Neurology

Front 1

The main difference between neurons and glia is tin the means that.....
-Neuronal Cells differ bc....
*Glial cells lack the ability to...

Back 1

they transfer information.
-Neuronal cells have electrochemical signalling including changes in membrane receptor and ion channel activities leading to alterations in neuronal membrane potentials -- action potential
*Glial cells lack the ability to generate action potentials - but fluctuate in their resting membrane potential

Front 2

Astrocytes a type of ____cell, supports prominant ______ related to transmitter receptor, transporter and ion channel activity.
They also regulate the amount of neurotransmitters in _____ by uptake of _____ via transporters in their endfeet.

Back 2

1. glial cell
2. intra and intercellular calcium signalling
3. synaptic cleft
4. excess neuronal transmitters

Front 3

both neurons and glial cells are able to release. ____ to support their survival

Back 3

specific neurotrophic factors such as gliac cell derived neurotrophic factor GDNF, brain derived NF BDNF and neurotrophin-3

Front 4

most neurons _____ regenerate
-neurons have ____ roles and glia have _____ roles
*Cell processes for neurons are ____ and for glial cells are ____
-Neurons are excitable via ____ and glial cells via ____

Back 4

1. do not regenerate
2. signalling, glial have supportive and signalling
3. neurons = long, glial - short
4. neurons - action potentials and synaptic potentials, glial cells - transmitters and calcium signalling

Front 5

-Elementary structures in neurons are: ____ & ____
*structures important for information transfer are the (5)

Back 5

- dendrites and axons leaving the soma
* axon hillock, myelin, synapses, dendritic spines, synaptic boutons

Front 6

-Multipolar neurons - are found _____ and have ____ and one _____.
*Bipolar neurons - are ___ or ____ and have an _____ and two ____.
-Pseudo-Unipolar: Two axon-type branches out of the cell body of which one is towards_____ and other is toward _______. Examples are:_______
*Unipolar Neurons: is ____ in mammalian vertebrates; axons arise from____

Back 6

-in the brain, dendrites and one long axon.
*sensory neurons OR retinal bipolar cells; have an elongated cell body and two processes one axon and one ending in dendrites
-CNS other is to PNS; examples are dorsal root ganglia and baroreceptor sensitive cells in nodose ganglion
*Rare, the same spot with dendrites

Front 7

-Afferent Neuron is a neuron with an axon carrying impulses ______ the CNS
*Efferent Neuron is a neuron with an axon carrying impulses ______ the CNS
-Interneuron is a neuron mediating information between ________

Back 7

-in towards the CNS from PNS
*outwards from CNS to PNS
-between two other neurons within PNS or CNS

Front 8

Cytoskeleton has three types of filaments:
1._____ is alpha, beta or gamma; grow by addition of tubulin dimers at their ___ ends; behave as transport tracks for two ____ transport systems; ______ proteins play key roles in fast axonal transport.
2. ______ are intermediate filaments - NF's, vimentin; highly stable polymerized and undergo l_____turnover (unlike the other 2);
they create a _______of the cytoskeleton and determine the axon's ____.
3. _________ such as actin and spectrin, actin forms a network beneath the _____ and probably participate in advancement of the ____

Back 8

1. Microtubules; postive; axonal; MAPS, kinesin and dynein
2. Neurofilaments, little, scaffolding, diameter
3. Microfilaments, cell membrane, growth cone

Front 9

______ is a MAP that is repsonsible for fast anterograde transport from soma to nerve ending and is akin to myosin in muscle - it becomes inactivated and is carried back to soma via. _____.
2. ________ is responsible for fast retrograde transport from nerve ending to soma, and is the motor protein in cilia and flagella.

