Nervous Tissues

Front 1

Functions of Nervous Tissues

Back 1

1. sensing changes with sensory receptors (sensation)
2. interpreting & remembering changes (integration center)
3. reacting to those changes with effectors
In short: communication system, regulator/control system, and command system)

Front 2

What is a ligand?

Back 2

ion molecule that bind with protein

Front 3

2 types of Ion Channels

Back 3

1. Leakage (non-gated) channel)
2. Gated channels:
- voltage gated
- ligand gated
- mechanically gated

Front 4

Leakage (non-gated) Channel

Back 4

* passive (facilitated diffusion)
* always open
* nerve cells have more K+ than Na+ leakage channel
* resulting membrane permeability to K+ is higher
* resting membrane potential is -70mV in nerve tissue

Front 5

Gated Channels

Back 5

1. active open/close in response to a stimulus resulting in neuron excitability
2. Types of Gated Channels:
a. Voltage channel:
* open/close in response to change in voltage
* in membranes of sarcolemma/axolemma (skeletal muscle cells), not in motor-end plates
b. Ligand Gated:
* open/close in response to particular chemical stimuli (hormone, neurotransmitter) bind on receptors
* only on motor-end plates
c. Mechanically-gated channel:
* open/close with mechanical stimulations (stretching, pressure, vibrations)
* on smooth muscle cells

Front 6

Electrical Signals in Neurons

Back 6

* Neurons are highly excitable due to Voltage Difference Across the Membrane
* Communicate with 2 types of electrical signals:
1. Action-Potential: all/nothing, travel long distances
2. Graded Potential: local membrane changes only
* In living cells, flow of ions occurs via ion channels in the cell membranes

Front 7

Resting Membrane Potential

Back 7

* Is the negative ions along inside of cell membrane and positive ions along the outside
--potential energy difference at rest is -70mV
--cell is then "polarized"

Front 8

Resting Membrane Potential Exist Because:

Back 8

1. concentration of ions is different inside and outside
--ECF si rich in Na+ and Cl-
--Cytosol is full of K+, Phosphate and amino acids

2. Membrane permeability is different between Na+ and K+
-- greater permeability for K+ (50-100)
-- inflow of Na+ can't keep up with outflow of K+
-- Na/K pump removes Na+ as it leaks into cell
-- Na/K pump ejects 3Na+ for each 2K+ ions into the cell (ratio is 3:2 for Na+ entry to K+loss via passive channels)
--Resting membrane potential is -90mV (equilibrium potential for K+)
--Typical neuron has resting membrane potential of -70mV

Front 9

Graded Potentials

Back 9

= Small deviations from resting potential of -70mV
* hyperpolarization = membrane has become more negative
* depolarization =
membrane has become more positive (less negative)

Front 10

Local Potentials:

Back 10

= Local disturbances in membrane potential
-- aka: graded potentials caused by depolarizing of the inside of plasma membrane
-- happens when neuron is stimulated by chemicals, light, heat or mechanical disturbance.
-- depolarization decreases potential across cell membrane due to opening of gated Na+ channels
* Na+ rushes in down concentration and electrical gradients
* Na+ diffuses for short distance inside membrane producing a change in voltage called a LOCAL POTENTIAL

Front 11

Local Potential (L/P or G/P)
vs
Action Potential (A/P)

Back 11

* L/P are graded (vary in magnitude accord. to stimulus strength)
* L/P are decremental (get weaker the farther they spread)
* L/P are reversible as K+ diffuses out of the cell
* L/P can either excitatory or inhibitory

Front 12

How do Graded Potentials Arise?

