Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

B&B 3 > CNS Neurotransmitters > Flashcards

CNS Neurotransmitters Flashcards

1
Q

glutamate: inhibitory or exitatory?

GABA: inhibitory or excitatory?

enzyme that converts glutamate to GABA

A

glutamate- excitatory

GABA- inhibitory

glutamic acid decarboxylase (GAD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

neuropeptide that functions as pain perception

A

substance P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

EPSP vs IPSP; which one is hyperpolarizing? which is depolarizing?

A

EPSP- excitatory postsynaptic potential (glutamate); depolarizing

IPSP- inhibitory post synaptic potential (GABA); hyperpolarizing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

are EPSPs or IPSPs fast or slow?

A

both can be fast or slow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

acetylcholinergic receptors- nicotinic vs muscarinic: where are each found? are IPSPs/EPSPs slow or fast?

A

nicotinic: in PNS on NM junction; fast EPSP
muscarinic: in CNS in brain & autonomy. ganglia; fast IPSP, slow EPSP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

location of glutamate neurons and the locations of their terminals

A

cns interneurons- local and long tract connections

primary sensory neurons- second-order neurons in CNS

pyramidal cells of cerebral cortex- basal ganglia, thalamus, spinal cord, other cortical areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

location of GABA neurons and their terminals

A

CNS interneurons- local connections

cerebellar cortex (purkinje cells)- deep cerebellar nuclei

caudate nucleus, putamen- globus pallidus, substantia nigra

globus pallidus, substantia nigra- thalamus, subthalamic nuclei

thalamic reticular nucleus- other thalamic nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

believed to be the source of learning

A

glutamate NMDA receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

the NMDA receptors requires these 2 things

A

glutamate/NMDA
AND
depolarization (voltage-gated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

the depolarization of the Glutamate NMDA receptor frees…

A

Mg2+ that blocks the channel at rest, allowing influx of Ca2+, which augments transmission at the synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

regulation of the strength of connection between two synapses

A

synaptic plasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe pathology and causes of glutamate toxicity

A

excessive Ca2+ intake triggers neuronal injury/death; stems from excessive glutamate release, or poor glutamate reuptake; stroke anoxia can release toxic amts of glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

GABA hyperpolarizes the cell by influx od

A

Cl-

GABAa- ligand gated

GABAb- GPCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

benzos and barbituates bind to these receptors

GHB, alcohol, baclofen bind to these types of receptors

A

GABAa

GABAb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

disease models of GABA excess or inhibition

A

huntingtons- destruction of GABA nerons

tetanus and strychnine- inhibit presynaptic GABA release

stiff-person syndrome- antibodies to GAD prevent GABA production, causing autoimmune or paraneoplastic syndrome

excess- seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

treat seizures (too much glutamate) with more GABA via these drugs..

A

benzos- increase GABA efficiency

valproate- inhibit GABA-deactivating enzymes

topiramate- inhibit GABA reuptake

side effects: sedation, cognitive slowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

non-therapeutic GABA

A

anxiolysis, hypnosis, amnesia; date rate drugs (GHB, benzos)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

nuclei of origin of dopamine

A

substantia nigra, ventral tegmental area, hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

nigrostriatal tract function of dopamine

A

fluid, smooth muscle action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

mesolimbic tract function of dopamine

A

fear and reward responses

21
Q

mesocortical tract function of dopamine

A

motivation and response

22
Q

tubero-infundibular tract function of dopamine

A

secretion of hormones, notably prolactin

23
Q

pathology of Parkinson’s disease

A

death of PARS COMPACTA within the SUBSTANTIA NIGRA

24
Q

drugs that block dopamine reuptake, and cause exocytosis of dopamine, leading to excess dopamine

A

cocaine, methamphetamine- can cause paranoia, hallucinations, delusions, disorganized thoughts

25
Q

why give L-DOPA to Parkinson’s patients?

A

increases dopamine by skipping the rate-limiting step (tyrosine hydroxylase)

26
Q

drugs for depression and ADHD

A

buproprion/methylphenidate to prevent dopamine reuptake

27
Q

many psychotics operate via..

A

D2 receptor antagonism- blocking the inhibition of adenylate cyclase, so cAMP is formed and PKA activated

28
Q

nuclei of origin of serotonin; serotonin tracts

A

raphe nucleus (pons/midbrain)

brain: cortex, cerebellum, hypothalamus; spinal column, PNS

29
Q

receptor subtypes for serotonin

A

5HT-1 and 2: mood, appetite, energy, sexual function

5HT-3: localized in area postrema/nausea

30
Q

therapeutics for major depressive disorder

A

SSRIs, TCA and MAOIs

31
Q

DOC for anxiety disorders

A

benzos

32
Q

drug for nausea; its mechanism of action

A

ondansentron - 5HT-3 receptor antagonist

33
Q

serotonin toxicity induced by excessive serotonin causes these symptoms

A

headache, delirium

autonomic: hyperthermia, hypertension
somatic: tremor, hyperreflexia, clonus

34
Q

drugs and compounds that can be abused and cause serotonin syndrome

A

LSD, MDMA

tyramine “cheese effect”: MAOs decrease, tyramine increases, hypertension ensues

35
Q

nuclei of origin of norepinephrine; tracts

A

locus ceruleus

broad projections throughout frontal cortex, limbic, spinal

36
Q

norepinephrine receptors function to induce sympathetics or parasympathetics?

A

sympathetics

37
Q

panic attacks may be caused by deficiency in

A

norepinephrine reuptake

38
Q

antidepressants increase the availability of

A

norepinephrine

39
Q

a selective norepinephrine and dopamine reuptake inhibitor drug

A

buproprion (wellbutrin)

40
Q

selective serotonin/norepinephrine reuptake inhibitor drugs

A

venlafaxine (Effexor)

duloxetine (Cymbalta)

41
Q

acetylcholine nuclei of origin

A

nucleus basalis of Mynert

pedunculopontine nucleus

42
Q

acetylcholine tracts

A

pedunculopontine projects to thalamus, basal ganglia

nucleus basalis of mynert (NBM) projects to cortex

43
Q

NMB/acetylcholine is associated with

A

memory, learning, deficits with Alzheimer’s, LIMBIC SYSTEM, HOMEOSTASIS

44
Q

effect of acetylcholine in CNS and PNS

A

PNS: parasympathetic stimulation

CNS: inhibitory OR excitatory

45
Q

acetylcholine toxicity symptoms, and what causes them

A

SLUDGE-M (pupil constriction)

organophosphates, sarin gas

46
Q

disease involving degeneration of ACh-producing neurons at nicotinic receptors

A

Alzheimer’s

47
Q

anti-muscarinic toxicity symptoms and causes

A

hot as a hare, blind as a bat, dry as a bone, mad as a hatter

anti-nausea meds, anti-depressants, anti-psychotics, antihistamines, atropine

48
Q

stiff person syndrome associated with this transmitter

A

GABA

B&B 3 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions