Neuro Final Review

Front 1

5 steps of neurotransmission

Back 1

1. Sodium channels open in presyn to cause an action potential
2. Calcium channels open
3. Ca causes vesicle fusion and release of NT
4. NT crosses cleft and open transmitter receptors
5. Depolarization of postsynaptic cell triggers an action potential

Front 2

Size of the endplate potential depends on two things

Back 2

Number of vesicles released
Response of muscle to one vesicle

Front 3

The response of a muscle to 1 vesicle is dependent on 4 variables

Back 3

1. How much NT in vesicle
2. How many postsyn receptors
3. How much current through open ion channel
4. NT catabolism rate

Front 4

What is the reversal potential of Na? K?

Back 4

+55. -100. Together the combined reversal potential is 0

Front 5

When does repetitive stimulation cause depression? Faciliation?

Back 5

When the amount of extracellular Ca is normal. When the amount of extracellular Ca is low, repeated stimulation can actually causes a larger end-plate potential, since fewer vesicles are released each time, not depleting NT as fast

Front 6

Define the safety factor

Back 6

The throwaway voltage above the minimum needed to induce a postsynaptic potential

Front 7

Difference between MG and LEMS

Back 7

In MG, there is a depletion of ACHR, all rates of stimulation will be depressed. In LEMS, Ca entry in presynapse is reduced. Depresses at low rates, facilitates at high rates.

Front 8

What is the insular lobe involved in?

Back 8

Pain processing and addictive behavior

Front 9

4 fxnal areas of frontal lobe

Back 9

1. Primary (precental) motor cortex
2. Premotor/Supplementary motor areas
3. Broca's
4. Prefrontal cortex

Front 10

3 fxns of parietal lobe

Back 10

1. Primary (postcentral) sensory cortex
2. Inf. parietal lobule of dominant hemisphere: Wernicke's
3. The rest is spacial orientation/perception

Front 11

Four fxns of the temporal lobe

Back 11

1. Primary auditory cortex: transverse temporal
2. Wernicke's (posterior w/parietal)
3. Inferior surface: visual processing
4. Learning/memory: medial temporal lobe

Front 12

Function of the occipital lobe

Back 12

Primary visual cortex.

Front 13

Fxn of the hippocampus? Amygdala? What lobe are we talking about here?

Back 13

Memory consolidation. Drive/emotional memory/affect. Limbic

Front 14

What kind of fibers are in the corpus callosum?

Back 14

Cortical Interhemispheric

Front 15

Generally, what kind of fibers are in the interal capsule?

Back 15

All input and output from the cortex to other parts of the body.

Front 16

Contents of posterior limb of IC?

Back 16

corticospinal fibers and sensory fibers from the body.

Front 17

Contents of retrolenticular limb of IC?

Back 17

The retrolenticular part contains fibers from the optic system, coming from the lateral geniculate nucleus of the thalamus. More posteriorly, this becomes the optic radiation

Front 18

Contents of the anterior limb of IC?

Back 18

* 1) frontopontine (corticofugal) fibers project from frontal cortex to pons;
* 2) thalamocortico fibers connect the medial and anterior nuclei of the thalamus to the frontal lobes (these are severed during a prefrontal lobotomy).

Front 19

Contents o fthe genu of the IC?

Back 19

corticobulbar fibers, which run between the cortex and the brainstem.

Front 20

What induces ectodermal cells to become nervous tissue?

Back 20

That is their default fate. They are prevented from that fate by BMP, except in the region overlying the notochord. Chordin and noggin BLOCK BMP, thus allowing the overlying ectoderm to become nervous tissue.

Front 21

Chemical responsibile for caudalizing the neural tube?

Back 21

Retinoic acid

Front 22

Once the nervous tissue has differentiated, what dorsalizes the neural tube? Ventralizes?

Back 22

BMP dorsalizes (sensory) the neural tube
SHH ventralizes (motor) the neural tube

Front 23

Why is SHH a morphogen?

Back 23

It changes the fate of cells dependent on gradient.

Front 24

What makes the dopaminergic neurons of the substantia nigra?

Back 24

Sonic hedgehog

Front 25

Caudal induction proteins. What do these turn on?

Back 25

Wnt, RA, FGF. Rostralization occurs in the relative absence of these inducers. They activate Hox genes which then determine spinal cord levels and brainstem divisions.