Back 12

1. Source of stimuli:
-- mechanical stimulation of membranes with mechanical gated ion channels (pressure)
-- chemical stimulation of membranes with ligand gated ion channels (neurotransmitter)
2. Graded/post-synaptic/ receptor or generator potential
-- ions flow through ion channels and change membrane potential locally
-- amount of change varies with strength of stimuli
3. Flow of current (ions) is local change only

Front 13

Action Potential

Back 13

-- Series of rapidly occurring events that change and then restore the membrane potential of a cell to its resting state
-- Ion channels open, Na+ rushes in (depolarization), K+ rushes out (repolarization)
-- All-or-none principal = with stimulation, either happens one specific way or not at all (lasts 1/1000 of a second)
-- Travels (spreads) over surface of cell without dying out

Front 14

Depolarizing Phase of Action Potential

Back 14

-- Chemical or mechanical stimulus causes a graded potential to reach at least threshold (-55mV)
-- Voltage-gated Na+ channels open & Na+ rushes into cell
* in resting membrane, inactivation gate of sodium channel is open & activation gate is closed (Na+ can not get in)
* when threshold (-55mV) is reached, both open & Na+ enters
* inactivation gate closes again in few ten-thousandths of second
* only a total of 20,000 Na+ actually enter the cell, but they change the membrane potential considerably (up to +30mV)
--Positive feedback process

Front 15

Re-polarizing Phase of Action Potential

Back 15

* When threshold potential of
-55mV is reached, voltage-gated K+ channels open
* K+ channel opening is much
slower than Na+ channel
opening (which causing depolarization)
* When K+ channels finally do open, the Na+ channels have already closed (Na+ inflow stops)
* K+ outflow returns membrane potential to -70mV
* If enough K+ leaves the cell, it will reach a -90mV membrane potential and enter the after-hyperpolarizing phase
* K+ channels close and the membrane potential returns to the resting potential of -70mV

Front 16

What is Refractory Period of Action Potential?

Back 16

period of time during which neuron can't generate another action-potential

Front 17

Types of Refractory Periods

Back 17

1. Absolute refractory period
-- even very strong stimulus will not begin another AP
-- inactivated Na+ channels must return to the resting state before they can be reopened
-- large fibers have absolute refractory period of 0.4 msec and up to 1000 impulses per second are possible
2. Relative refractory period
-- a supra-threshold stimulus will be able to start an AP
-- K+ channels are still open, but Na+ channels have closed

Front 18

Summary of Action Potential

Back 18

* Resting membrane potential is -70mV
* Depolarization is the change from -70mV to +30 mV
* Repolarization is the reversal from +30 mV back to -70 mV)

Front 19

Propagation of Action Potential

Back 19

= An action potential spreads (propagates) over the surface of the axon membrane
* as Na+ flows into the cell during depolarization (voltage of adjacent areas is effected and their voltage-gated Na+ channels open)
* self-propagating along the membrane

-- The traveling action potential is called a NERVE IMPULSE

Front 20

(Local) Anesthetics

Back 20

-- Prevent opening of voltage-gated Na+ channels
-- Nerve impulses cannot pass the anesthetized region
-- i.e: Novocaine and lidocaine

Regional Anesthetics:
-- chemicals given @ spinal cord/plexus to affect several nerves (ie: epidural)
General Anesthetics:
-- affect synaptic transmission some ESPS (depolarized), some are IPSP (hyper-polarized) >>deals with perception

Front 21

Continuous Conduction
vs
Saltatory Conduction

Back 21

1. Continuous conduction (unmyelinated fibers):
step-by-step depolarization of each portion of the length of the axolemma
2. Saltatory conduction
-- depolarization only at nodes of Ranvier where there is a high density of voltage-gated ion channels
-- current carried by ions flows through extracellular fluid from node to node (conduction hops between node of Ranvier

Front 22

Speed of Impulse Propagation

Back 22

the propagation speed of a nerve impulse is not related to stimulus strength
>> larger, myelinated fibers conduct impulses faster due to the size and saltatory conduction

Front 23

Fiber types

Back 23

1. Type A fibers
-- largest (5-20 microns, 130m/sec)
-- myelinated somatic sensory and motor to skeletal muscle
2. Type B fibers
-- medium (2-3 micron, 15m/sec)
-- myelinated visceral sensory and autonomic pre-ganglionic fibers
3. Type C fibers
-- smallest (.5-1.5 micron, 2m/sec)
-- un-myelinated sensory and autonomic motor fibers

