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PMCOL 371 - Cellular Neuroscience > 12 - Neurotransmitters > Flashcards

12 - Neurotransmitters Flashcards

1
Q

3 fates of neurotransmitters after synaptic transmission?

A
  1. Neurotransmitters can be returned to axon terminals for reuse or transported into glial cells
  2. Enzymes inactivate neurotransmitters
  3. Neurotransmitters can diffuse out of the synaptic cleft
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2
Q

6 criteria for neurotransmitter substance:

A
  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
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3
Q

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
A
  1. Presence and synthesis
    • The presynaptic neuron should contain the putative NT and be able to synthesize it
  2. Release
    • The putative NT should be released on stimulation of the presynaptic axons
  3. Identity of action
    • Application of the putative NT to the postsynaptic cell should reproduce the effects of normal transmission
  4. Pharmacology
    • The action of a putative NT and the effect of presynaptic nerve stimulation should e altered in the same way by antagonists (eg acetylcholine on NMJ => EPSP | Curare drug inhibit ACh)
  5. Inactivation
    • There should be a mechanism for inactivation of the NT (uptake or metabolism)
  6. Behavioural criteria
    • Drugs which affect NT systems should have observable effects on whole animal
      • (eg GABA → inhibit CNS)
      • GABA blocker → Convulsions
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4
Q

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
A

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
    • The presynaptic neuron should contain the putative NT and be able to synthesize it
  2. Release
    • The putative NT should be released on stimulation of the presynaptic axons
  3. Identity of action
    • Application of the putative NT to the postsynaptic cell should reproduce the effects of normal transmission
  4. Pharmacology
    • The action of a putative NT and the effect of presynaptic nerve stimulation should e altered in the same way by antagonists (eg acetylcholine on NMJ => EPSP | Curare drug inhibit ACh)
  5. Inactivation
    • There should be a mechanism for inactivation of the NT (uptake or metabolism)
  6. Behavioural criteria
    • Drugs which affect NT systems should have observable effects on whole animal
      • (eg GABA → inhibit CNS)
      • GABA blocker → Convulsions
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5
Q

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
A

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
    • The presynaptic neuron should contain the putative NT and be able to synthesize it
  2. Release
    • The putative NT should be released on stimulation of the presynaptic axons
  3. Identity of action
    • Application of the putative NT to the postsynaptic cell should reproduce the effects of normal transmission
  4. Pharmacology
    • The action of a putative NT and the effect of presynaptic nerve stimulation should e altered in the same way by antagonists (eg acetylcholine on NMJ => EPSP | Curare drug inhibit ACh)
  5. Inactivation
    • There should be a mechanism for inactivation of the NT (uptake or metabolism)
  6. Behavioural criteria
    • Drugs which affect NT systems should have observable effects on whole animal
      • (eg GABA → inhibit CNS)
      • GABA blocker → Convulsions
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6
Q

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
A

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
    • The presynaptic neuron should contain the putative NT and be able to synthesize it
  2. Release
    • The putative NT should be released on stimulation of the presynaptic axons
  3. Identity of action
    • Application of the putative NT to the postsynaptic cell should reproduce the effects of normal transmission
  4. Pharmacology
    • The action of a putative NT and the effect of presynaptic nerve stimulation should e altered in the same way by antagonists (eg acetylcholine on NMJ => EPSP | Curare drug inhibit ACh)
  5. Inactivation
    • There should be a mechanism for inactivation of the NT (uptake or metabolism)
  6. Behavioural criteria
    • Drugs which affect NT systems should have observable effects on whole animal
      • (eg GABA → inhibit CNS)
      • GABA blocker → Convulsions
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7
Q

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
A

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
    • The presynaptic neuron should contain the putative NT and be able to synthesize it
  2. Release
    • The putative NT should be released on stimulation of the presynaptic axons
  3. Identity of action
    • Application of the putative NT to the postsynaptic cell should reproduce the effects of normal transmission
  4. Pharmacology
    • The action of a putative NT and the effect of presynaptic nerve stimulation should e altered in the same way by antagonists (eg acetylcholine on NMJ => EPSP | Curare drug inhibit ACh)
  5. Inactivation
    • There should be a mechanism for inactivation of the NT (uptake or metabolism)
  6. Behavioural criteria
    • Drugs which affect NT systems should have observable effects on whole animal
      • (eg GABA → inhibit CNS)
      • GABA blocker → Convulsions
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8
Q