Back 9

1. Kinesin, carried back via retrograde axonal transport
2. Dynein

Front 10

1. Fast Anterograde Transport is _____ drive and materials transported are____&______.
2. Fast Retrograde transport is _____ drive and transports: (3)
3. Slow Anterograde transport of 0,1 - 1 mm/day transports: _____.
4. Slow Anterograde transport of 1-10 mm/day transports: _____

Back 10

1. kinesin drive; vesicles and mitochondria
2. dynein driven; lysosomes, enzymes, recycled vesicular membrane
3. cytoskeleton molecules
4. soluble proteins and enzymes

Front 11

Influence of influx of sodium ions on the rising phase of the action potential

Back 11

at threshold - Na+ causes the rising phase of the impulse.
--the increased opening of these channels causes an increased influx of Na+ ions down the electrochemical gradient (Vm-Ena) - driving the membrane potential in a self regenerative manner toward Ena (depolarized

Front 12

describe the influence of the efflux of K+ ions on the repolarizing phase of the action potential

Back 12

the presence of open K+ channels along the axon ensures that the efflux of K+ ions down their electrochemical gradient will REPOLARIZE the membrane - producing the falling phase of the impulse
-unmyelinated axons have voltage gated K+ channels that are also induced by depolarization but the kinetics of opening are delayed relative to opening of the Na+ channels.-the delayed efflux of K+ ions drives the potential towards Ek - hyperpolarizing undershoot
--> potential change first moves toward E(Na) to E(k)

Front 13

time courses of changes in sodium and potassium conductances:

Back 13

Na+: peaks when action potential is peaked
K+ has a lower peak and does not occur until Na+ is half way through hyperpolarizing -- see notes page 16-5

Front 14

Structural features of voltage gated sodium channels related to influence of depolarization

Back 14

there is a voltage sensor and another voltage sensitive part of the channel that mediates its later closure during depolarization --> inactivated closure state is DIFFERENT from open active state
-Ball and chain model of inactivation the bally carring the positive charge moves into the pore during depolarization
"inactivation following depolarization

Front 15

Refractory Period
Relative Refractory Period

Back 15

Refractory Period - when sodium channel reverts from inactivated state to the normal closed state; when virtually all Na+ channels are inactivated
Relative - follows the absolute refractory period, that is longer, during which a new impule can be evoked by a LARGER stimulus. - some Na+ channels remain open and tend to hod the potential close to Ek - opposing excitation of the axon.

Front 16

Locations of voltage gated channels in myelinated and unmyelinated axons

Back 16

Myelinated: clustering of Voltage gated Na+ channels is found at Nodes of Ranvier
- Na+ channels are in the axon initial segment (initiation zone), presynaptic terminals and enriched in nodes of ranvier
K+ channels are found in paranodal (spot where myelination begins again) and juxtaparanodal (just under the myelin) of peripheral and central myelinated axons, presynaptic terminals and axon initial segment
---> impulses only occur at nodes
-impulses in myelingated axons are repolarized by pos. charge leaving axon in para and juxta nodal regions w opne K+ channels
-k_ channels in paranodal are responsible for maintaining resting membrane
-impulse conduction impaired with demyelination
Unmyelinated : distributed uniformly throughout the axon - channel densities are less than in myelinated

Front 17

Impulse conduction in myelinated and unmyeltinated axons is related to:

Back 17

myelinated: positive charge enters each node of ranvier during impulse moves internally - the larger the myelinated fiber diameter, the easier the positive charge moves along its interior during impulse propagation; regeneration of impulses at each node ensures conduction of impulses without decrement - Saltatory Conduction; CONDUCTION VELOCITY IS ABOUT 6 TIMES FIBER DIAMETER
Unmyelinated: impulse in one regions caues positive charges to flow ahead cell's interior and depolarize adjacent region. Continuous conduction; there are smaller diameters that limite effectiveness - CONDUCTION VELOCTIY IS TWICE THE FIBER DIAMETER

Front 18

IMPULSES in unmyelinated v myelinated:

Back 18

unmyelinated: continuous conduction

myelinated: saltatory conduction

Front 19

Advantages of Myelination

Back 19

1. enhanced velocity of conduction becuase impulses are generated only at nodes - about 1 mm apart
2. Large velocity is acheived in fibers with relatively small diameters - hence space saving without fall in velocity
3. confining impulses to nodes means Na+ loading during intense impulse traffic is minimized in myelinated axons