Front 24

How do we differentiate a light touch from firmer touch?
(Encoding of Stimulus Intensity)

Back 24

1. Frequency of impulses
-- firm pressure generates impulses at a higher frequency
2. Number of sensory neurons activated
-- firm pressure stimulates more neurons than does a light touch

Front 25

Action Potentials in Nerve and Muscle

Back 25

1. Entire muscle cell membrane versus only the axon of the neuron is involved
2. Resting membrane potential
-- nerve is -70mV
-- skeletal & cardiac muscle is closer to -90mV
3. Duration:
-- nerve impulse is 1/2 to 2 msec
-- muscle action potential lasts 1-5 msec for skeletal & 10-300msec for cardiac & smooth
3. Fastest nerve conduction velocity is 18 times faster than velocity over skeletal muscle fiber

Front 26

Comparison of Graded & Action Potentials

Back 26

1. Origin
-- GPs arise on dendrites and cell bodies
-- APs arise only at trigger zone on axon hillock
2. Types of Channels
-- AP is produced by voltage-gated ion channels
-- GP is produced by ligand or mechanically-gated channels
3. Conduction
-- GPs are localized (not propagated)
-- APs conduct over the surface of the axon
4. Amplitude
-- amplitude of the AP is constant (all-or-none)
-- amplitude of GP vary depending upon stimulus
5. Duration
-- The duration of the GP is as long as the stimulus lasts
6. Refractory period
-- AP has a refractory period due to the nature of the voltage-gated channels, and the GP has none.

Front 27

Signal Transmission @ Synapses -- 2 Types of Synapses

Back 27

1. Electrical
-- ionic current spreads to next cell through gap junctions
-- faster, two-way transmission & capable of synchronizing groups of neurons
2. Chemical
-- one-way information transfer from a presynaptic neuron to a postsynaptic neuron
* axodendritic: from axon to dendrite
* axosomatic: from axon to cell body
* axoaxonic: from axon to axon

Front 28

Chemical Synapses

Back 28

-- Action potential reaches end bulb and voltage-gated Ca+ 2 channels open
-- Ca+2 flows inward triggering release of neurotransmitter
-- Neurotransmitter crosses synaptic cleft & binding to ligand-gated receptors
(the more neurotransmitter released, the greater the change in potential of the postsynaptic cell)
-- Synaptic delay is 0.5 msec
-- One-way information transfer

Front 29

Nervous System Divisions

Back 29

1. Central nervous system (CNS): brain and spinal cord
2. Peripheral nervous system (PNS): cranial and spinal nerves that contain both sensory and motor fibers
-- connects CNS to muscles, glands & all sensory receptors

Front 30

Subdivisions of PNS

Back 30

1. Somatic (voluntary) nervous system (SNS):
-- neurons from cutaneous and special sensory receptors to the CNS (voluntary effectors)
-- motor neurons to skeletal muscle tissue
2. Autonomic (involuntary) nervous systems
-- sensory neurons from visceral organs to CNS
-- motor neurons to smooth & cardiac muscle and glands:
a. sympathetic division (speeds up heart rate)
b. parasympathetic division (slow down heart rate)
3. Enteric nervous system (ENS)
-- involuntary sensory & motor neurons control GI tract
-- neurons function independently of ANS & CNS

Front 31

Neurons

Back 31

* Functional unit of nervous system
* Have capacity to produce APs (electrical excitability)
* Cell body
-- single nucleus with prominent nucleolus
-- Nissl bodies (chromatophilic substance)
-- abundant rough ER & free ribosomes for protein synthesis
-- neurofilaments give cell shape and support
-- microtubules move material inside cell
-- lipofuscin pigment clumps (harmless aging)
* Cell processes = dendrites & axons
* Amitotic (your cell is as old as you are)

Front 32

Dendrites

Back 32

-- Conducts impulses towards the cell body
-- Typically short, highly branched & unmyelinated
-- Surfaces specialized for contact with other neurons
-- Contains neurofibrils & Nissl bodies

Front 33

Axons

Back 33

-- Conduct impulses away from cell body
-- Long, thin cylindrical process of cell
-- Arises at axon hillock (trigger zone)
-- Impulses arise from initial segment (trigger zone)
-- Side branches (collaterals) end in fine processes (=axon terminals)
-- Swollen tips called synaptic end bulbs (synaptic terminals/ boutons) contain vesicles filled with neurotransmitters

Front 34

Axonal Transport (Axoplasmic Flow Diffusion)

Back 34

* Cell body is location for most protein synthesis
-- neurotransmitters & repair proteins
* Axonal transport system moves substances
1. slow axonal flow
-- movement in one direction only: away from cell body (remove waste)
-- movement at 1-5 mm per day
2. fast axonal flow
-- moves organelles & materials along surface of microtubules (200-400 mm per day)
-- transports in either direction
-- for use or for recycling in cell body

Front 35

Axonal Transport & Disease

Back 35

-- Fast axonal transport route by which toxins or pathogens reach neuron cell bodies
1. Tetanus (Clostridium tetani bacteria)
-- disrupts motor neurons causing painful muscle spasms
-- bacteria enter the body through a laceration or puncture injury
-- more serious if wound is in head or neck because of shorter transit time

Front 36

Functional Types of Neurons

Back 36

1. Sensory (afferent) neurons
-- receptors detect changes in body and external environment
-- this information is transmitted into brain or spinal cord
2. Interneurons (association neurons)
-- lie between sensory & motor pathways in CNS
-- 90% of our neurons are interneurons
-- process, store & retrieve information
3. Motor (efferent) neuron
-- send signals out to muscles & gland cells
-- organs that carry out responses called effectors

Front 37

Functional Classification of Neurons

Back 37

1. Sensory (afferent) neurons
-- transport sensory information from skin, muscles, joints, sense organs & viscera to CNS
2. Motor (efferent) neurons
-- send motor nerve impulses to muscles & glands
3. Interneurons (association) neurons
-- connect sensory to motor neurons
-- 90% of neurons in the body

Front 38

Variation in Neuronal Structure

Back 38

1. Multipolar neuron
-- most common
-- many dendrites/one axon
2. Bipolar neuron
-- one dendrite/one axon
-- olfactory, retina, ear
3. Unipolar neuron
-- sensory from skin & organs to spinal cord
4. Anaxonic neuron
-- many dendrites/no axon
-- help in visual processes

Front 39

Structural Classification of Neurons

Back 39

Based on number of processes found on cell body:
1. multipolar = several dendrites & one axon
most common cell type
2. bipolar neurons = one main dendrite & one axon
found in retina, inner ear & olfactory
3. unipolar neurons = one process only(develops from a bipolar)
are always sensory neurons

Front 40

Neuroglial Cells

Back 40

* Half of the volume of the CNS
* Smaller cells than neurons
50X more numerous
* Cells can divide
-- rapid mitosis in tumor formation (gliomas)
* 4 cell types in CNS
-- astrocytes
-- oligodendrocytes
-- microglia
-- ependymal
* 2 cell types in PNS
-- schwann cells
-- satellite cells

Front 41

Astrocytes

Back 41

* Star-shaped cells
* Form blood-brain barrier by covering blood capillaries
* Metabolize neurotransmitters
* Regulate K+ balance
* Provide structural support

Front 42

Oligodendrocytes

Back 42

* Most common glial cell type
* Each forms myelin sheath around more than one axons in CNS
* Analogous to Schwann cells of PNS

Front 43

Microglia (smallest)

Back 43

* Small cells found near blood vessels
* Phagocytic role -- clear away dead cells
* Derived from cells that also gave rise to macrophages & monocytes