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
A

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
    • The presynaptic neuron should contain the putative NT and be able to synthesize it
  2. Release
    • The putative NT should be released on stimulation of the presynaptic axons
  3. Identity of action
    • Application of the putative NT to the postsynaptic cell should reproduce the effects of normal transmission
  4. Pharmacology
    • The action of a putative NT and the effect of presynaptic nerve stimulation should e altered in the same way by antagonists (eg acetylcholine on NMJ => EPSP | Curare drug inhibit ACh)
  5. Inactivation
    • There should be a mechanism for inactivation of the NT (uptake or metabolism)
  6. Behavioural criteria
    • Drugs which affect NT systems should have observable effects on whole animal
      • (eg GABA → inhibit CNS)
      • GABA blocker → Convulsions
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9
Q

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
  2. Release
  3. Identity of action
  4. Pharmacology
  5. Inactivation
  6. Behavioural criteria
A

Describe how each of the criteria for a neurotransmitter are defined:

  1. Presence and synthesis
    • The presynaptic neuron should contain the putative NT and be able to synthesize it
  2. Release
    • The putative NT should be released on stimulation of the presynaptic axons
  3. Identity of action
    • Application of the putative NT to the postsynaptic cell should reproduce the effects of normal transmission
  4. Pharmacology
    • The action of a putative NT and the effect of presynaptic nerve stimulation should e altered in the same way by antagonists (eg acetylcholine on NMJ => EPSP | Curare drug inhibit ACh)
  5. Inactivation
    • There should be a mechanism for inactivation of the NT (uptake or metabolism)
  6. Behavioural criteria
    • Drugs which affect NT systems should have observable effects on whole animal
      • (eg GABA → inhibit CNS)
      • GABA blocker → Convulsions
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10
Q

Which receptors have a NT binding site that is intrinsic to the ion channel protein?

A

Ionotropic Receptors

GABAA

Nicotinic ACh

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11
Q

In ________ receptors, the NT interacts directly with the ion channel

A

In ionotropic receptors, the NT interacts directly with the ion channel

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12
Q

Ionotropic receptors are involved in the generation of _________

A

Ionotropic receptors are involved in the generation of fast epsp’s and ipsp’s

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13
Q

Ionotropic receptors involve increases in _________ to ____ or _____

A

Ionotropic receptors involve increases in conductance to anions or cations

NT binds channel mol → channel opens → Pos in = depol | Neg in = hyperpolarization | Neg out = depol | Pos out = hyperpol

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14
Q

Five examples of ionotropic receptors:

A
  1. Nicotinic ACh
  2. GABAA
  3. Glycine
  4. 5-HT3 (serotonin)
  5. NMDA, AMPA, and Kainate receptors for glutamate (excitatory ion channels)
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15
Q

Binding site of metabotropic receptors?

A

Binding site remote so information from the NT binding site is “transduced” via G-proteins and sometimes via second messenger systems

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16
Q

With metabotropic receptors, neurotransmitter interacts ______ with the ion channel

A

With metabotropic receptors, neurotransmitter interacts indirectly with the ion channel

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17
Q

Metabotropic receptors are involved in _______ effects

A

Metabotropic receptors are involved in neuromodulatory effects

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18
Q

Activation of metabotropic receptors often leads to decreases in ______ of _______

A

Activation of metabotropic receptors often leads to decreases in conductance of K+ or Ca2+ channels

→ electrical effects => more often close (reduce conductance)

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19
Q

Because NT’s of metabotropic receptors activate second messenger systems - can orchestrate a change in the physiological status of the ___________

NT can affect a variety of _____, _____, _____ and ______

A

Because NT’s of metabotropic receptors activate second messenger systems - can orchestrate a change in the physiological status of the postganglionic neuron (pleiotropic action)

NT can affect a variety of ion channels, ion pumps, enzymes and gene expression

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20
Q

What are four examples of metabotropic receptors?

A
  1. Muscarinic ACh receptor
  2. alpha and beta adrenoceptors (NE/E)
  3. Metabotropic aminoacid receptor
  4. Peptide receptors
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21
Q

Some neurotransmitters such as ____, ___, ____ and _____ act at both ionotropic and metabotropic receptors

A

Some neurotransmitters such as ACh, GABA, Glutamate, and 5-HT act at both ionotropic and metabotropic receptors

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22
Q

_______ and _______ work only on metabotropic receptors

A

peptides and catecholamines work only on metabotropic receptors

→ no ionotropic receptors for peptides

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23
Q

How can nt’s change the activity of neurons over prolonged periods?

