulting in overactivity
5. Removed by a re-uptake mechanism

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seratonin (5Ht/5 hydroxytryptamine) characteristics

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1. EXCITATORY/INHIBITORY
2. involved in a variety of CNS systems
a. sleep, mood, emotional behavior (Limbic system)
b. Closely related to depression
3. Prozac prevents the reuptake of serotonin, resulting in higher levels

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GABA (gamma amino butyric acid) characteristics

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1. Major inhibitory NTM of NS
2. Most extensive
3. Derivative is inhibitory
4. Removed by selective uptake from the synaptic cleft
a. Can be taken up by the neuron and/or glial cells

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glutamate characteristics

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1. Amino acid
2. Major excitatory NT (a lot of EPSPs)

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glycine characteristics

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1. Amino acid
2. Generally inhibitory
3. Found in the spinal cord

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Neuromodulator (NM) definition

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a. Chemicals that interact with pre and postsynaptic membranes and are usually linked to G-Protein and Second Messenger Systems

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neuromodulator characteristics

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b. Slow system, take longer than NT to influence the synapses
c. NT initiate activity, NM modulate activity (NOT initiate)
d. Make receptors on a protein more or less sensitive to NT

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Neuromodulator (NM) process

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i. Initial binding with receptor proteins (at the pre and post synaptic membranes)
ii. The receptor contacts and activates molecules called G-proteins which are located on the inner surface of the cell membrane
iii. G-proteins become involved with cAMP (cyclic adenosine monophosphate) which is called a second messenger molecule
iv. The second messenger molecules (cAMP) set into action very complicated cascades of metabolic activity utilizing kinases and phosphorylation (signal transduction)
v. The increased activity results in changes in the biochemical nature of the neuron

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Examples of biochemical changes of neurons

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i. Produces changes in the molecular nature of the protein receptor mc resulting in opening or closing the channels. The result is a change in sensitivity to NT.
ii. Alteration of gene expression
iii. Alterations of protein synthesis
iv. Long term effects associated with memory and learning (permanent changes in the cell membrane)

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common NM

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i. Dopamine
ii. Norepinephrine
iii. Epinephrine
iv. Serotonin
v. Nitric Oxide
vi. Adenosine
vii. Neuroactive Peptides

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receptor characteristics

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• Determines if a substance that binds to it will behave as Nt or NM
o Ach to a nicotinic receptor on NMJ  NT
o Ach to muscarinic receptor  acts as NM
• Receptor always facing outward so they can interact w ligands
• Protein molecules
• Found on outer surface of cell membrane (receptor pore)

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2 parts of receptor

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o Binding component: active site, specific for diff transmitter substances
o Ionophore component: pore component (protein pore)

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ionotrophic receptors bind to

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to NT

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Metabotrophic receptor bind to

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to NM

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Properties of Amino Acid Ligand Gated Channels (receptors)

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• Pharmacology of binding sites
o Channels, pore, receptors
o Which neurotransmitters/drugs influence the receptors
• Kinetics
o Binding process and channel gating and ultimately the duration of the effect (gating process-rate of interaction)
• Selectivity
o Which ions flow through the receptor
o IPSP or EPSP
• Conductance
o Magnitude of effect
o Quantity of ions passing through

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Neural processing: coding definition

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initial algebraic, temporal, and spatial summation.

Used to determine excitatory or inhibitory activities of 2nd order sensory neuron

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1st order sensory neurons characteristics

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1. Found in PNS
ii. Enter CNS and synapse with 2nd order
1. synapse in SC or brainstem

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2nd order sensory neurons characteristics

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i. Coding begins here
1. algebraic addition using temporal & spatial summation must take place to determine excitatory/inhibitory activity of the 2nd order sensory neurons
2. cell body decides whether or not to fire on to 3rd.
ii. Found in CNS – grey area of SC
iii. Form ascending sensory pathways
1. generally go to thalamus (synapse here)

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3rd order sensory neurons characteristics

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i. Found in CNS (starts in thalamus and ends in the cortex)
ii. End up at cortex in the post central gyrus
1. Primary sensory cortex, responsible for perceiving sensation.