Front 44

Ependymal Cells

Back 44

* Form epithelial membrane lining cerebral cavities & central canal
* Modify cerebrospinal fluid (CSF)
-- Coroid Plexus produces CSF

Front 45

Satellite Cells

Back 45

* Flat cells surrounding neuronal cell bodies in peripheral ganglia
* Support neurons in the PNS ganglia

Front 46

Schwann Cells

Back 46

* Cells encircling PNS axons
* Each cell produces part of the myelin sheath surrounding an axon in the PNS

Front 47

Axon Coverings in PNS

Back 47

* All axons surrounded by a lipid & protein covering (myelin sheath) produced by Schwann cells
* Neurilemma is cytoplasm & nucleus of Schwann cell
(gaps are called nodes of Ranvier)
* Myelinated fibers appear white
-- jelly-roll like wrappings made of lipoprotein (myelin is 20% protein, 80% lipid)
-- acts as electrical insulator
-- speeds conduction of nerve impulses
* Unmyelinated fibers
-- slow, small diameter fibers
-- only surrounded by neurilemma but no myelin sheath wrapping

Front 48

Myelination in PNS

Back 48

* Schwann cells myelinate (wrap around) axons in the PNS during fetal development
* Schwann cell cytoplasm & nucleus forms outermost layer of neurolemma with inner portion being the myelin sheath
* Tube guides growing axons that are repairing themselves

Front 49

Un-myelinated Axons

Back 49

* Schwann cells hold small nerve fibers in grooves on their surface with only one membrane wrapping

Front 50

Myelination in CNS

Back 50

* Oligodendrocytes myelinate axons in the CNS
* Broad, flat cell processes wrap about CNS axons, but the cell bodies do not surround the axons
* No neurilemma is formed
* Little regrowth after injury is possible due to the lack of a distinct tube or neurilemma

Front 51

Regeneration and Repair

Back 51

1. Plasticity maintained throughout life
-- sprouting of new dendrites
-- synthesis of new proteins
-- changes in synaptic contacts with other neurons
2. Limited ability for regeneration (repair)
-- PNS can repair damaged dendrites or axons
-- CNS no repairs are possible

Front 52

Neurogenesis in the CNS

Back 52

1. Formation of new neurons from stem cells was not thought to occur in humans
-- in 1992 a growth factor was found that stimulates adult mice brain cells to multiply
-- in 1998 new neurons found to form within adult human hippocampus (area important for learning)
2. Factors preventing neurogenesis in CNS
-- inhibition by neuroglial cells, absence of growth stimulating factors, lack of neurolemmas, and rapid formation of scar tissue

Front 53

Repair Within the PNS-- part I

Back 53

1. Axons & dendrites may be repaired if
-- neuron cell body remains intact
-- schwann cells remain active and form a tube
-- scar tissue does not form too rapidly
2. Chromatolysis
-- 24 to 48 hours after injury, Nissl bodies break up into fine granular masses

Front 54

Repair Within the PNS -- part II

Back 54

3. Between 5 to 5 days:
-- Wallerian degeneration occurs (breakdown of axon & myelin sheath distal to injury)
-- retrograde degeneration occurs back one node
4. Within several months, regeneration occurs
-- neurolemma on each side of injury repairs tube (schwann cell mitosis)
-- axonal buds grow down the tube to r

Front 55

Gray and White Matter

Back 55

* White matter = myelinated processes (white in color)
* Gray matter = nerve cell bodies, dendrites, axon terminals, bundles of unmyelinated axons and neuroglia (gray color)
-- In the spinal cord = gray matter forms an H-shaped inner core surrounded by white matter
-- In the brain = a thin outer shell of gray matter covers the surface & is found in clusters called nuclei inside the CNS

Front 56

Excitatory Cholinergic Synapse

Back 56

* Nerve signal opens voltage-
gated calcium channels
* Triggers release of ACh which crosses synapse
* ACh receptors trigger opening of Na+ channels producing local potential (postsynaptic potential)
* When reaches -55mV, triggers AP

