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268 Cards in this Set

  • Front
  • Back
Forebrain
Telencephalon + Diencephalon
Mesencephalon
Midbrain
Metencephalon
Pons + cerebellum
Myelencephalon
Medulla
Rhombencephalon
Metecephalon + Myelencephalon (Pons, Cerebellum, Medulla)
Brainstem
midbrain, pons, medulla
Brain
Brainstem, cerebellum, forebrain
White matter
myelinated axons (cortex inwards, spinal cord outwards)
Grey matter
cell bodies (cortex outwards, spinal cord inwards)
Association (White matter)
Mediates communication between areas WITHIN a hemisphere
Commissural (white matter)
Mediates communication between areas BETWEEN hemispheres

Major Commissural = Corpus Collosum
Projection (white matter)
Mediates communication between cortical and subcortical sites

Major Projection - Internal capsule
Lateral Geniculate Nucleus
Location?
Function?
Lateral Geniculate Nucleus
Location: Thalamus (Diencephalon)
Function: relay station between retina and primary visual cortex
Suprachiasmatic nucleus
Location?
Function?
Suprachiasmatic nucleus
Location: hypothalamus (Diencephalon)
Function: trigger circadian clock
Pretectal Nucleus
Location?
Function?
Pretectal Nucleus
Location: Midbrain (Mesencephalon)
Function: afferent limb of pupillary light reflex
Superior Colliculus
Location?
Function?
Superior Colliculus
Location: Midbrain (Mesencephalon)
Function: Contribute to Eye Movements
Magnocellular
- Dorsal (parietal pathway)
- Depth and Motion (location & movement)
- 1st 2 layers
- detects fast moving stimulus
Parvocellular
- Ventral (temporal pathway)
- Form & Color (Color vision & acuity)
- projects deeper into the primary visual cortex
-layers 3-6
What portion of the visual field is lost at lesion 1?
Monocular Blindness
Lesion: Optic Nerve

total blindness in 1 eye
What portion of the visual field is lost at lesion 2?
Lesion: Optic Chiasm
Bitemporal hemianopia
Cut Nasal Retina Input.
What would be lost on the visual field in lesion 4?
Superior Homonymous Quandrantanopia
What part of the visual field would be lost at lesion 7?
Macular Sparing
Fovea Spared.
notched hemifield
Where part of the visual field is lost in lesion 3?
Homonymous hemianopia
Lesion in Optic tract or Posterior cerebral artery dysfunction
Inferior colliculus
Location?
Function?
Inferior colliculus
Location: Midbrain (Mesencephalon)
Function: involved in the localization of sound
Type of receptor on ON bipolar cells
E (Glutamate [metabotropic receptor])
Superior Visual Field
is temporal/parietal radiation?
is above/below calcarine sulcus?
Superior Visual Field
is temporal radiation
is below calcarine sulcus
Inferior Visual Field
is temporal/parietal radiation?
is above/below calcarine sulcus?
Inferior Visual Field
parietal radiation
above calcarine sulcus
Ocular Dominance Columns
Alternating by which eye input comes from [ipsilateral & contralateral]
Orientation Columns
Light Orientation (horizontal, vertical)
Dark Current
- photoreceptors are depolarized and releasing glutamate in the dark.
What is the neurotransmitter for photoreceptors?
glutamate
Protanopia
Red cone color blindness
Deuteranopia
Green Cone Color Blindness
What is the rarest type of color blindness?
Blue
What kind of receptor is a ON Bipolar cell?
Glutamate (metabotropic)
What kind of receptor is a OFF Bipolar cell?
Ionotropic
Epidural Hematoma
- Hemorrhage of ARTERY (usually Middle Meningeal)
- Biconvex shape
- Lucid for a while and then die suddenly
Subdural Hematoma
- Hemorrhage of bridging VEIN
- Crescent Shaped
- Venous System - lower pressure than arterial. = takes approx 4-6 weeks for symptoms.
- Vague Symptoms.
- Chronic rather than acute
- Trauma or Elderly
emx
homeobox gene
- deficiency = schizencephaly (split cortex)
otx
homeobox gene
- deficiency = epilepsy
hox genes
direct fate of cells within a segement
- ie. master gene in drosophilia
BMP (Bone morphogenic Protein)
- induction of neural plate
- Early - suppress neural differentiation and promotes epidermal tissue
- Later - is blocked so that ectoderm can form neural plate
PMP22
mutation of PMP22 = Charcot Marie Tooth Syndrome

-PMP22 =produced in schwann cells for myelination
Sonic Hedgehog
- NOT a homeobox gene

- influences development of serotonergic neurons - hindbrain
dopaminergic neurons - posterior midbrain
oculomotor neurons - anterior midbrain
- secreted by notochord
- acts on floor plate to induce netrin formation
is a protein
Hensen's Node
Anterior-Posterior Hox gene expression
Radial Glia persist in adults as
Muller cells (Retina)
Bergman Glia (cerebellum)
astrotactin
proteins that mediate neuronal migration

if blocked = no cell migration

Receptor = Integrin
Reeler
large extracellular matrix glycoprotein

If Mutated - neurons fail to migrate past each other
- positions inverted

- Expressed in Cajal-Retzius cells - tell cells to 'get off' the glial monorail
Kallman's Syndrome
- no sense of smell
- no sexual maturation
PNS neural crest cells migrate along pathways that
LACK
1) axons tracts
2) organized glial structure
laminin
- made by Schwann cells after injury
- promotes neural outgrowth

Antibody against laminin = block neurite extension and outgrowth
What activates transcription of Hox genes?
Retionic Acid
- creates a Anterior- posterior gradient
What kind of neurons can move without radial glial cells?
neurons with Gonadotropin-releasing hormone

failure of GnRH migration = Kallman Syndrome = ↓ olfactory and sterile
Axon growth is influenced by:
Diffusible Molecules and Proteins from Extracellular Matrix

1. Pioneer Axon - leads the way. has extensive filopodia
2. Netrin - released by floor plate. causes axons to cross anterior commissure
3. Laminin - secreted by Schwann cells after accident; promotes neural outgrowth
4. Growth cone - enlarged axon extension. Receptors are on axon surface. cones may release enzymes to clear pathway and change substrate
Growth cone
enlarged axon extension. Receptors are on axon surface. cones may release enzymes to clear pathway and change substrate

- in axonal growth
Netrin
released by floor plate. causes axons to cross anterior commissure


- in axonal growth
Pioneer Axon
leads the way. has extensive filopodia


- in axonal growth
Leukemia Inhibitory Factor
- peptide secreted to change crest cells
- induces differentiation in immune system
agrin
released by nerve.
makes receptors on NMJ concentrate on end plate
semaphorin
short range inhibitory signal
Trembler mouse
- myelin formed to fail
- genetic defect in Schwann cells
Sciatic nerve tansplant experiment
Charcot Marie Tooth Diease
PMP22 mutation
gly to asp (amino acid substitution
- peripheral myelin fails to form properly
NCAM
Neural Cell Adhesion Molecule
- binds to itself and causes axons to stick to one another

- bound axons are wrapped by shared glia

-Fab part of antibody can disrupt bundling of growing axons
Nerve Growth Factor
- from snake venom and salivary glands
- causes growth of neurites
- required for sensory cell outgrowth
- antiNGF = smaller Dorsal Root Ganglion
- affects Sympathetic NS but not Parasympathetic
- each cell types CRITICAL PERIOD = survival depends on supply of NGF
- Transported into Soma, regulates synthesis of NORE via
1 tyrosine hydroxlase, dopamine b-hydroxylase
Brain derived neurotropic factor (BDNF)
- protein in CNS that promotes survival of DRG
- very similar to NGF
- can rescue cells from neuronal death if administered
Neurotrophin
- Family of growth factors, including BDNF and NGF
- dimers with basic regions held together by cysteine residues