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different types of synapses- inhibitory or excitatory

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i. Axosomatic->Inhibitory
ii. Axodendritic->excitatory
1. most common form
iii. Axoaxonic->inhibitory
iv. Dendodendritic->excitatory

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2 ways coding is expressed

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i. Rate (frequency)= impulse/sec
ii. Pattern = variation in rate

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brains most fundamental capability

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a. Charles Sherrington described the brain’s ability to choose between competing alternatives (suppress one and activate the other)
i. Brain decides to be excited or not excited
ii. This is the brain’s most fundamental capability (very important)

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if brain could not decide to be excited or not excited:

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1. Could not have any mm activity
2. Could not make sense out of special sensory input, the brain would be blurry
iv. Not the same concept as not using all of your brain (that is a load of crap)
1. It takes energy to inhibit neurons!!!!!

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disinhibition definition

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mechanisms which prevent inhibition
a. Important under certain conditions to eliminate inhibition to increase activity

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examples of disinhibition

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i. Examples:
1. maximize movement
2. increase awareness of special senses
b. Parkinsons is example of disinhibition
i. Dopamine via Basal ganglia inhibits activity (has been disinhibited pathologically)

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Negative feedback loop characteristics

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(Involves one excitatory and one inhibitory)

Uses Renshaw cells (interneurons) : inhibitory; a means by which the neuron can influence its own activity (shut itself down)

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renshaw cells location and fxn

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ii. Renshaw cells are located between the collateral branch of LMN & dendrite of the cell body of the same LMN and other LMNs
1. LMN (collateral branch) releases ACh (causing EPSP)onto Renshaw cell (an excitatory NTM) & the Renshaw cell fires
2. Assuming an AP occurs, Renshaw cells release glycine (a inhibitory NTM) at the synapse (axodendritic)
a. This causes a resultant hyperpolarization, causing an inhibition on the NTM (IPSP)
b. This makes the cell fire less

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Presynaptic Inhibition- involves axoaxonic synapse steps

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1. excitatory NTM is released from presynaptic axon of #3 to postsynaptic axon (terminal area) of #1
2. This causes a graded potential (EPSP; partial depolarization) on the distal part of #1
a. Vesicles open to release NT
b. Ca++ released
3. When AP arrives from #1, the RMP is at lower amplitude due to the prior depolarization from #3.
4. Since #1 is partially depolarized, there is less Ca++ than normal to enter the postsynaptic membrane & flux inward. (Due to the pre-release earlier)
5. With less Ca++, there will be less NTM (exocytosis) released between #1 and #2.
a. Tendency for it to not fire because we have not released enough NT  Therefore EPSP is not what you would expect

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Feedback Inhibition (Lateral/Recurrent Inhibition) characteristics

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i. Utilizes Renshaw cells (inhibitory interneurons)
1. The most rapidly firing 2nd Order sensory neuron depresses the activity of adjacent, less-active 2nd Order sensory neurons
ii. A contrast between active and less-active neurons is enhanced
1. results in an enhancement of the discrimination of stimuli (i.e. crunching noise in ear when eating)
a. Signal:Noise ratio becomes larger
b. Allows for better discrimination of sensations

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Feedforward Inhibition (Reciprocal Inhibition) characteristics

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i. One or more than one neuron inhibits another neuron or another group of neurons
ii. There are a limited # of competing responses are expressed while the others are inhibited
iii. Must shut down antagonist (extensors if wanting to use flexors)
iv. Monosynaptic reflex arc: knee jerk
1. Renshaw cells send an inhibitory message to knee flexors
2. LMN sends an excitatory message to knee extensors

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Descending Supraspinal Inhibitory Mechanisms (Distal inhibition) characteristics

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i. Information coming from brain or brain stem and tells things in spinals cord what to do
ii. Involves 2nd order sensory neuron to send less info (ex: Pain after initial injury is high and it decreases over time due to this mechanism)
iii. Information coming from above inhibits mechanisms in the spinal cord & LMN fire less
iv. Naturally occurring pathway that deals with pain must be activated
v. Activated via thought process that sends neurons to influence activity
vi. Activation releases endorphins to reduce noxious stimulation