Front 57

Inhibitory GABA-ergic Synapse

Back 57

* Nerve signal triggers release of GABA (GamaAminoButyric Acid) which crosses synapse
* GABA receptors trigger opening of Cl- channels producing hyper-polarization
* Postsynaptic neuron now less likely to reach threshold

Front 58

Excitatory Adrenergic Synapse

Back 58

* Neurotransmitter is NE (Norepinephrine)
* Acts through 2nd messenger systems (cAMP: cyclic AMP)
* Receptor is an integral membrane protein associated with a G protein, which activates adenylate cyclase, which converts ATP to cAMP
* cAMP has multiple effects
-- synthesis of new enzymes
-- activating enzymes
-- opening ligand gates
-- produce a postsynaptic potential

Front 59

Cessation & Modification of the Signal

Back 59

1. Mechanisms to turn off stimulation
-- diffusion of neurotransmitter away from synapse into ECF where astrocytes return it to the neurons
-- synaptic knob reabsorbs amino acids and monoamines by endocytosis & breaks them down with monoamine oxidase
-- acetylcholinesterase (AChE) degrades ACh in the synaptic cleft (choline reabsorbed & recycled)
2. Neuromodulators modify synaptic transmission
-- raise or lower number of receptors
-- alter neurotransmitter release, synthesis or breakdown
>> nitric oxide stimulates neurotransmitter release

Front 60

Neural Integration

Back 60

1. More synapses a neuron has the greater its information-processing capability
-- cells in cerebral cortex with 40,000 synapses
-- cerebral cortex estimated to contain 100 trillion synapses
2. Chemical synapses are decision-making components of the nervous system
-- ability to process, store & recall information is due to neural integration
3. Neural integration is based on types of postsynaptic potentials produced by neurotransmitters

Front 61

Post-synaptic Potentials

Back 61

1. Excitatory postsynaptic potentials (EPSP)
-- a positive voltage change causing postsynaptic cell to be more likely to fire (result from Na+ flowing into the cell)
-- glutamate & aspartate are excitatory neurotransmitters
2. Inhibitory postsynaptic potentials (IPSP)
-- a negative voltage change causing postsynaptic cell to be less likely to fire (hyper-polarize) >>result of Cl- flowing into the cell or K+ leaving the cell.
-- glycine & GABA are inhibitory neurotransmitters
3. ACh & norepinephrine vary depending on cell

Front 62

Excitatory & Inhibitory Potentials

Back 62

* The effect of a neurotransmitter can be either excitatory or inhibitory
1. a depolarizing postsynaptic potential is called an EPSP
-- it results from the opening of ligand-gated Na+ channels
-- the postsynaptic cell is more likely to reach threshold
2. an inhibitory postsynaptic potential is called an IPSP
-- it results from the opening of ligand-gated Cl- or K+ channels
-- it causes the postsynaptic cell to become more negative or hyper-polarized
-- the postsynaptic cell is less likely to reach threshold

Front 63

Removal of Neurotransmitter

Back 63

1. Diffusion
-- move down concentration gradient
2. Enzymatic degradation
-- acetylcholinesterase (AChE)
3. Uptake by neurons or glia cells
-- neurotransmitter transporters
-- Prozac = serotonin reuptake
inhibitor

Front 64

Spatial Summation

Back 64

Summation of effects of neurotransmitters released from several end bulbs onto one neuron (at once), multipolar neuron

Front 65

Temporal Summation

Back 65

Summation of effect of neurotransmitters released from 2 or more firings of the same end bulb in rapid succession onto a second neuron (over time/ in succession)

Front 66

Three Possible Responses

Back 66

1. Small EPSP occurs
-- potential reaches -56 mV only
2. An impulse is generated
-- threshold was reached
-- membrane potential of at least -55 mV
3. IPSP occurs
-- membrane hyper-polarized
-- potential drops below -70 mV