Front 26

Cause of holoprosencephaly

Back 26

Failure of the prosencephalon to separate into di and tele

Front 27

8 key stages of neurogenesis

Back 27

1. Mitosis/Proliferation
2. Migration (gradient)
3. Differentiation
4. Axon guidance
5. Synaptogenesis
6. Neuronal Death
7. Synapse Rearrangement
8. Myelination

Front 28

Netrins, semaphorins, and eph

Back 28

Netrin - long-term attractant
Semaphorins - long term repulsant
Eph - short term attract/repulse

Front 29

Characteristics of early development errors

Back 29

Neural tube defects, holoprosencephaly, mortality

Front 30

Characteristics of late development errors

Back 30

Migration/proliferation (epilepsy)
Savantism
Retardation

Front 31

Agenesis of the corpus callosum leads to?

Back 31

Savantism in the style of Rain Man

Front 32

CSF production characteristics

Back 32

1. Independent of arterial/intercranial pressure
2. Dependent on HCO3 and energy

Front 33

CSF absorption characteristics

Back 33

1. Highly dependent on pressure
2. If production > absorption = hydrocephalus

Front 34

Do astrocytes comprised the BBB?

Back 34

No, their end feet assist capillaries in maintaining the barrier

Front 35

Circumventricular organs

Back 35

Areas of the brain that do not have a BBB for practical purposes (release and receipt of hormones and chemical signals)

Front 36

Why is the ECF concentration of K so low in the brain?

Back 36

The proximity of neurons to each other means that even a slight increase in K concentration would dangerously depolarize too many cells. (One theory of epilepsy)

Front 37

ECF K buffering?

Back 37

Performed by astrocytes that take up the K in the brain and either dump it in the blood or CSF (end-feet). Astrocytes also pick up excess neurotransmitters

Front 38

Excitotoxicity

Back 38

Accumulation of K and NT leading to neuronal death

Front 39

How do glial cells microscopically regulate blood flow? Why?

Back 39

Glutamate released by neurons activates Ca influx in GLIA, who communicate with each other to release ArachA/prostagladins at end feet = vasodilation. Areas of the brain with increased neuronal firing require energy from the blood.

Front 40

How much of the cranial circulation is provided by the internal carotids?

Back 40

About 2/3 or 80% according to Nolte of the anterior circulation

Front 41

How can blood continue to supply the brain in the event of an IC occlusion?

Back 41

From the external carotid -> Orbit -> opthalmic artery -> ICA

Front 42

Where does the basilar artery begin?

Back 42

Pontomedullary jxn

Front 43

Branches of the PCA

Back 43

Pchoroidal
Thalamogeniculates
Thalamoperforating
Pcomm

Front 44

Branches of the BA

Back 44

SCerebellar
Pontine
--the labyrinthine feeds the inner ear
AICerebellar A

Front 45

Branches of the VA

Back 45

Aspinal
Pspinal
PIcerebellar A

Front 46

Superficial veins drain into the? Deep?

Back 46

Sagittal sinus. Straight sinus.

Front 47

What kind of stroke can lead to reperfusion injury?

Back 47

Embolic (as the embolus is lysed, so goeth the tissue)

Front 48

Cause of venous thrombosis

Back 48

Contraceptives and estrogen theapy

Front 49

Major locations of berry aneurysms

Back 49

ACommA, Internal carotid, middle cerevreal branch point, Circle of Willis

Front 50

Rupture of berry aneurysms =

Back 50

sub-arachnoid hemorrhage

Front 51

If an intracerebral hemorrhage occurs in the lobe . . .

Back 51

Hypertension is probably not the cause

Front 52

Most common location for an intracerebral hemorrhage

Back 52

Putamen

Front 53

Symptoms of left cerebral hemisphere stroke

Back 53

Aphasia, L gaze preference, R visual field deficit, R hemiparesis, R hemisensory loss

Front 54

Symptoms of right cerebral hemisphere stroke

Back 54

L Neglect, R gaze preference, L visual field deficit, L hemiparesis, L hemisensory loss

Front 55

Common lacunar infarct syndromes

Back 55

Pure motor hemiplegia, pure hemisensory loss, sensorimotor deficits (posterior IC), ataxic hemiparesis, clumsy-hand dysarthria

Front 56

4 main NIH stroke benchmarks

Back 56

1-4 = mild
5-10 = mild/moderate
10-20 = moderate
>20 severe

Front 57

Cerebrocerebellar damage

Back 57

movement decomposition, x pinching motion, movement initiation delays

Front 58

Spinocerebellar damamge (intermediate)

Back 58

Dysdiadochokinesia, no RAM, dysmetria, tremors

Front 59

Spinocerebellar damage (vermis)

Back 59

Truncal ataxia (thiamine deficient breakdown of flocculonodular), ataxia and tremor of legs while walking

Front 60

Vestibulocerebellum damage

Back 60

Inability to stand upright and maintain gaze (imbalance/nystagmus)