Front 20

Different ways impulse conduction can be impaired

Back 20

1. TTX and Saxitoxin - block Na+ channels at an extracellular site. - in japanese puffer fish (TTX) binds to channels and blocks entry and so does STX
2. Local anesthetics block channels at intracellular site - lidocaine and procaine - uncharged form can cross the membrane readily and each moelcule acts as a charge molecule from inside at the site within Na_ channel to block Na+ entry ---small myelinated (A delta) and large (C delta) pain perception reflects impulse traffic in A and C delta fibers - sensation is blocked
3. Demyelination impairs conduction
4. Demeylination may cause decreased conduction velocity
5. frequency related block
6. total conduction block
7." crosstalk between axons"

Front 21

Describe the chemical nature of transmitters

Back 21

transmitters can be amino acids, amines, neuropeptides or gases.
-they are all synthesized, stored in vesciles and released by exocytosis, then bind to receptors in postsynaptic cell
-some are degraded, but most are taken up by presynaptic cell or glial cell
-receptors may be ionotropic or metabotropic
-ME and Serotonin taken up and broken down by MAO, NE also broken down by COMT
-ACh broken down in synaptic cleft
-all others reabsorbed by presynaptic neurons

Front 22

main features of the life cycle of neurotransmitters

Back 22

-they are all synthesized, stored in vesciles and released by exocytosis, then bind to receptors in postsynaptic cell

Front 23

ACh mechanisms on exocrine glands, smooth muscle and pacemaker cells

Back 23

ACh on exocrine: postganglionic sympathetic cholinergic neurons stimulate exocrine glands - such as salivary, lacrimal glands, and eccrine glands by binding ACh to muscarinic receptor M3 in secreotry cells. Activated receptor interacts with G protein that raises activity of PLC - IP3 and DAG are produced ensuing the increase of Ca2+ in Smooth ER which causes an increase in [Ca2+] --> causes an enhanced secretion of stored enzymes accompanied by ion and water transport
-Smooth Muscle: in GIT, circular muscle of iris, ciliary muscle, bronchiolar msucle, ballder wall, all have M3 receptors mediating contraction again by PLC IP3 and DAG pathway
-Pacemaker Cells: have M2 reecptors innervated by parasympthetic neurons - M2 activates inhibitory G protein that reduces the activity of adenylyl cyclase and there is a fall in cAMP --> closure in Ca2+ channels leading to weaker depolarization of cells -- couple to shortcut pathway - inhibitory unit of G protein directly gates the opening of K+ channels leading to hyperpolarization of pacemaker cells = prolongs time it takes for cells to reach threshold.
ACh STIMULATES EXOCRINE AND SMOOTH MUSCLE, INHIBITS CARDIAC PACEMAKER CELLS

Front 24

Mechanism of action on NE on cardiac pacemaker cells and cardiac muscle

Back 24

NE on Pacemaker cells - these cells have beta 1 adrenoceptors linked to adenylyl cyclase - G protein is stimulatory and receptor activation leads to rise in cAMP, phosphorylating membrane protein increasing Ca2+ and decreasing K+ - NE from postganglionic sympathetic neurons increases rate of spontaneous depolarization of pacemaker and enahcnes Ca2+ in ventricular walls to lead to a stronger contraction.
Cardiac Muscle: Ne from postgang sympath activated adrenoreceptors in smooth muscle and cardiac muscle. Same process as pacemaker cells

Front 25

Differences between nAChRs and muscarinic Receptors and cellular distribution of the receptors:

Back 25

Nicotinic receptors are located at the neuromuscular junction (somatic nervous system), at the autonomic ganglia (autonomic synpase site) for both parasympathetic and sympathetic nerves, and in the adrenal medulla. They are ionotropic receptors that are excitatory and respond to Ach and nicotine, with tubocurarine as an antagonist.
Muscarinic receptors are located in heart, smooth muscle, and glands and receive Ach from the postganglionic neurons of the parasympathetic system. They may be inhibitory M2, M4 or slow excitatory M1,M3, and M5. They are metabotropic receptors and M2 causes an inhibition of adenylate cyclase, decrease of cAMP, closure of Ca channels (slower depol-INDIRECT), increased K channel opening (greater starting hyperpol- DIRECT), and therefore a slowing of the heartrate. M1 and M3 lead to increase in PLC activity, more IP3, more intracellular Ca, so increased gut wall contractions, contractions of pupillary and ciliary muscle, increased gland secretion, or bladder wall contraction. Main agonists are Ach and muscarine and antagonist is Atropine

Front 26

Locate the cellular distribution of the receptors for Ach and catecholamines and describe the nature of the responses they mediate in heart, glands and smooth muscle.