Front 67

Strychnine Poisoning

Back 67

* In spinal cord, Renshaw cells normally release an inhibitory neurotransmitter (glycine) onto motor neurons preventing excessive muscle contraction
* Strychnine binds to and blocks glycine receptors in the spinal cord
*Massive tetanic contractions of all skeletal muscles are produced
-- when the diaphragm contracts & remains contracted, breathing can not occur

Front 68

Neurotransmitter Effects

Back 68

1. Neurotransmitter effects can be modified
-- synthesis can be stimulated or inhibited
-- release can be blocked or enhanced
-- removal can be stimulated or blocked
-- receptor site can be blocked or activated
2. Agonist (work with)
-- anything that enhances a transmitters effects
3. Antagonist (work against)
-- anything that blocks the action of a neurotransmitter

Front 69

Small-Molecule Neurotransmitters (part I)

Back 69

1. Acetylcholine (ACh)
-- released by many PNS neurons & some CNS
-- excitatory on NMJ but inhibitory at others
-- inactivated by AChE (acetylcholinesterase)
2. Amino Acids
-- glutamate released by nearly all excitatory neurons in the brain (inactivated by glutamate specific transporters)
-- GABA is inhibitory neurotransmitter for 1/3 of all brain synapses (Valium is a GABA agonist -- enhancing its inhibitory effect)

Front 70

Small-Moleculle Neurotransmitters (part II)

Back 70

3. Biogenic Amines
-- modified amino acids (tyrosine)
* norepinephrine: regulates mood, dreaming, awakening from deep sleep
* dopamine: regulating skeletal muscle tone
* serotonin: control of mood, temperature regulation, & induction of sleep
-- removed from synapse & recycled or destroyed by enzymes (monoamine oxidase or catechol-0-methyltransferase)

Front 71

Small-Molecule Neurotransmitters (part III)

Back 71

4. ATP and other purines (ADP, AMP and adenosine)
-- excitatory in both CNS & PNS
-- released with other neurotransmitters (ACh & NE)
5. Gases (nitric oxide or NO)
-- formed from amino acid arginine by an enzyme
-- formed on demand and acts immediately
**diffuses out of cell that produced it to affect neighboring cells
**may play a role in memory & learning
-- first recognized as vasodilator that helps lower blood pressure

Front 72

Neuropeptides

Back 72

* 3-40 amino acids linked by peptide bonds
* Substance P: enhances our perception of pain
* Pain relief
-- enkephalins: pain-relieving effect by blocking the release of substance P
-- acupuncture may produce loss of pain sensation because of release of opioids-like substances such as endorphins or dynorphins

Front 73

Neuronal Circuits

Back 73

* Neurons in the CNS are organized into neuronal networks
* A neuronal network may contain thousands or even millions of neurons.
* Neuronal circuits are involved in many important activities
-- breathing
-- short-term memory
-- waking up

Front 74

Types of Neuronal Circuits

Back 74

1. Diverging -- single cell stimulates many others
2. Converging -- one cell stimulated by many others
3. Reverberating -- impulses from later cells repeatedly stimulate early cells in the circuit (short-term memory)
4. Parallel-after-discharge -- single cell stimulates a group of cells that all stimulate a common postsynaptic cell (math problems)

Front 75

Multiple Sclerosis (MS)

Back 75

* Autoimmune disorder causing destruction of myelin sheaths in CNS and PNS
-- sheaths becomes scars or plaques
-- 1/2 million people in the U.S
-- appears between ages 20 and 40
-- females twice as often as males
* Symptoms include muscular weakness, abnormal sensations or double vision
* Remissions & relapses result in progressive, cumulative loss of function

Front 76

Epilepsy

Back 76

* The second most common neurological disorder
-- affects 1% of population
* Characterized by short, recurrent attacks initiated by electrical discharges in the brain
-- lights, noise, or smells may be sensed
-- skeletal muscles may contract involuntarily
-- loss of consciousness
* Epilepsy has many causes, including;
-- brain damage at birth, metabolic disturbances, infections, toxins, vascular disturbances, head injuries, and tumors

Front 77

Pre-Synaptic Inhibition

Back 77

One presynaptic neuron suppresses another one.
-- Neuron I releases inhibitory neurotransmitter GABA
prevents voltage-gated calcium channels from opening in neuron S so it releases less or no neurotransmitter onto neuron R and fails to stimulate it.