In Early development, before sensory neurons innervate target, Neurotrophin needed for:
- neural crest cells
-sensory neurons
-Dorsal Root Ganglion
-Trigeminal Ganglia
p75
low affinity, fast NGF receptor
found on neurons and non-neuronal cells
p140prototrk (trk)
high affinity receptor

- found only in neurons
- mediate cell survival and neurite outgrowth
- intracellular domain has Tyrosine Kinase
- activates Intracellular Signalling Pathways:
1. PLC
2. Phosphatidylinositol 3 Kinase
3. MAP Kinase
trkA
High affinity receptor for NGF
trkB
High affinity receptor for BDNT and NT-4/5
trkC
High affinity receptor fro NT-3
BDNF influences
retinal ganglion cell branching and remodeling

dendritic growth of cortical neurons

formation of ocular dominance columns within developing visual cortex
Ephrin
- responsible for repulsive interactions during cell signaling
- cell migration, axon pathfinding and cell intermingling
- part of receptor tyrosine kinases

ephrin-A2 and ephrin A-5 are in tectum
Thalidomide
- reduce limbs to flipper like appendages

1. primary effect = neurons
2. secondary effect = bone growth
Albinism
frequent miswiring of retinogeniculate connections
Microglia
macrophage of CNS
Astrocytes
- homeostatis at synapse
- regulates chemicals
- recycles Neurotransmitter
- building block of BBB
- Release antioxidants to protect neurons
- uptake of excess Neurotransmitters via transporters
- secretes cholesterol for neural development
Signals via IP3/Ca2+
oligodendrocytes
coats CNS with myelin
Ependymal Cells
Secretes CSF
Radial Glia
- Scaffold that developing neurons climb on

Persists in the adult as:
- Muller cells - retina - bidirectional communication with neurons

- Bergmann Glia - cerebellum - regulate synaptic plasticity
Bergmann Glia
Radial Glial cells in the cerebellum - regulate synaptic plasticity
Muller cells
Radial glia in retina - bidirectional communication with neurons
Schwann Cells
myelinate PNS axons
phagocytic activity
Satelitte cells
regulates external chemical environment.

- surround sensory, sympathetic, parasympathetic
Tanycytes
ependymal cells in 3rd ventricle. Bipolar cells that link CSF to neuroendrocrine events
Enteric Glial
analagous to CNS astrocyte but in Enteric Nervous system
Tripartite Synapse
close proximity of pre, post and glial cell

- both neuron and glia can release neurotropic factors
- Glial-cell derived neurotropic factor (GDNF)
- Brain derived Growth Factor (BDNF)
- Neurotropin-3
Perivascular Astrocytes
astrocytes that maintain blood flow and osmotic balance in brain
Tanycyte
bipolar cells that link CSF to neuroendocrine events.

- radial glial that differentiate with astrocyte like properties
Schwann cells
in PNS
- myelinate AND phagocytic activity
glial scar
- During trauma or ischemia
- astrocyte form scar to isolate neurons from each other

- presence of glial scar = limits the possibility of axonal regeneration in CNS
Astrocytes store _____________
glycogen
- can be converted to lactate and be used as an alternate supply of ATP
Astrocytes have what kind of receptors:

1. Ionotropic
2. Metabotropic
both
Spatial Buffering/Potassium Siphoning
- astrocytes take in K+ from extracellular fluid and redistributes to its neighbors (via gap junction)
- K+ from action potentails
Amyotrophic lateral sclerosis
loss of brain and spinal cord motor neurons

- mutation in Superoxide Dismutase and astrocytes
Gliosis
hyperplasia and hypertrophy of astrocytes in response to injury in CNS

= Glial Scar
Glial Fibrillary Acidic Protein (GFAP)
- encodes filament protein for mature astrocytes

Disease = Alexander Disease
Anterograde Degeneration
degeneration of the neuron postsynaptic to the damaged neuron

- Wallerian degeneration
- after the axon has been cut
Retrograde Degeneration
degeneration of the neuron, before the lesion
Chromatolysis
when lesion next to cell body
- swelling and movement of cell organelles away from the cell body
Multipolar neurons are

Efferent/Afferent
Efferent
Pseudounipolar neurons are:
Afferent
Bipolar cells are:

Motor/Sensory
Sensory
synaptic potentials

1. do not spread with decrement
2. spread with decrement
spread with decrement
action potentials

1. do not spread with decrement
2. spread with decrement
do not spread with decrement
Collateral Axon branch
branch of main axon that feeds back onto soma providing modulation of cell firing
Nissl body
histological sign of rough ER; site of protein synthesis
What is the main determinant of shape of the neuron?
cytoskeleton

ie. microtubules, neurofilaments, microfilaments"
Multiple Sclerosis
- degeneration of myelin in CNS
- autoimmune
- reduced axonal velocity
- CN II is only cranial nerve demyelinated in MS
as well as problems with hearing and balance (caused in brainstem, not CN)
Guillain-Barr Syndrome
-degeneration of myelin in PNS
- affects both myelin and axons themselves
Neurofilament
-most common filament in neurons
-highly stable
-undergo little turnover
- Scaffolding for cytoskeleton of neuron
Microtubule
-13 protofilaments forming a tubule (α/β)
- associated with dynein and kinesin
- damage to microtubule = cell death
- transport between nerve cell and soma"
Remak Fiber
unmyelinating Schwann cells that envelope small axons to regulate [K+]
Choroid Plexus
Ependymal cells - Group 1
Secretory, grouped by TIGHT JUNCTIONS
Ventricles & Central Canal
Ependymal cells - group 2
- Assists in CNS CSF circulation
joined by GAP JUNCTIONS
- solutes pass paracellularly
Resting potential of neuron
-65
Resting potential of skeletal muscle
-90
Resting membrane potential of photoreceptor
-40
In neurons, membrane potentials are affected by which ion?

K+
Ca2+
Na+
H+
K+
The main difference between neurons and glia is:
The main difference between neurons and glia is how they transfer info

Neurons: Action Potentials
Glial cells - Intra/Inter-cellular Ca2+ signalling
Dynein
"- fast RETROGRADE transport
- nerve ending back to soma
- motor protein for movement in cilia and flagella
- inactivated in soma and carried back to nerve ending
-ATPase
- carries lysozymes, enzymes and recycled vesicle membranes"
Kinesin
fast ANTEROGRADE transport
- soma to nerve ending
- ATPase
- allows attachment of large structures (vesicles, mitochondra)
- Kinesin is inactivated at nerve ending and carried back via retrograde"
What excites astrocytes?
[Ca2+] not voltage
Which is faster: electrical signaling or axonal transport?
Electrical Signaling
Channelopathies
dysfunctional ion channels
Cytotoxic Edema
edema following ischemia (interrupted blood supply)
- affects Grey more than white
- edema b/c failure to supply Na+/K+ pump with ATP = ions dissipate
- Increased Intracellular water and Na+ in edema fluid
- Clinical Disorders: Hypoxia, Water intoxication, Ischemia
Vasogenic Edema
blood vessels become permeable and fluid accumulates in extracellular space
The Membrane Potential (Vm) depends on
number of open channels for ions
conductances of the open ion channels
equilibrium potentials for those ions
What happens with lethal injection?
- Lethal Injection = KCl
-raise extracellular K+
- depolarizes excitable cells
- fails to generate another action potential b/c voltage gated Na+ channels are inactivated
Efferent neurons and Interneurons
have membrane proteins that are chemoreceptors for NT
Afferent
membrane receptors responding to a specific type of stimulus
Golgi Tendon Organ
Mechanoreceptor in muscle
- measure TENSION
- muscle mechanoreceptor measures stretch
Mechanoreceptors in muscle
measure STRETCH

- golgi tendon organs measure TENSION
anosmia
loss of olfactory sensation
spasticity
increase of muscle tone.
hyperexcitability of stretch reflex with decrease in reflex threshold
Enkephalin
regulates nociception
made in hindbrain
opoid pepetide
Biogenic amines
catecholamines, indoleamine, imidazoleamine, purine
Neuropeptide Y
- in CNS and PNS