Back 26

Ach receptors found in neuromuscular junction, adrenal medulla, autonomic ganglia for symp and parasymp, and effector organs that parasymp neurons are acting on. Those binding to nicotinic receptors have ionotropic effect and are excitatory. They will cause formation of EPP on muscle cell, release of epinephrine from adrenal medulla, and excitation of postganglionic ANS neurons. Those binding to muscarinic receptors in the parasympathetic organs (either excitatory or inhibitory ) will cause slowing of heart rate, less contraction force, longer time delay in AV node, release of secretions from glands, and contraction of smooth muscle in gut and bladder wall, pupillary and iris muscle.
Receptors for catecholamines are all metabotropic and may be excitatory or inhibitory. (see above). In B-1, they may be excitatory to increase heart rate, heart muscle contraction, and increase AV node conduction rate. Those in a-1 are excitatory and lead to constriction of vascular smooth muscle in the skin, sphincters of bladder and gut. Those in a-2 are inhibitory and lead to relax GI walls and decrease insulin. B-2, leads to relaxation of vascular smooth muscle in the skeletal muscle, relaxation of bladder wall and gut wall, bronodilation.

Front 27

List the main agonists and antagonists for nicotinic, muscarinic and adrenoceptors.

Back 27

Nicotinic receptors have Ach and nicotine as agonists and Tubocurarine as antagoinst
Muscarinic receptors have Ach and muscarine as agonists and Atropine as antagonist
Adrenoceptors have noradrenaline, adrenaline as agonists.

Front 28

Understand that inhibition in the central nervous system is mediated by glycine and GABA acting on ionotropic glycine and GABA(A) receptors and also by GABA on metabotropic GABA(B) receptors.

Back 28

Glycine and GABA(A) operate by opening Cl channels that hyperpolarize the cell and inhibit impulse formation by making IPSPs. GABA(B) receptors operate in a metabotropic manor by indirectly opening K channels through a second messenger.

Front 29

Clinical correlations of pilocarpine, beta blockers, relief of broncho constriction during asthma, relief of nasal congestion, Horner's Syndrome

Back 29

Pilocarpine is an agonist for muscarinic receptors of the parasymp nervous system. They help the ciliary muscle to contract, to drain fluid from the eye and are used to treat glaucoma.
Beta 1 antagonists (propranolol) can be used to treat hypertension bc they block the sympathetic effects such as increased heart rate, contractility, and vasoconstriction.
Bronchoconstriction during Asthma can be treated by giving patients agonists to B2 receptors, like salbutamol. This leads to relaxtion of smooth muscle of the bronchioles.
Alpha 1 agonists are used to treat nasal congestion by causing vasoconstriction in nasal covity and thereby reduce congestion (phenylephrine).
Horner's syndrome results from unilateral lesion of the path from hypothalamus to spinal cord, to superior cervical gangion, part of face. Leads to paralysis of radial iris muscle (miosis), droopy eyelids (ptosis) from loss of tarsal muscle, and dry face (no sweat), and retracted eyeball.

Front 30

Roles of Amines in the Arousal System:

Role of Amines that influence Mood:

Back 30

Role of Amines: NE and Serotonin are transmitters in the ascending arousal system

Mood: Neurons in the locus ceruleus and rostral raphe nuclei innervate neurons in the limbic lobe and coretx that are involved in our mood and level of anxiety - when noradrenergic and serotonergic transmission is below par, mood is altered to give feelings of despair, fear and anxiety.