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neural regulation definition

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mechanism by which CNS channels and sorts/focuses information

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neural processing- Convergence definition

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i. Many neurons synapse on a single neuron
ii. Result in focused input (gets concentrated)

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neural processing- divergence definition

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i. Means by which information from one neuron is spread to others
ii. Enhancing spread of information

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neural processing- serial

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i. Neurons are arranged sequentially (i.e. 1st-2nd-3rd Order neurons)
ii. Ascending (sensory) & descending (motor) pathways

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neural processing- parallel

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i. Information is conveyed in parallel sequences
ii. More than one pathway; two serial pathways that run parallel
iii. Involved with rehabilitation

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Alzheimer’s disease & the Neuronal Cytoskeleton characterized

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characterized by the disruption of the cytoskeleton of neurons in the cerebral cortex, a region of the brain crucial for cognitive function.

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severity of the dementia is correlated w/

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the # & distribution of neurofibrillary tangles, the “tombstones” of dead & dying neurons.

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causes of mental retardation

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-genetic disorders
-accidents during pregnancy & childbirth
-poor nutrition during pregnancy
-environmental impoverishment (the lack of good nutrition, socialization & sensory stimulation)

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dendritic spines characteristics in mental retardation

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a. there are changes in dendritic structure – fewer dendritic spines & the spines they do have are unusually long & thin
b. extent of spine changes is well correlated w/the degree of mental retardation
c. resemble those of a fetus in mentally retarded children
d. normal synaptic development depends on the environment during infancy & early childhood.
e. Deprivation-induced changes in the brain can be reversed if intervention occurs early enough

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Scorpion toxin functions as:

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plug on the pore (potassium channels) & it interacts w/ions inside the pore

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Intracellular recording of AP characteristics

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requires impaling the neuron/axon w/a microelectrode.
a. Challenging due to the small size of neurons
b. Goal – to measure the potential difference between the tip of the intracellular electrode & another electrode place din a solution bathing the neuron
c. Potential difference is displayed using an oscilloscope

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extracellular recording of AP characteristics

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a. Measure using an electrode & ground – electrode can be a thin insulated wire or fine glass capillary filled w/a salt solution
b. w/out AP the difference is w/AP characterized by a brief, alternation voltage difference
c. when AP arrives positive charges flow away from electrode into the neuron, & after AP passes positive charges flow out across the membrane toward the electrode.

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hydrocepalus mechanism

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1. CSF from choroid plexus -> ventricular system-> subarachnoid space -> if impaired, fluid will back up & cause a swelling of the ventricles = hydrocephalus “water head”

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hydrocephalus treatment

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inserting a tube into the swollen ventricle & draining off the excess fluid

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hydrocephalus symptoms

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-Typically accompanied by severe headache, caused by the distention of nerve ending in the meninges

-more serious in adults b/c skull cannot expand & intracranial pressure increases; brain tissue is compressed, impairing function & leading to death if left untreated

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Anencephaly definition

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failure of the anterior neural tube to close
a. Characterized by degeneration of the forebrain & skull; always fatal

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spina bifida definition

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– failure of the posterior neural tube to close
a. Characterized by defect in the meninges & vertebrae overlying the posterior spinal cord
b. Usually not fatal but does require extensive & costly medical care

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folic acids while pregnant importance

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green leafy vegetables, liver, yeast, eggs, beans, & oranges
a. Average intake is only ½ what is recommended to prevent birth defects (0.4 mg/day)
b. Recommend taking multivitamins w/ folic acid before planning pregnancy.

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Critical period of development definition

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may be defined as a period of time in which intercellular communication alters a cells fate.
a. Found when transplanting a piece of an early embryo from one location to another often caused the “donor” tissue to take on the characteristics of the “host,” but only if transplanted during a well-defined time period.
b. The intercellular communication that altered the physical characteristics (phenotype) of the transplanted cells was mediated by both contact & chemical signals