Pbd Neuro Dr Peris & Cranial Nerves

Front 1

The rate limiting step for Ach?

Back 1

Choline uptake

Front 2

Metabolism of Ach?

Back 2

extracellular acetylcholinesterase AChE

Front 3

These Ach R are linked through Gq to activate phopholipase C

Back 3

M1 & M3

Front 4

2 functions of M2 & M4

Back 4

1. linked through Gi to inhibit adenylate cyclase
2. Stimulate G coupled potassium channels

Front 5

what are the Ach R?

Back 5

M1, M2, M3, M4 & Nicotinic

Front 6

ligand gated ionophore for sodium, potassium, and calcium in the Ach mechanism

Back 6

nicotinic

Front 7

where is choline found more in the body?

Back 7

extracellularly

Front 8

How can the Ach mechanism be affected with drugs?

Back 8

Drugs can affect ChAT to inhibit it and therefore decrease Ach
Drugs can affect ChAT to stimulate it and therefore increase Ach
Drugs can affect AchE to inhibit it and therefore increase Ach
Drugs can affect AchE to stimulate it and therefore decrease Ach

Front 9

Which Ach R is the autoR?

Back 9

M2 b/c its affect on adenylate cyclase is to decrease vesicular transport

Front 10

Which of the AchR are inhibitory?

Back 10

M2 & M4 b/c it decreases cAMP and decreases K+

Front 11

Which AchR are excitatory?

Back 11

M1, M3 and N

Front 12

Fxn of of M1 & M3?

Back 12

Increase DAG and IP3

Front 13

Fxn of M2 & M4?

Back 13

decrease cAMP and K

Front 14

Fxn of Nicotinic AchR?

Back 14

increase Na & Ca and decrease K

Front 15

the 4 cholingergic pathways?

Back 15

1, short interneourons in caudate/putamen
2. basal nucleus to frontal and parietal cortex & thalamus
3. septal nucleus to hippocampus
4. pons to thalamus & hypothalamus

Front 16

this cholinergic pathway is important for motor control

Back 16

short interneurons in caudate/putamen

Front 17

cholinergic pathway that is important in actual formation of long term potentiation

Back 17

basal nucleus to frontal and parietal cortex and thalamus

Front 18

this cholinergic pathway is important for learning and memory

Back 18

septal nucleus to hippocampus

Front 19

This cholinergic pathway is unknown in its fxn?

Back 19

pons to thalamus & hypotalamus

Front 20

these types of transmittors are very selective in how they interact and how they are released?

Back 20

endogenous opioid peptides

Front 21

what is the uptake and metabolism of endogenous opioid peptides?

Back 21

uptake: none
metabolism: rapidly degraded by extracellular peptidases

Front 22

what are the endogenous opioid peptide receptors?

Back 22

Mu, kapa, and delta subtypes

Front 23

how do the opioid peptide R work?

Back 23

all linked through Gi to inhibit adenylate cyclase & stimulate G coupled K channels
also linked through Go to inhibit Ca channels

Front 24

the 8 CNS effects of endogenous opioid peptides

Back 24

1. analegsia
2. respiratory depression
3. euphoria/dysphoria
4. miosis
5. sedation
6. mm rigidity
7. nausea
8. endocrine

Front 25

the mu kappa and delta R in SC, PAG, thalamus, cortex, and limbic system have this CNS effect

Back 25

analgesia

Front 26

T/F: Mu R stimulation in the medulla can cause respiratory depression

Back 26

True

Front 27

mu, kappa and delta R stimulation in ______ & _______ can cause either euphoria or dysphoria.

Back 27

VTA (ventral tegmental area)
NAc (nucleus accumbens)

Front 28

The CNS effect of miosis can be stimulated by what opioid peptide R?

Back 28

mu & kappa in the edinger westphal nucleus

Front 29

T/F: Sedation can be caused by stimulation of mu and delta R when the locus ceruleus is excited.