Front 31

Therapeutic Use of drugs to influence mood, thought and movement via actions on synapses where GABA and amines are released

Back 31

Dopaminergic neurons make projections into the basal ganglia to influence movement control, and those in the ventral tegmentum go to hippocampus, and frontal lobe to influence thought. Dopamine agonists (D2) can be used to treat movement disorders like parkinson's where there is less dopamine present. Dopamine antagonists (for D2) are used to treat psychosis.

Patients with mood disorders now treated with serotonin re-uptake inhibitors (SSRI's) based on the fact that thee patients have impaired serotonergic transmisstion in the CNS. Reuptake inhibitors, especially SSRIs, help to keep serotonin in the synaptic space so that it can continue to act. This will eventually lead to upregulation of receptors in the postsynaptic neuron which explains the delayed benefits of taking SSRIs

Front 32

what structures in the nervous system develop from the neural tube and neural crest cells?

Back 32

1. neurons and glia

2. neural crest cells give rise to neurons of the ANS

Front 33

what is the origin of the neural plate, neural fold neural tube and neural crest cells?

Back 33

ectoderm

Front 34

what is the origin of the notocord

Back 34

mesoderm

Front 35

what does bone morphogenic protein in ectoderm differentiation?
what is it inhibited by

Back 35

BMP is secreted by ectodermal cells and its inhibition causes the neural plate to form.
-inhibited by proteins secreted by Hensen's node (not retinoic acid), this blockage allows the cells to follow their neural pathway to become the neural plate

Front 36

what does BMP4 do

What is it inhibited by?

Back 36

BMP4 stimulates differentiation of overlying ectodermal tissue (inhibition of the BMP4 signal by chordin, noggin or follistan) causes the extoderm to differenetiate into the neural plate

Front 37

What effect does BMP have on the spinal cord?

Back 37

BMP is secreted by the ectodermla cells, so they diffuse nearest to the dorsal horn - they specify cells of the dorsal horn!

Front 38

What does the notochord due in developing babies

Back 38

induces ventral spinal cord characteristics, --> motor neurons and floor plate in embryos (which separate the left and right sides of the ventral tube)

Front 39

what does the notocord secrete

what else secretes this protein

what does the notocord turn into

Back 39

sonic hedgehog protein
-then floor plate secretes sonic hedgehog protein
-notocord --> nucleus pulposus

Front 40

What is the role of the Sonic the Hedgehog protein?

Back 40

establish the dorsal - ventral axis in developing neurons
-responsible for motor neurons and floor plate formation

Front 41

consequence of failed neural tube closure
rostal end
caudal end

Back 41

rostal - anencephaly

caudal - spina bifida

Front 42

What are homeotic/ Hox genes?

Back 42

responseible for segmentation of the pro, mes, and rhombencephalon
-- they are MASTER GENES - control expression of many other genes during development - responsible for proper placement and number of embryotic segment structures (leg, antennae, eye), (over expression of the 'eye' gene in flies will cause dropshila - many eyes)
---HOX GENES known for their roles in assigning segmental identity, telling cells which segment they are in along the AP axis, turning on downstream target genes to make the appropriate appendages for that segment -> mutations of these cause the wrong types of cell ls to be formed in the wrong places

Front 43

What does an ideal Hox system have?

Back 43

1. genetic colinearity: all hox genes are found on one chromosome, one after the other - separated by a promotor/repressor gene,
-Hox 1 is at the 3'end, hox 14 is at the 5' end
2. ANATOMICAL COLINEARITY - hox genes are expressed in the same order along the anterior to posterior axis, hox1 at front of head, hox 14 at tail
3. TEMPORAL COLINEARITY: hox genes are also expressed in the same sequence in time, hox 1 first, hox 14 last

Front 44

what would a mutation of EMX Hox gene cause?

What would a mutation of OTOX hox gene cause

Back 44

EMX - schizencephaly - deep cervices in the cortex

OTX - epilepsy

Front 45

What role does retinoic acid play in the differential expression of Hox genes?

Back 45

1. the diffusion of retnoic acid from HENSONS NODE sets up the gradient along the embryo that conributes thte anterior - posterior sequence of the hox gene expression in the -hindbrain-
2. activates the transcription of Hox genes: Hox genes have different sensitivities to it

Front 46

What comes first - dorsal -ventral positioning of cells or anterior posterior?

Back 46

Anterior posterior by Hox genes, then dorsal ventral by proteins like sonic hedgehog and BMP

Front 47

What are the primary and secondary vesicles in the NS
3

Back 47

1 proencephalon - tele & di
2. mesencephalon
3. rhombencephalon - met and myel

Front 48

How can rhombencephalon be so segmented (in the hindbrain?)

Back 48

during development several genest identified whos pattern of expression correlate the segmental boundries of the hindbrain:
1. metencephalong - pons and cerebellum
2. myelencephalong - medulla

Front 49

Where does a neural crest cell start at the marginal or ventricular zone?

what happens during cell proliferation?

Back 49

1. Ventricular Zone

2. cell in the ventricular zone extens a process that reaches upward toward the pial surface - nucleus of the cell migrates upward
once it reaches the top it travels back down too the ventricular zone
it retracts its arm from pial surface and cell divides in two

Front 50

what are the only neurons (other than stem cells) that can continue to divide

Back 50

olfactory neurons

Front 51

What roles do radial glial cells have in cell migration?

what are they called in cerebellum?
retina?

Back 51

in the cortex and other regions the migrations of neurons is dependent on them -
once cells have stopped dividing, the neurons will migrate on them like a train on tracks
Cerebellum: Bergmanns Cells
Retina: Mueller Cells

Front 52

How do cortex layers develop 'inside out'

Back 52

each successive generation of neurons migrate past the older ones, toward the pial surface
-youngest neurons on near the pial surface and oldest are near layer VI

Front 53

How do cells know where to get off the radial glia in the cortex

aka cortical neuron migration

Back 53

CAJAL FETZIUS cells in marginal zone of the cortex secrete REELIN, (from the gene reeler).
when cells are close enough to the marginal zone to come in contact with this diffusible protein - REELIN signals them to get off the glial cells to take their final position

Front 54

Cells of CNS need radial glial cells to migrate to their positions,
cells that express gnRH are an exception -
how do GnRH cells migrate?

Back 54

they travel from the olfactory pit, into the CNS, along a previously established axon tract.

Front 55

What determines what type of NT the neuron will produce

Back 55

once a cell has migrated, its environment influences its development

neurons will release the correct transmitter for the tissue/targets they are innverating

Front 56

Leukemia Inhibitory Factor LIF' phenotype is influence by local peptides

- What nerves does it have an effect on?

Back 56

LIF , released by cardiac tissue, causes neural crest cells to become cholinergic (changes phenotype of neural crest cells from secreting NE to ACh)

Front 57

what is the role of laminin in axonal outgrowth?

What happens if it is blocked?

Back 57

laminin is present along pathways in the extracellular matrix that neural axons follow - PROMOTING NEURAL OUT GROWTH (found at the NMJ and makes pathways for axonal regrowth following axotomy)
-neural crest cells migrate to PNS via path from laminin
-INTEGRINS on axons bind LAMININ promoting axonal elongation
-synthesized by Schwann cells, particularly after injury
-Blocked --> with an antibody, you will block the neurite extension and outgrowth

Front 58

What is fasiculation? How does it occur?

Back 58

Fasiculation is a mechanism that causes axons growing together to stick together due to the epxression of neural cell adhesion molecules NCAMS
--N-CAMS in the membrane of neighboring asons bind tightly to one another causing axons to grow in unison

Front 59

What is the role of PMP-22 (peripheral myelin protein) in myelination of peripheral nerves?
Who makes it?

Back 59

Schwann cells make it

it is expressed in Schwann cell membranes when axons are around, these axons will fuse, forming myelin
-ESSENTIAL FOR MYELINATION OF AXONS
- if neuron is not around Schwann cells will break it down

Front 60

In patients with Charcoat Marie Tooth - they have a mutated PMP-22, what is the result?

