Neurotransmitters Flashcards

1
Q

How does Clostridium Botulism prevent the pre-synaptic terminal from signalling the post-synaptic terminal?

A

Binds to nicotinic cholinergic receptors prevents the binding, docking and fusion of vesicles causing flaccid paralysis.

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

How does Clostridium tetanii cause uncontrolled muscle contraction?

A

Targets inhibitory Renshaw interneurons of the spinal cord

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

what type of receptor are nicotinic ACh receptors?

A

ionotropic, non-selective

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

What type of receptor are muscarinic receptors?

A

metabotropic

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

Name the agonists and antagonists for Nicotinic cholinergic receptors

A

Agonist: ACh, nicotine
Antagonist: curare

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

Name the agonists and antagonists of muscarinic ACh receptors.

A

Agonist: ACh, muscarine
Antagonists: atropine, ipratropium

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

What is the clinical application of curare?

A

muscle relaxant: used in capturing prey and seizures

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

Where do nicotinic ACh receptors occur?

A

Skeletal muscle: nAChRm

Neuronal (CNS, PNS): nAChn

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

Where do muscarinic ACh receptors occur?

A

M2 receptors: heart

M3 receptors: bronchioles, destrusor muscle, salivary gland, pancreatic duct, GI tract, occular SM

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

What is the action of M2 muscarinic receptors of the heart?

A

decrease HR

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

What are the overall actions of M3 muscarinic ACh receptors ?

A

Increased secretion of salivary glands, pancreatic duct, gastric acid

Increased contraction of bronchioles, GI tract and ocular smooth muscle

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

How do organophosphates affect ACh?

A

Prevents termination of ACh by acetycholinesterase –> refractory depolarised state

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

What would be the effects of reduced ACh termination?

A

refractory depolarised state –> muscle: muscle tremors, stiff gate, muscle spasms

parasympathetic and central synapses: salivataion (M3), lacrimation (M3), pupillary constriction (M3), diarrhea (M3), bradycardia (M2)

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

How does curare affect ACh binding to the post-synaptic terminal?

A

competitively binds to ACh receptors and blocks receptors that have already been activated by ACh

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

What is the consequence of preventing ACh signalling at the post-synaptic membrane?

A

relaxation of skeletal msucle

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

What is the function of myasthenia gravis?

A

ACh receptor degradation: exacerbates conditions where ACh competitive agonists are present as in the case of curare

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

What is atropine typically used for in veterinary medicine?

A

treats bradycardia, AV block and organophosphate poisoning (acetycholiesterase degradation)

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

How does atropine induce tachycardia?

A

Competitive binding of M2 muscarinic receptors of the heart prevent binding of ACh and consequentially reduce parasympathetic stimulation of HR and contractility.

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

What is the function of glutamate?

A

main stimulatory neurotransmitter of the CNS. Acts in opposition to GABA (inhibitor)

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

How is glutamate synthesised?

A

1) excitatory amino acid trasnporters (EAATs) –> glutamine (glial cells) –> system A transporter (SAT2) –> pre-synaptic terminal –> glutaminase –> glutamate –> vesicular glutamate transporters (VGLUT) –>
2) glucose –> transamination of a-ketoglutarate ((krebs cycle) –> glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Name the Ionotropic glutamate receptors.

A

AMPA

NMDA

Kainate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name which ions pass through the ionotropic glutamate receptor NMDA .

A

Ca influx
Na influx
K efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name the general function of all glutamate ionotropic receptors.

A

excitatory stimulation (Na influx and K efflux)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the function of metabotropic glutamate receptors.

A

excitatory and inhibitory signals of post-synaptic vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the action of ketamine?

A

Binds to NMDA ionotropic glutamate receptor at PCP binding site causing inhibition of the excitatory signals (Na, Ca)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the function of Mg2+ at the NMDA glutamate ionotropic receptor?

A

Mg2+ acts as to block transmission during resting membrane potential therefore receptors are only able to be activated during states of depolarisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is long term potentiation?

A

With continual Ca influx, synaptic connections between neurons become stronger
mechanism underlying memory and learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

WHat are the consequences of excess glutamate?

A

Glutamate toxicity:

activation receptors –> destruction neurons –> stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What causes excess glutamate?

A

reduced enzymatic decomposition

increased glial cell uptake (EAAT) –> inflammation + further release glutamate

pathologic conditions with inappropriate activation of microglia and astrocytes –> relelase glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the function of GABA (y-aminobutyric acid/glycine)?

A

Reduces anxiety, stress and fear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How does GABA reduce anxiety, fear and stress?

A

signal inhibition in the brain –> calming effect + reduce hyperactivity

32
Q

What are the precursosrs of GABA?

A

Glucose

Glutamate

33
Q

Where are GABA receptors located?

A

Brain and spinal cord interneurons incl cerebellum.

34
Q

How do GABA ionotropic and metabotropic receptors differ in their ability to inhibit synapse signaling?

A

ionotropic: Cl- influx
metabotropic: K efflux

35
Q

How are GABA neurotrasnmitters terminated?

A

Na dependent co transporters at glial cells and pre-synaptic terminals

36
Q

List the ionotropic and metabotropic GABA type receptors.

A

ionotropic: GABAa, GABAc
metabotropic: GABAb

37
Q

What is the function of dopamine?

A

motor control ,

reward (addiction, arousal, motivation, memory, mood, attention)

38
Q

How is dopamine synthesised?

A

tyrosine –> dihydroxyphenylalanine (DOPA)

dopamine (hypothalamus)

39
Q

How might inappropriate dopamine activity appear clinically?

A

Parkinsons disease
Hypokinetic syndrome
Pituitary pars intermedia dysfunction (cushings): reduced inhibition of ACTH

40
Q

List the receptors for Dopamine.

A

D1 like: D1, D5

D2 like: D2, D3, D4

41
Q

What are the function of D1 like receptors (dopamine)?

A
Excitation --> 
activation adenylate cyclase -->
cAMP activation -->
PKA activation -->
cAMP regulatory binding protein  (CREB) phosphorylation -->
CREB translocation to nucleus -->
activation of CREB dependent trascription genes -->
synaptic plasticity -->
learning and memory
42
Q

What are the effects of D2 like (dopamine) receptors?

A

inhibition of CREB activation pathways involved in memory and learning

43
Q

how is dopamine neurotransmitters terminated?

A

presynaptic terminal: reuptake via dopamine transporters (DAT)

post-synaptic terminal: conversion to HVA (homovanillic acid)

diffusion into circulation: metabolised by hepatic monamine oxidase (MAO) and catechol O methyl trasnferase (COMT) into HVA

44
Q

What is the function of noradrenaline?

A

attention, arousal, memory, learning, mood, anxiety, pain, sleep wake cycles.

45
Q

How is norepinephrine synthesised?

A

tyrosine –> dihydoxyphenyllalanine–> dopamine –> norepinephrine

46
Q

Name the receptors involved in noradrenaline.

A

a (adrenergic): a1, a2 subtypes

b (adrenergic: G protein): B1, B2, B3 subtypes)

47
Q

How is noradrenaline terminated?

A

pre and post synaptic uptake
diffusion
MAO and COMT metabolism

48
Q

What is the formal name for serotonin?

A

5-hydroxytryptamine

49
Q

Name the functions of serotonin

A

emotions, mental arousal, fullness (satiety) and motor behaviours

50
Q

How is serotonin synthesised?

A

tryptophan –>
5-hydroxytryptophan –>
5-hydroxytryptamine (serotonin)

51
Q

Are the receptors for serotonin mostly metabotropic or ionotropic?

A

metabotropic except HTH3 which is ionotropic

52
Q

How is serotonin terminated?

A

serotonin reuptake transporter (SERT)

53
Q

How do antidepressant drugs function?

A

selective serotonin reuptake inhibitors (SSRI) inhibit serotonin uptake by SERT

54
Q

Name one compound used in antidepressants.

A

Fluoxetine hydrochloride (prozac)

55
Q

What is the function of a2 adrenergic receptors at the sympathetic postganglionic neurons.?

A

presynaptic inhibition of noradrenaline release

56
Q

Name where you might find a2 adrenergic receptors?

A
blood vessel SM
adipose tissue
sympathetic post ganglionic neurons
sphincters
urethra
57
Q

Name where you might find B1 adrenergic receptors?

A

myocardium
SA node
Kidney

58
Q

Name where you might find B2 receptors and what its function is?

A

relaxation:
smooth muscle of bronchioles
intestine
some blood vessels (skeletal muscle)

59
Q

Name where you might find B3 adrenergic receptors?

A
detrusor muscle (relaxation, enables bladder filling) 
adipose tissue (lipolysis)
60
Q

What are the 5 categories of neuropeptides?

A
Brain/gut
opioid
pituitary peptides
hypothalamic releasing hormones
miscellaneous
61
Q

What is a neurotrasnmitter from the brain/gut peptide group of neuropeptides?

A

substance P

62
Q

What is a neurotrasnmitter from the opioid neuropeptide category?

A

endorphins
enkephalins
dynorphins

63
Q

Name a neurotransmitter from the group of pituitary peptides.

A

ADH
oxytocin
ACTH

64
Q

Name the neurotrasnmitters from the group of neuropeptides: hypothalamic releasing hormones.

A

Gonadotropin releasing hormone (GnRH)

Thyropropin-releasing hormone (THR)

65
Q

Name a neurotrasnmitter from the neuropeptide group classed “ miscellaneous”.

A

angiotensin 2

66
Q

How is Nitric oxide synthesised?

A

arginine converted to NO and citrulline via NO synthesase

67
Q

How does NO function at the terminal membrane?

A

activation of soluble guanylyl cyclase –> cGMP –> protein kinase G

68
Q

NO is stored in vesicles. T or F?

A

F: generated as needed

69
Q

NO is released from the pre-synaptic terminal via Ca dependent exocytosis. T or F.

A

F: diffuses through lipid membrane.

70
Q

NO decays spontaneously into nitrites, nitrates and O and H20 and therefore does not require enzymatic degradation. T or F.

A

T

71
Q

NO does not interact with specific receptors and is therefore not confined to the post synaptic membrane. T or F.

A

T

72
Q

NO acts as retrograde messenger: regulates function of axon terminals presynaptic to neuron in which produced. T or F.

A

T

73
Q

Which receptors does Diazepam function on and what is its mode of action?

A

GABA

enhance mode of transmission –> trasnquiliser

74
Q

Which receptor is involved in Xylazine and what is its action?

A

a2 adrenergic agonist –>
presynaptic inhibition of noradrenaline release –>
tranquiliser

75
Q

Which receptor does Domperidone bind to and what is its effect?

A

blocks D2 receptor preventing fungus of fescue binding –> prolactin formation –> milk production