Back 29

F: sedation can be caused by stimulation of mu and kappa R when the locus ceruelus is inhibited.

Front 30

Stimulation of the mu kappa and delta R in nigrostriatal tract will cause ____________

Back 30

mm rigidity

Front 31

Stimulation of mu receptors in chemoR trigger zone will cause:
a. nausea
b. sedation
c. miosis of the eyes
d. all of the above

Back 31

A. nausea

Front 32

Fxn of mu R in hypothalamus?

Back 32

They have an effect on the endocrine system by inhibiting gonadotrophins

Front 33

From the proopiomelanocortin (POMC) precursor protein, you can get:
a. gamma MSH
b. alpha MSH
c. ACTH
d. beta LPH
e. A & C
f. all of the above

Back 33

F. all of the above

Front 34

What's interesting about the POMC precursor?

Back 34

for every precursor of POMC, one gets an beta LPH which is stress releasing and also get an ACTH which is stress enhancing

Front 35

What are all the peptides that you can get from POMC?

Back 35

gamma MSH
alpha MSH
ACTH
beta LPH
beta MSH
MET-ENK

Front 36

T/F: from the MET-ENK peptide made from POMC, one can cleave MET from ENK & make 2 different proteins

Back 36

False: you can't cleave the MET-ENK apart

Front 37

What are the active peptides that are formed from Proenkephalin?

Back 37

you get 3 types of MET-ENK and 1 type of LEU-ENK

Front 38

The 4 peptides formed from prodynorphin?

Back 38

1. alpha neoendorphin
2. beta neoendorphin
3. DYN A
4. DYN B

Front 39

T/F: You can't make LEU-ENK from prodynorphin but prodynorphin can take LEU-ENK & make 4 active peptides

Back 39

True

Front 40

T/F: The precursor protein uses the ER to form the actual opioid peptides

Back 40

True

Front 41

Opioid peptides are degraded by what enzyme?

Back 41

peptidases

Front 42

What is the overall effect of the opiode peptide R?

Back 42

all inhibitory b/c decreases cAMP, decreases, Ca, & decreases K

Front 43

All of the cell bodies for the beta endorphin opioid peptides are found where?

Back 43

Arcuate nucleus

Front 44

The arcuate nucleus sends beta endorphin opioid projections to what parts of the brain? (6 projections)

Back 44

hippocampus
hypothalamus
periaqueductal grey (PAG)
Raphe nucleus
Striatum
nucleus accumbens

Front 45

This area of the brain is responsible for motor rigidity with beta endorphin?

Back 45

striatum

Front 46

The_________ is associated with stress when beta endorphin is around

Back 46

hypothalamus

Front 47

The PAG and raphe are important in__________ when beta endorphin is around

Back 47

pain

Front 48

which nucleus is associated with euphoria and addiction?

Back 48

nucleus accumbens

Front 49

proenkephalin precursor have interneurons where in the brain?

Back 49

hypothalamus
PAG & substantia gelationosa
nucleus tractus solitarious
striatum
nucleus accumbens
cortex
hippocampus
limbic system

Front 50

proenkephalin interneurons in hypothalamus

Back 50

endocrine fxns

Front 51

When proenkephalin is around, the _______ _______ and ________ ________ are associated with pain

Back 51

periaqueductal grey & substantia gelatinosa

Front 52

T/F:the proenkephalin interneurons associated with the nucleus tractus solitarious bring on pain

Back 52

False: bring on autonomic reflexes

Front 53

Besides the brain, proenkephalin is also seen where?

Back 53

adrenal medulla
posterior pituuitary
stomach
GI tract

Front 54

when it comes to the nucleus accumbens, prodynorphin is different from the other precursors how?

Back 54

when the interneurons going to the nucleus accumbens are stimulated, they bring about dysophoria

Front 55

With the prodynrophin precursor, interneurons go where in the brain? (6 pathways)

Back 55

hypothalamus
ventral spinal cord
striatum
substantia nigra
nucleus accumbens
limbic system

Front 56

with dynorphin, stimulation of the______ ________ _______ is associated with pain.