Back 60

Peripheral myelin fails to form properly, -- CMT is a demyelinating disesae

Front 61

What releases netrin?
How does netrin influence axonal growth?

Back 61

Netrin is released by the floor plate (floor plate also releases sonic hedgehog)

floor plate is ventral to midline
attacks neurons - that cross teh anterior commissure -- become attached with NETRIN - ATTRACTS THE DORSAL NEURONS

Front 62

HOW DO EXPERIMENTS with trembler mouse (with genetic deficiencies) illustrate importance of Schwann cell's role
4

Back 62

1. when u cut a good sicatic nerve, the distal axon degenerates - leaving behind the schwann cels wihtout a neruone these shcwaan cells will breakd won their PMP-22 causing demylination where there is no axon - if you graft a trembler axon to that spot the axon will travel down the nerve and beocme myelinated
2. if you cut a trembler nerve, and try to graft a good axon to it, the axon will grow into the growth tube of teh trebler nerve and not induce myelination
3. you can say that schwaan cells is responsible for the myelination and not the neuron (or the good axon would have become myelinated in the bad growth tube)
4. PMP - schwaan cells on their won can make PMP22 but break it down instead of letting it become transported to their membranes, once neurons are around they no longer break it down, instead express it in their membrane which fuse to form myelin

Front 63

How does the growing motor neuron influence the muscle fiber it synapses on?

Back 63

1. first ACh receptors are distributed all across the fiber so sensitivity is widespread
2. when motor neurons secrete AGRIN into the basal lamina the AGRIN interacts with ACh receptors causing them to aggregate across from the neuron forming the endplate
3. denervation happens, the sensitivity becomes widespread again but the focal sensitivity at the end of the plate does not -- the sever axon will still regenerate tot he correct plate
-- if the muscle cell is destroyed it will regenerate to the correct place because the agrin in the ECM and the laminin and ACh esterase

Front 64

What is the mechanism of Nerve Growth Factor NGF

Back 64

1. it is taken up by nerve terminals and transported to the soma, there it induces tyrosine hydroxylase and dopamine hydroxylase to make NE
-- it is produced by sympathetic neurons
2. it enhances the outgrowth of neurites from sensory and sympathetic neurons -
essential for their survival as well during development
--growth of sensory neurons to their receptive site

Front 65

What is the role of NGF onthe sympathetic and dorsal root gangion structures?

Back 65

1. NGF is needed for survival of sensory neurons during the fetal stage
2. NGF is needed for survival of sympathetic neurons in INFANCY
3. in adults, antibodies to NGF were much less effective on their cell population
-anti NGF given to mouse - doesnt react well to stress, but has almost normal sensation

Front 66

What is the importance of the Neurotropin family of growth factors>

Back 66

they promote the survival of neurons - signal survive differentiate or grow

act at specific receptors (tRk) that phosphorylate tyrosine residues, leading to second messenger cascade that alters gene expression
they switch off the cells instructions for apoptosis
NT3 receptor = tRKc
NGF - - TRKc

Front 67

What is apoptosis
what is its importance in neurodevelopment?

Back 67

Apoptosis is programmed cell death - important for making the right synpases and number of enurons per target
-reflects competition for trophic factors a vital substance for survival released by the target tissue

2 important in development of making sure only one motor neuron innervates a muscle fiber
initially 5-6 neurons innervate a motor fiber then only one survives after apoptosis
elimination si mediated by the muscle fiber - silencing the activity of the fiber leads to retention of the polyneuronal innervation
stimulation of the muscle accelerates the elimination of all but one input

Front 68

What is the example regarding frog ganglion cells in the retina innervating neurons in the tectum?

Back 68

-The temporaal retinal cells only grow to anterior tectum
- based on a repulsive factor --> they are repelled by EPH (ephrin) ligands that are present along an anterior - posterior gradient, with higher concentrations of ephrin being at the posterior tectum
-temporal retinal cells have a higher concentration of Eph receptors in the growth cone - when they bind to ephrin they detach from it and retreat
2. retinal cells in the nasal part of the retiina grew to the posterior tectum because they were not repelled by ephrin ligands located their - they lack the Eph receptors
--in a petri dish, nasal retinal cells will grow on both the anterior and posterior tectum equally because it lacks eph receptors

Front 69

What is the role of the Eph family of receptor tyrosine kinases?