Front 78

Neural Coding

Back 78

* Qualitative information (salty or sweet) depends upon which neurons are fired
* Qualitative information depend on:
-- strong stimuli excite different neurons (recruitment)
-- stronger stimuli causes a more rapid firing rate
>>CNS judges stimulus strength from firing frequency of sensory neurons (600 APs /sec instead of 6 APs/sec)

Front 79

Learning & Memory

Back 79

* Learning is acquiring new knowledge
* Memory is retaining that knowledge:
1. short-term memory:
-- recall phone number while dialing
-- depends upon electrical events (reverberating circuits)
2. long-term memory
-- frequent retrieval of specific information helps with memory consolidation (learning)
-- structural or biochemical changes occurs (ie: increase in dendrites, enlarge end bulbs, increase in presynaptic terminals or formation of additional membrane receptors)
* Recently acquired memory lost first with coma or shock treatments

Front 80

Memory & Synaptic Plasticity

Back 80

* Memories are not stored in individual cells
* Physical basis of memory is a pathway of cells (aka: memory trace/engram)
-- new synapses or existing synapses have been modified to make transmission easier (synaptic plasticity)
* Synaptic potentiation
-- process of making transmission easier
-- correlates with different forms of memory (immediate, short term, and long term memory)

Front 81

Immediate Memory

Back 81

* Ability to hold something in your thoughts for just a few seconds
* Feel for the flow of events (sense of the present)
* Our memory of what just happened “echoes” in our minds for a few seconds
-- reverberating circuits

Front 82

Short Term Memory

Back 82

1. Lasts from a few seconds to several hours
-- quickly forgotten if distracted with something new
2. Working memory allows us to keep something in mind long enough search for keys, dial the phone
-- reverberating circuits
3. Facilitation causes memory to longer lasting
-- tetanic stimulation (rapid, repetitive signals) causes Ca+2 accumulates & cell becomes more likely to fire
4. Post-tetanic potentiation (to jog a memory)
-- Ca+2 level in synaptic knob has stayed elevated long after tetanic stimulation, so little stimulation will be needed to recover that memory

Front 83

Long Term Memory

Back 83

* May last up to a lifetime
* Types of long-term memory
1. Declarative: retention of facts as text/words
2. Procedural: retention of motor skills (ie:keyboard)
* Physical remodeling of synapses with new branching of axons or dendrites
* Molecular changes called long-term potentiation
-- Tetanic stimulation causes ionic changes (Ca+2 entry)
1. neuron produces more neurotransmitter receptors
2. synthesizes more protein used for synapse remodeling
3. releases nitric oxide signals presynaptic neuron to release more neurotransmitter

Front 84

Alzheimer Disease

Back 84

* 100,000 deaths/year
* 11% of population over 65; 47% by age 85
* Symptoms
-- memory loss for recent events, moody, combative, lose ability to talk, walk, and eat
* Diagnosis confirmed at autopsy
-- atrophy of gyri (folds) in cerebral cortex
-- neurofibrillary tangles & senile plaques
* Degeneration of cholinergic neurons & deficiency of ACh and nerve growth factors
* Genetic connection confirmed for some forms

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Parkinson's Disease

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* Progressive loss of motor function beginning in 50’s or 60’s -- no recovery
-- degeneration of dopamine-releasing neurons in substantia nigra (prevents excessive activity in motor centers/ basal ganglia)
-- involuntary muscle contractions (pill-rolling motion, facial rigidity, slurred speech, illegible handwriting, slow gait)
* Treatment is drugs and physical therapy
-- dopamine precursor can cross blood-brain barrier
-- deprenyl (MAO inhibitor) slows neuronal degeneration
-- surgical technique to relieve tremors