Back 56

ventral spinal cord

Front 57

The 2 neurons associated with motor rigidity with dynoprhin

Back 57

striatum, substantia nigra

Front 58

which interneuron is involved with endocrine by dynorphin

Back 58

hypothalamus

Front 59

why does stimulation of nucleus accumbens lead to dysphoria with dynorphin?

Back 59

the kappa R are directly on the DA neuron which inhibits DA & give a dysphoric effect

Front 60

pain R comes from skin and goes to ___________ tract which is found in________ ________.

Back 60

spinothalamic tract
substantia Gelatinosa (SG)

Front 61

4 ways opioids affect pain pathways?

Back 61

1. ENK neuro in SG----- release MET---- bind to pre & post R & stop pain transmission
2. dinorphin affect post R of the spinothalamic tract to stop pain
3. mu kappa and gamma R when one stops transmission of signal to thalamus, cortex, and limbic system to decrease pain
4. PAG & raphi have mu R to turn ON NE & 5HT which inhibits pain

Front 62

peptide that is released from the dorsal root ganglia?

Back 62

Substance P

Front 63

These peptide transmitters are involved in feeding, metabolism, and weight gain?

Back 63

CCK
neuropeptide
VIP
Leptin

Front 64

with this cranial nerve lesion, a patient won't see anything in the hemispace

Back 64

CN II

Front 65

what is gaze conjugate?

Back 65

when both eyes move together

Front 66

define smooth pursuit?

Back 66

how smoothly are the eyes tracking a moving finger

Front 67

to test for gaze conjugate, smooth pursuit & sacades, you would be looking at which CNs?

Back 67

CN III, IV, & VI

Front 68

Define herniation syndrome?
Affects which CN?

Back 68

it's a big mass involving the one side of the brain which pushes on the brain stem. The pressure increases--- pupils blow up--- CN III paralysis. THIS IS AN EMERGENCY!!!!. patient only has hours to get help or they will die.
CN III is affected

Front 69

tracts for smooth pursuit go to which part of the brain?

Back 69

medial vestibular nucleus

Front 70

Scadic eye movement is read in which part of the brain

Back 70

frontal lobe

Front 71

how are the eyes affected if there is a lesion in the pre-frontal area of the brain?

Back 71

eyes may become stuck where they can't move past the midline

Front 72

T/F: periphal movement is seen by the eye & controlled by the inferior colliculi and occipital lobe.

Back 72

False: controlled by superior colliculi and parietal lobe

Front 73

Flashing a lite in the eye tests which CNs?

Back 73

CN II & III

Front 74

What happens with peripheral vision if the frontal lobe is damaged.

Back 74

Since the frontal lobe controls main vision, if it is damaged and there is peripheral movement, a person would not be able to focus ahead but their parietal & superior culliculi will dominate & therefore will always be distracted by peripheral movement

Front 75

What do you see when shining a light and the right CN II is damaged?

This condition is diagonostic in which disease?

Back 75

if you shine the lite in the rt eye---- lite comes in--- produces weak stimulus in rt side of brain---pupils dilate a bit with the light shining.
when you test the good eye---- will see full transmission and full constriction of the pupils

seen very early on in MS

Front 76

when testing CN V, what are you testing?

Back 76

simple touch of the face, sensation, vibration. Also test for coolness and heat of something on the face. Could also test for corneal brushing.

Front 77

pathway of testing CN V from the face to the brain?

Back 77

Test face--- cavernous sinus----subarchnoid

Front 78

CN VII innervates what?

Back 78

mm of facial expression

Front 79

crc of Bell's Palsy

Back 79

can't raise eyebrow, face drooping, worry about cornea b/c can't close the eye. will only be able to move one side of the mouth

Front 80

how can you differentiate Bell's palsy from a stroke in the brain?