- CNS - cortical excitability, circadian rhythm, stress response, pain processing, emotion, food response

- PNS - cardiovascular function, blood pressure, vasoconstriction
Vasopressin
from hypothalamus
-stored in posterior pituitary
Vasopressin = ADH
Dynorphin
regulates nociception
opoid
Leu-Enkephalin
Nitric Oxide
not stored in vesicles
made on demand
release not Ca2+ dependent
doesn't interact with postsynaptic cleft
Synapsin
Gets phosphorylated. release vesicles from cytoskeleton
Rab Protein
transports vesicle to site of exocytosis
(moves vesicle to active site)
Synaptobrevin
Docking of vesicle of nerve membrane.
(partially docked)

- Binds to syntaxin.
Synptotagmin
Docking of vesicle of nerve membrane.
(fully docked)

- Binds to neurexin.
Synaptotophyin
forms fusion of vesicular and nerve membrane.

Fully docked to nerve membrane
small clear vesicles
- AcH, serotonin, glycine
- recycled locally (at the synapse)
- low nerve stimulation (10Hz) causes a rise in Ca2+ near active zone and causes exocytosis
dense core vesicles
- peptides (NE, Serotonin)
- high nerve stimulation rate (100Hz)
cause a rise in Ca2+ near active zone = exocytosis
Botulinum Toxin
- blocks Ach release
- blocks synaptobrevin (Ach can't dock)
- diplopia, dysphasia, dysphagia dry mouth

= botox injection
Tetanus Toxin
blocks glycine release
- blocks synaptobrevin (glycine can;t dock)
-
α-Latrotoxin
massive release of AcH = depletes all of Ach
then nothing. flaccid paralysis
4-aminopyridine (4-AP)
- blocks K+ channels and increases duration that Ca2+ release = more AcH
neomycine/streptomycin
inhibit Ach exocytosis at high concentration = blocks nACHr
Monoamine Oxidase breaks down:
norepinephrine, epinephrine, dopamine, serotonin
Catechol O-methyltransferase (COMT) degrades:
norepinephrine, epinephrine, dopamine,

Does not degrade serotonin (unlike MAO)
M2 Receptor
Ach receptor
In Heart
↓ cGAMP
inhibits pacemaker cells
coupled to K+ and Ca2+ Channels = closure of Ca2+ channels
Inhibitory - slower spontaneous depolarization and slower HR
M3 receptor
Ach Receptors
- stimulates exocrine glands and eccrine glands
- also stimulates smooth muscle
↑ PLC = ↑ IP3 and DAG
↑ Ca2+ release
Excitatory M receptors
M1, M3, M5
via phospholipase

M1, M3 = brain
M3 - secretory and smooth muscle
Inhibitory M receptors
M2, M4

M2 = heart
Dopamine
mostly in CNS. not much in PNS
Norepinephrine
activates adrenoceptors of smooth muscle, glands, cardiac
(Sympathetic)
Ephinephrine
released by chromaffin cells
enters circulation
ultimate activates adrenoceptors
Isoprenaline
synthetic catecholamine
similar structure to ephinephrine
D1 and D5 Dopamine Receptors
↑ cAMP production
D2 (D3, D4) Dopamine receptors
↓ cAMP production

↑ D2 = psychosis - give D2 anatagonist
↓D2 = parkinsons. - give D2 agonist
Glycine
inhibitory in the spinal cord
- ionotropic - permeable to Cl-
- 3 glycines to bind
- resembles nACHr
GABA
- inhibitory in the brain and brainstem
- 2 GABA to bind
- mediates FAST IPSP
-metabotropic - indirect K+ channels open thru 2nd messenger
- mediate slow inhibition of postsynpatic neuron

