Brainscape's Knowledge GenomeTM

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


See full index

Brain and Behaviour > Chemical Signalling > Flashcards

Chemical Signalling Flashcards

You may prefer our related Brainscape-certified flashcards:
The Brain flashcards
1
Q

What are the types of neurotransmitter?

A

amino acids
monoamines
acetylcholine
neuropeptides

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

What are the types of neurotransmitter?

A

amino acids
monoamines
acetylcholine
neuropeptides

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

What are amino acids?

A

chains of proteins e.g. GABA and glutamate (responsible for fast transmission)

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

What are examples of monoamines?

A

dopamine and serotonin

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

Where are acetylcholine’s synthesised and stored?

A

they are synthesised in the presynaptic terminal and stored in synaptic vesicles

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

When are acetylcholine’s released?

A

when there is a local increase in Ca2+

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

Where are neuropeptides synthesised and released?

A

they are synthesised in the cell soma and transported to the terminal where they are stored in secretory granules

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

When are neuropeptides released?

A

when there is a global increase in Ca2+

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

Give an example of a neuropeptide

A

endorphins

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

What are amino acids?

A

chains of proteins e.g. GABA and glutamate (responsible for fast transmission)

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

What are examples of monoamines?

A

dopamine and serotonin

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

Where are acetylcholine’s synthesised and stored?

A

they are synthesised in the presynaptic terminal and stored in synaptic vesicles

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

When are acetylcholine’s released?

A

when there is a local increase in Ca2+

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

Where are neuropeptides synthesised and released?

A

they are synthesised in the cell soma and transported to the terminal where they are stored in secretory granules

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

When are neuropeptides released?

A

when there is a global increase in Ca2+

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

Give an example of a neuropeptide

A

endorphins

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

What are the criteria for neurotransmitters?

A

chemically synthesised presynaptically
electrical stimulation leads to the release of a chemical
chemical produces physiological effect
terminate activity

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

How is glutamate synthesised?

A

it is synthesised from glucose or glutamine in the nerve terminals

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

How is glutamate stored?

A

it is loaded and stored in vesicles by vesicular glutamate transporters

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

How is glutamate released?

A

exocytosis

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

What is neuromodulation?

A

alteration of the presynaptic cell’s ability to release neurotransmitter or the postsynaptic cell’s ability to respond

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

What is the reuptake mechanism for glutamate?

A

excitatory amino acid transporters reuptake glutamate in the plasma membrane of presynaptic cell and surrounding area

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

What can too much glutamate/too little GABA cause?

A

hyperexcitability (epilepsy) or excitotoxicity

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

What is cerebral ischemia?

A

insufficient blood flow in the brain caused by plaques/tumors

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

What are some symptoms of ischemia?

A

weakness
visual impairment
release of glutamate
excitotoxic cell death

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

What is an agonist?

A

a drug which can combine with a receptor on a cell to produce a cellular reaction

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

What is an antagonist?

A

a drug that reduces or completely block the activity of the agonist, no cellular effect after interacting with a receptor a.k.a. endogenous ligand

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

What is an excitatory post synaptic potential?

A

glutamate ionotropic receptors flux Na+ depolarising the postsynaptic neuron

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

What is an inhibitory post synaptic potential?

A

GABA ionotropic receptors flux Cl- hyper polarising the postsynaptic neuron

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

What happens at an AMPA receptor?

A

an ionotropic receptor
the binding of glutamate leads to the opening of a Na+ channel and hence depolarisation
has slight K+ permeability
a fast opening channel

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

What are the features of an NMDA receptor?

A 
an ionotropic receptor
voltage dependent blockade
permeable to Na+, K+, Ca2+
slow opening channel
requires glutamate and glycine (cofactor) to open the gate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What can be caused by the dysregulation of NMDA?

A

Schizophrenia symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do we know NMDA receptors are linked with schizophrenia?

A

phencyclidine and MK801 block NMDA receptors and produce schizophrenia like symtpoms

34
Q

What happens during glutamate exciotoxicity?

A

excessive Ca2+ influx activates calcium dependent proteases and phospholiphases which damage the cell

35
Q

Where is GABA stored?

A

it is loaded and stored into synapses by a vesicular GABA transporter

36
Q

How is GABA synthesised?

A

from glutamate

37
Q

When is GABA released?

A

during excytosis (Ca2+ dependent)

38
Q

Where does GABA act?

A

ionotropic GABAa receptor
metabotropic GABAb receptor
both are on the postsynaptic membrane

39
Q

How is GABA cleared from the synapse?

A

reuptake using transporters on glia and neurons including non-GABAergic neurons

40
Q

What are the effects of too much GABA?

A

sedation/coma

anxiolytic

41
Q

What are 2 features of the ionotropic receptors?

A

GABA ligand gated Cl- channels

fast IPSP’s

42
Q

What is a feature of metabotropic receptors?

A

slow IPSP’s

43
Q

What does GABA do?

A

increase the permeability of Cl- and hypolarises the neuron

44
Q

What is an indirect agonist?

A

An agonist which only works in the presence of a particular neurotransmitter

45
Q

What do barbiturates do?