Back 80

if it's a stroke of the brain, you would also see problems with the forehead

Front 81

how do you test CN VIII

Back 81

test by lite sounds near each ear

Front 82

if there is a problem with CN X, how would it affect the palate of the mouth?

Back 82

it would not be lifted symmeterically

Front 83

with this damage, you see impairment to pain & temp on opposite side of the body below the lesion level

Back 83

damage to one side of the spinal cord

Front 84

when testing the motor system, the patient closes his eyes and you see an arm drift and change in small fine movements, it tells us what?

Back 84

the problem or lesion is in the brain

Front 85

when there is instability of gate after a long time of alcohol abuse, the damage is where?

Back 85

cerebellum

Front 86

touching own nose and then touching the doctor's finger several times tests this part of the brain?

Back 86

cerebellum

Front 87

when it comes to memory, how can you differentiate where the lesion would be?

Back 87

if lesion is in the hippocampus, one would have trouble forming new memories.
if lesion is in the whole cortex, whole information would be lost (seen in cases of dimensia)

Front 88

True / False
In the spinal cord, dynorphin neurons are located in the substantia gelatinosa cell layer whereas enkephalin interneurons are located more ventrally.

Back 88

False

Front 89

T/F: Activation of mu opioid receptors leads to activation of potassium channels and IPSPs, via mediation by Gs.

Back 89

False

Front 90

T/F: Light energy entering the eye interacts with photopigments and cause sodium channels to open and produce a negative generator potential.

Back 90

False

Front 91

T/F: Intraocular pressure is created by the rates of secretion of aqueous humor by the ciliary processes and the rates of outflow by the trabecular meshwork.

Back 91

True

Front 92

T/F: The dioptric media of the eye includes the cornea, aqueous media vitreous humor, choroid and lens.

Back 92

False

Front 93

Third-order sensory neurons have their cell bodies located in sensory nuclei of the ________.

Back 93

THALAMUS

Front 94

Regardless of etiology, the most prominent and specific pathological changes observed in brains of Parkinson’s disease are:
A. Dilation of ventricles due to a massive loss of neurons in the brain.
B. Formation of tangles and plaques in the affected neurons/regions.
C. Degeneration of the dopaminergic pathway between ventral tagmental area and nucleus accumbens area.
D. Degeneration of the dopaminergic pathway between substantia nigra and striatum.

Back 94

D

Front 95

Dopamine is a key neurotransmitter in relation to the pathogenesis of Parkinson’s disease because:
A. It binds dopamine receptors on neurons in the substantia nigra to regulate movements.
B. It binds dopamine receptors on neurons in the striatum to send out a stimulative signal to neurons in other regions to regulate movements.
C. It interacts with dopamine receptors on neurons in the striatum to maintain a fine balance between two opposing pathways to precisely regulate movements.
D. It interacts with other neurons in the brain to suppress the inhibitory signal sent out of basal ganglia to fine tune the movements.

Back 95

C

Front 96

The ability of a drug to increase the activity of this transmitter leads to drug addiction and drug cravings

Back 96

Dopamine

Front 97

. What are the two afferent nuclei of the basal ganglia?
___________________ and __________________.

Back 97

caudate nucleus and putamen

Front 98

Name the rate-limiting step in the synthesis of acetylcholine: _____________

Back 98

the choline transporter or choline reuptake

Front 99

T/F: In the spinal cord, dynorphin neurons are located in the substantia gelatinosa cell layer whereas enkephalin interneurons are located more ventrally

Back 99

false

Front 100

T/F: Activation of mu opioid receptors leads to activation of potassium channels and IPSPs, via mediation by Gs.

Back 100

false

Front 101

List 2 of the 3 opioid peptide precursor proteins:
a. _________________________
b. _________________________

Back 101

pro-opiomelanocortin (POMC), pro-enkephalin, pro-dynorphin (any two