-anti-anxiety drugs
inhibits Amygdala (responsible for fear/anxiety)
Glutamate
has both metabotropic and ionotropic
AMPA
allows Na+ to enter
Ionotropic
NMDA
allows Ca2+ in
(blocked by Mg2+)
- when v. large depolarization, many EPSP = membrane induces Mg2+ to leave
Unblocked NMDA = Ca2+ enters = - long lasting physiological changes in cell
- activated during intense synpatic activity
SSRI
for clinical depression
- allows more available SEROTONIN in CNS
- slows down 5-HT receptor = ↓ reuptake
Pilocarpine
naturally occurring alkaloid
mimics AcH - agonist at all muscarinic receptors
- used for glaucoma
(faciliates fluid drainage from eye via canal of schlem)
Beta blockers
antagonist of B1 receptors
treat hypertension
- antagonize vasoconstriction action of Norepinephrine
how does the composition of CSF compare to serum (in terms of Protein, K+, Na+, Ca2+ and Cl-)?
CSF
- less protein
- less cations (K+, Na+, Ca2+)
- more Cl-
- produced by direct secretion
Presence of RBC and high [protein] in CSF is a sign of
Subarachnoid hemmorhage
Glucose crosses the BBB via
GLUT1 transporter.
facilitated diffusion
L-dopa crosses the BBB via
facilitate diffusion
Glycine crosses BBB via
(From brain to blood)
Na+ dependent secondary active transport
CSF is absorbed by
arachnoid villi in the superior sagittal sinus
Presence of ↑[cell] and ↓ [protein] in CSF is a sign of
Bacterial meningitis
Presence of ↑[cell] and normal [protein] in CSF is a sign of
Viral Meningitis or brain tumor
Papilloma
tumor in CSF
- communicating hydrocephalus
- all ventricles enlarged
Normal Pressure hydrocephalus
- no rise in intracranial pressure
- reduction of brain volume
- usually in elderly only
- enlarged ventricles, sulci and fissures with flattening cortical gyri against skull
ependymal cells transfer water and nutrients via
paracellular/transcellular
paracellular
Dandy Walker Syndrome
Foramina of Luschka and Magendie fail to develop
- Dilatation of all 4 ventricles
- congenital
Congenital Hydrocephalus
Usually due to blockage of cerebral aqueduct
How is Intracranial Pressure measured?
Spinal tap (L4/L5 or L3/L4)
1A afferents
- excite motor neurons & interneurons
in spinal cord
- release glutamate
EPSP

metabotropic or ionotropic
Ionotropic - CATION receptors
IPSP is invoked by which neurotransmitter?
Glycine or GABA
Renshaw Cell
Interneuron

signals from a motor neuron running collaterally back via the ventral horn into the spinal cord, there were interneuron’s firing with a high frequency, resulting in inhibition
Transient Ischemic Attack
acute loss of cerebral functions for ~24 hours
-caused by temporary blockage of cerebral circulation
-full recovery likely.
Reversible ischemic attack
neurological deficit is acute loss of cerebral or monocular function
-symptoms last longer than 24 hours; -recovery is still likely.
Striae medullares
strands of the vestibulocochlear nerve (CN VIII) which wind around inferior peduncle, disappearing into median sulcus.
Gracile tubercle
function is for fine touch and proprioception.

corresponds to neurons of gracile nucleus which is one of dorsal column nuclei
Cuneate tubercle
Cuneate nucleus is part of dorsal column-medial lemniscus system, which carries fine touch and proprioception information to thalamus and cerebellum.

- located inferior to gracile tubercle.
Blood supply of the Pons
branches of the Basilar artery
locked-in syndrome
- not enough blood supply (i.e. due to stroke) to ventral portion of pons

-horizontal eye movement and facial expression (along with all other voluntary muscle actions) will be non-functional
Ataxia
problem in performing smooth, coordinated muscle movements, generally resulting in a wide gait.

-Ataxia is caused by a problem with cerebellum or cerebellar peduncles.
Erlanger & Gasser
- used for spinal nerves, and can be both motor and sensory.

- A, B,C,D
- A = thickest and highest conduction velocity
Lloyd classification
- used for afferent nerves in skeletal muscle

- I-IV
I = thickest and highest conduction velocity
IV = thinnest. slowest
Membrane Conductance (equation)
membrane conductance = total # of open channels x conductance of each channel
Tetrodotoxin
blocks Na+ entry
Saxitoxin
blocks Na+ Entry
4-aminopyridine (4AP)
selectively block K+ channels = will prolong action potential.

- used for people with muscular weakness or disease at the NMJ
Anesthetics
block Na+ channels on pain receptors
safety factor
every excitatory signal is ~5x as strong as is needs to be. therefore it can still move thru an demyelinated area
Synaptic delay
occurs between arrival of impulse at synaptic bouton (nerve ending) and response of postsynaptic cell;

related to speed of diffusion, but mostly affected by transmitter release (exocytosis).

- Shorter in Ionotropic. Longer in Metabotropic
Which Neurotransmitter DIFFUSES out of synaptic cleft?
neuropeptides
Strychnine
blocks glycine receptors in CNS - no inhibitory signals = muscle spasm and inference with breathing
Morphine
binds to receptors of neuropeptide on C fibers (pain fibers) located in substantia gelatinosa
Cocaine
blocks reuptake of dopamine, serotonin, norephinephrine = prolonged activity

prolonged stimulation = down regulation of receptors
Botulinum
inhibits exocytosis by inhibiting docking of synaptic vesicles.
Lambert-Eaton syndrome
auto-immune disease characterized by muscle weakness due to attack on Ca2+ channels in motor nerve terminals.
Neostigmine
inhibits AchE in synaptic cleft allowing Ach concentration to remain high.
Myasthenia gravis
is auto-immune disease where anti-bodies recognize nAchR, reducing their number on end plate, resulting in condition where there is not enough cation channels to reach threshold.

- treated with neostigmine (also give atropine because achE is not good for Cardiovascular)
Merkel's disk
receptor for touch discrimination
Ruffini's Endings
receptor for skin stretch
Meissner's corpuscle
receptor for vibration
- highest sensitivity
- low frequency
Pacinian Corpuscle
receptor for vibration
- high frequency
- low sensitivity
Factors Contributing to High Spatial Resolution
1. High density of cutaneous mechanoreceptors
2. Small receptive field
3. Large cortical area involved
4. Special mechanisms, ie. lateral inhibition
stereognosia
ability to perceive properties of a coherent object, like its size, shape, texture, by holding it the hand
The first sense lost in peripheral neuropathies is usually:
vibration
Tabes Dorsalis
- Destruction of DRG cells with large diameter myelinated axons
- Consequence of Syphilitic infection
- severe deficit in touch and proprioception (large diameter myelinated axons)
- Nociception and temperature remain unaffected
Phantom limbs is due to:
reorganization of the cortical maps

ie. touching the face induced sensations that were perceived to have originated from amputated hand
- facial region takes over 'unused' cortex regions
Nociceptive Pain
from stimuli that have the potential to cause tissue damage
Neuropathic Pain
pain sensation from aberrant somatosensory processing in the PNS or CNS
First Pain vs. Second Pain
First Pain
- myelinated Aδ fibers (faster)
- sharp, pricking sensation
- activation of thermal or mechanical nociceptors

Second Pain
- unmyelinated C fibers (slower)
- burning sensation
- activation of polymodal nociceptors
Visceral Pain is carried on what type of fiber?
unmyelinated C fibers
- burning sensation
What activates three chemicals activate nociceptors?
1. K+ from damaged cells
(intracellular K+ leaks into extracellular. will depolarize surrounding cells)
2. Bradykinin from blood
3. Histamine from mast cells
What 3 chemicals cause hyperalgesia?
Hyperalgesia = increased sensitivity to pain after nociceptors have been activated

Leukotrienes - from damaged cells
Prostaglandin - from damaged cells
Substance P - from primary afferents
What are the effects of opioids?
- ↓ duration of action potential from afferent neurons
- ↓ amplitude of excitatory post synaptic potential
- hyperpolarize 2nd order neuron in pain pathway
How does aspirin regulate pain?
It inhibits cyclo-oxygenase

cyclo-oxygenase is the enzyme responsible for the synthesis of Prostaglandins.