A

enhance the effect of GABA

general depression of neuronal activity

46
Q

What are some risks involved with barbiturates?

A

small difference between therapeutic dose and overdose
high suicide risk
can lead to dependence and withdrawal

47
Q

What can benzodiazepines be used for?

A 
fast acting anxiolytics
anticonvulsant
sedative
muscle relaxant
amnestic
48
Q

What is some evidence for GABAergic dysfunction in anxiety disorders?

A

patients with panic disorder are shown to have less benzodiazepine binding sites

49
Q

What is a diffuse modulatory system?

A

populations of neurons that project diffusely and modulate the activity of glutamate and GABA neurons in their target areas

50
Q

What is the function of dopamine?

A

its is the pleasure/reward molecule which projects into the forebrain

51
Q

What is the nigrostriatal system’s involvement in dopamine?

A

the substantia nigra projects dopamine onto the neostratium which is involved in movement

52
Q

What effect does Parkinson’s disease have on dopamine?

A

it destroys the dopamine projections from the substantia nigra to the basal ganglia

53
Q

What effect does Huntington’s disease have on dopamine?

A

destroys the target dopamine neurons in the striatum

54
Q

What is the mesolimbic system’s involvement in dopamine?

A

the ventral tegmental area projects dopamine to the nucleus accumbent, this is involved in reinforcement and reward

55
Q

What happens withe dopamine during addiction?

A

drug abuse can lead to enhanced dopamine release in the nucleus accumbens

56
Q

What is the mesocortical system’s involvement in dopamine?

A

the ventral tegmental area projects dopamine to the prefrontal cortex, involved in working memory and planning

57
Q

How is dopamine synthesised?

A

tyrosine is converted into L-Dopa and then dopamine

58
Q

What is tyrosine and how is it catalysed?

A

it is an essential amino acid obtained through diet which is catalysed by tyrosine hydroxylase

59
Q

How is L-Dopa catalysed?

A

by dopa decarboxylase

60
Q

How is tyrosine hydroxylase reduced?

A

dopamine is competing for binding with an essential cofactor, too much dopamine lowers the tyrosine hydroxylase activity

61
Q

How is tyrosine hydroxylase activity increased?

A

presynaptic activity leads to the phosphorylation of TH increasing its activity
prolonged activity leads to an increase in TH gene transcription

62
Q

What effect does reserpine have on dopamine synthesis and storage?

A

impairs the storage of monoamines in synaptic vesicles leaving them empty

63
Q

What effect do amphetamines/methylphenidates have on dopamine synthesis and storage?

A

psychostimulants which block the reuptake of monoamines into the terminals so there is more dopamine in the synaptic cleft extending its action

64
Q

What effect does > selegiline/entacapone have on dopamine synthesis and storage?

A

prevents the breakdown of catecholamines increasing the releasable pool available

65
Q

How is dopamine released?

A

depolarisation of the presynaptic membrane
influx of Ca2+ through voltage gated channels
Ca2+ dependent vesicle docks to the membrane and releases the neurotransmitter

66
Q

What does the noradrenergic system control?

A

arousal and attention

67
Q

What can noradrenergic dysfunction lead to?

A

anxiety and depression

68
Q

What does the serotonergic system control?

A

appetite, pain, sleep and emotions

69
Q

How is serotonin synthesised?

A

tryptophan is converted into 5-hydroxytryptophan and then serotonin

70
Q

How does fluoxetine affect the serotonin system?

A

blocks the reuptake of serotonin and is used as an antidepressant/anti-anxiety medication

71
Q

How does fenfluramine affect the serotonin system?

A

induces the release of serotonin in the synaptic cleft and inhibits its reuptake used as an appetite suppressant

72
Q

How does MDMA affect the serotonin system?

A

causes transporters to run backwards releasing serotonin into the synapse

73
Q

What is acetylcholine synthesised from?

A

choline

74
Q

Where is acetylcholine stored?

A

in vesicles

75
Q

How is acetylcholine metabolised?

A

it is rapidly degraded in the synaptic cleft by acetylcholinesterase into choline

76
Q

How is acetylcholinesterase synthesised?

A

by the cholinergic neuron, secreted into the synaptic cleft and associated with the axonal membrane

77
Q

What to acetylcholinesterase inhibitors do?

A

block the breakdown of acetylcholine thus prolonging its action in the synaptic cleft

78
Q

What do botulinum and tetanus toxins do?

A

block the docking of vesicles by attacking SNARE proteins

79
Q

What does botox do?

A

acts at the euro-muscular junction causing the muscles to lose all input and become permanently relaxed

80
Q

What is the action of the tetanus toxin?

A

inhibits the release of glycine, disinhibiting the cholinergic neurons so they continuously fire causing permanent muscle contraction

81
Q

What is a disorder associated with the peripheral cholinergic system?

A

myasthenia gravis; an autoimmune disease which destroys cholinergic receptors in the muscle

82
Q

What is the cholinergic systems role in Alzheimer’s disease?

A

loss of cholinergic neurons in the basal ganglia, underlies deficits in in memory

Brain and Behaviour (9 decks)

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