Back 69

they act throughout the developing NS to influence the axon path finding, cell migration and intermingling all by repellent mechanisms

Front 70

What is the critical period in relation to visual projections from the lateral geniculate nucleus to the visual striate cortex?

Back 70

the time of plasticity in a young animal during which certain aspects of vision ca be altered and those changed can be revered before adult life
this is known to be within the FIRST 3 MONTHS -
cells in cortex are concerned with orientation, no growth of cells when deprived of orientation - need orientation to 'form vision'
-- with ocular deprivation of wone eye - there is a one eye dominance - due to loss of form vision - not due to no light
--when an infant is born the visual system is virutally intact

Front 71

What happens to an ocular dominance colum in monocular deprivation before the critical period -
what about after the critical period?

what is the ocular dominance column

what does a score of 4 and 7 represent on the ocular dominance histogram?

Back 71

Before: ocular dominance column in the affected eye will shring and you will get monocular vison
After: nothing will happen to the columns - retian binocular vision
-- ocular dominance column is a region of neurons in the striate/visual cortex that synapses with axons, receiving small signals from only one eye (left or right)
---they are off equal widths, that can be seen in a tangential section (basically horizontal)
----a value of 4 on the histogram means that the particular group of cells is stimulated by both eyes equally - a value of 7 means it is only stimulated by one eye

Front 72

How does binocular vision occur?

WHAT HAPPENS IN STABISMUS

Back 72

1. convergence of inputs from layer IV cells serving right and left eyes into layer III
2. THERE IS NO BINOCULAR VISION IN LAYER 4
3. binocular competition occurs, when inputs from two eyes actively compete for the synaptic control of the postsynaptic neuron - if the activity of the two eyes is correlated and equal in strength - the two inputs will be retained on the same cortical cell --- if this balance is disrupted by depriving one eye - the more active input will somehow make the deprived synapses less effective
--STRABISMUS - where two eyes never are aligned in the same visual field - lose their binocular receptive field - even tho both eyes will retian equal representation in the cortex
---this shows that disconnection of inputs results from competition - not disuse --> no shrinkage of ocular dominance columns if both eyes are closed
----it cane sharpen segregation of ocular dominance columns --- eliminate depth perception
-cataracts or ocular misalignment must be corrected in early childhood to avoid visual disability

Front 73

How does the geniculate axon retraction occur?

what is the effect of this process when monocular blindess occurs during the critical period

Back 73

1. when axons are not stimulated the monocular blindness will cause cell columns in unaffected eye to stay, while affected eye columns shrink - this can be reversed if you close the previously opened eye - and you open the previously shut eye -- you will get expanded columns of the formerly shrunked column adn shrinkage of the formally expanded column
--the ramining eye fails to retract its terminal fibers to the normal column borders
---there is reduction of binocularly driven neurons - they will all be contralateral or ipsilateral neurons

Front 74

How do you read a histogram>
what do cells 1 and 5 represent

group 3?
group 2 and 4?

if you deprive the ipsi lateral eye of stimulate ---
in strabismus:

Back 74

Cells in groups 1 and 5 are activated by the stimulation of either the contralateral or ipsilateral
eye, respectively, but not both
they are the only groups that completely monocular

ii. Cells in group 3 are activated equally well by either eye

iii. Cells in groups 2 and 4 are binocularly activated, but show a preference for either the
contralateral or ipsilaterl eye, resp.

iv. The histogram reveals that the majority of neurons in the visual cortex are driven binocularly.

v. If you deprive the ipsilateral eye of stimulation, the cells in the groups of it will leave few neurons responsive to that eye.

vi. In strabismus, where you don’t get binocular vision, groups 1 and 5 have almost every single
cell in layer III of the visual cortex. (layers 2 and 4 have less than 5% and layer 3 has none)