- Prostaglandins increase pain sensitivity
Dorsal rhizotomy
- surgical management of pain
- destroy dorsal root of spinal nerves
Miosis
constricted pupil
mydriasis
dilated pupil
What two structures in the eye are responsible for accommodation?
Ciliary muscle and Zonule Fibers (suspensory ligaments)
Optic disc
- only axons of retinal ganglion cells
- no photoreceptors = blind spot
- retina overlaying lamina cribrosa
Fovea
highest visual acuity
- no rods, only cones
- surrounded by macula
- 1.5 mm diameter
- all layers (except for photoreceptors) are pushed laterally so they don't interfere with photoreceptors
- on ophthalmoscope = area without blood vessels
Macula
- region of high acuity
Refractive Power
1/ focal length
unit = Diopter (D)
Far vision
Ciliary Muscle - Relax
Zonule fiber - Tighten
Lens = Flat - ↓ Refractive Power (13D)

F - Far, Flat
Near Vision
Ciliary Muscle Constricted
Zonule Fiber - Loose
Lens =
- Rounded (more convex)
- ↑ refractive power (26D)
Presbyopia
- inability to focus on near objects with age
- lens loose its elasticity with age
What is normal visual acuity?
an angle of 5 minutes of a degree
What factors determine visual acuity?
- low threshold for 2 point discrimination
- high density of photoreceptors
- proper functioning accommodation apparatus
Emmetropia
normal sightedness
-
Papilledema
Optic Disk Edema
- Indicates ↑ Intracranial Pressure

- compromised venous drainage = dilated retinal veins
= optic disk pushed forward and appears white (instead of pink)
scotoma
areas of lost visual acuity due to retinal detachment

ie. dead pixels
When looking at the ocular fundus, the optic disc is always on the ______ side.

a. Lateral
b. Medial
b. medial side.
Macular Degeneration
- loss of vision in macula due to damage to retina
- Neo-vascualr = abnormal blood vessel growth. Most severe type.
- Treatment: Laser Photocoagulation
- Leading cause of vision loss in US
Temporal Resolution
ability to distinguish subsequent stimuli from each other (time related)
Spatial Resolution
ability to distinguish adjacent stimuli from each other (relating to space)
Neurotransmitter for Photoreceptors
Glutamate
Which second messenger keeps the Na+ channel open in the dark current?

a. cAMP
b. cGMP
c. IP3
cGMP
True/False

More glutamate is released from photoreceptors in the dark.
true.
There is more convergence in:

a. Rods
b. Cones
Rods have more convergence.

Cones have less convergence = better visual acuity
Retinal
- light absorbing substance
- derived from Vitamin A
Superior Visual Field
- temporal radiation
- below the calcarine sulcus
Infereior Visual Field
- parietal radiation
- above the calcarine sulcus
Sparing of the macula
- vascular damage usually involves posterior cerebral artery
- the macula region is also supplied by the middle cerebral artery and therefore it is usually spared
Color Agnosia
inability to distinguish color hue
- lesion in area 17 or 18
Ocular Dominance columns
organization of primary visual cortex
- arranged in alternating contralateral/ipsilateral columns
Orientation columns
- primary visual cortex shows preference for certain stimuli
- ie. horizontal or vertical
Magnocellular Pathway
- Dorsal (parietal) pathway
- Depth & Motion (answers Where?)
(Location & Movement)
- detects fast moving stimulus
- synapse in first 2 layers of lateral geniculate nucleus
- Magno b/c larger cells
Parvocellular Pathway
- Ventral (Temporal) pathway
- Form & Color (answers What?)
- Color vision and acuity
- projects deeper into the primary visual cortex
- synapses in layers 3-6
(deeper and in more layers than magnocellular pathway)
otosklerosis
replacement of normal bone in labyrinth and stapes footplate with lamellar new bone

= fusion of stapes with border of oval window.
= conductive hearing loss ~ 40db
Vestibular schwannoma
Causes sensorineural hearing loss

- benign tumor from Schwann cells
- compresses vestibulo-cochlear nerve within internal meatus
- symptoms = sensorineural hearing loss and tinnitus