A
  • Seconds or minutes in the case of slow synaptic responses or Ca2+ channel modulation
  • Almost permanently following alterations of gene expression
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24
Q

4 ways to inactivate neurotransmitter:!@

A
  • Enzymatic (eg cholenesterase → Ach)
  • Uptake into presynaptic terminals or glial cells (Reuse/recycle)
  • Diffusion
  • Receptor desensitization
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25
Q

What happens at autoreceptors?

A

Receptors on presynaptic membrane

Released transmitter feeds back on presynaptic terminal → inhibits own release of presynaptic Ca++ by inhibiting presynaptic Ca++ channels

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26
Q

Provide an example of autoregulation

A

Noradrenaline from sympathetic neuron also acts on presynaptic membrane of parasympathetic neuron to alter ACh release

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27
Q

Nicotinic receptors are blocked by ______ and ________

A
  • Nicotinic receptors are blocked by d-tubocurarine and _alpha-bungarotoxin (_snake toxin)
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28
Q

Muscarinic receptors are blocked by ________

A

Muscarinic receptors are blocked by Atropine

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29
Q

What are the five Muscarinic receptor subtypes?

A

M1, M2, M3, M4, M5

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30
Q

Where are nicotinic synapses located?

A
  • Neuromuscular junction
  • Autonomic ganglia (SNS/PNS)
  • Brain and Spinal cord (all nerves leaving CNS release ACh)
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31
Q

Where are Muscarinin synapses located?

A
  • Parasympathetic neuroeffectors
  • Brain and Spinal Cord
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32
Q

What enzyme is involved in synthesis of Acetylcholine ACh?

A

Chat/CAT - Choline-acetyltransferase

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33
Q

What enzyme inactivates ACh?

A

AChE - Acetylcholinesterase

34
Q

______ is taken up by presynaptic terminal for re-synthesis of ACh

A

Choline is taken up by presynaptic terminal for re-synthesis of ACh

35
Q

What happens if anticholesterases are introduced to the system?

A

Anticholinesterases inhibit cholinesterase

→ unable to breakdown ACh => excess ACh stops heart

36
Q

How is ACh related to alzheimers?

A

ACh plays a role in memory

Some central cholinergic neurons are lost in Alzheimer’s disease

37
Q

ACh can be found in cell bodies in the ____ and ______ and travel to spinal motoneurons

A

ACh can be found in cell bodies in the septum and nucleus basalis and travel to spinal motoneurons

38
Q

ACh can be found in cell bodies in the septum and nucleus basalis and travel to __________

A

ACh can be found in cell bodies in the septum and nucleus basalis and travel to spinal motoneurons

39
Q

____ is the go between of NS and mm

A

ACh is the go between of NS and mm

40
Q

Noradreneline/Norepinephrine acts on which two receptors?

A
  • Alpha and beta receptors
  • GPCR’s
41
Q

Which NT is the main sympathetic neuroeffector?

A

Noradrenaline/Norepinephrine

42
Q

Noradrenaline acts on ______ ; cell bodies in _______

A

Noradrenaline acts on brain and spinal cord ; cell bodies in Locus Coeruleus

43
Q

How is norepinephrine synthesized?

A

In the cytoplasm:

  • Tyrosine is converted to Dopa by tyrosine hydroxylase
  • Dopa is converted to Dopamine by Dopa decarboxylase
  • Dopamine enters synaptic vesicle

In Synaptic Vesicle:

  • Dopamine is converted to Norepinephrine by dopamine beta-hydroxylase
44
Q

How is Norepinephrine inactivated? (2)

A
  • Uptake 1 into presynaptic terminal
    • Reused or inactivated by monoamine oxidase
  • Uptake 2 into postsynaptic neuron or tissue
    • Metabolized by Catechol-o-methyltransferase
45
Q

What happens to norepinephrine that is taken into the presynaptic terminal?

A

It is reused or inactivated by monoamine oxidase

46
Q

What happens to Norepinephrine that is taken up into the postsynaptic neuron or tissue?

A

It is metabolized by Catechol-o-methyltransferase

47
Q

What are two examples of pharmacological blockers of noradrenaline uptake (potentiate actions of noradrenalin)

A

Cocaine

Some antidepressants

48
Q

An example of a pharmacological method that blocks the inactivation of norepinephrine?

A

Monamine oxidase inhibitors

Recall: monoamine oxidase inactivates norepinephrine that is taken back into the presynaptic vesicle

49
Q

Dopamine receptors are present in cell bodies in the _________, ______ and ________

A

Dopamine receptors are present in cell bodies in the Substantia nigra, Ventral tegmental area and Arcuate nucleus of hypothalamus

50
Q

5 dopamine receptors?

A

D1, D2, D3, D4, D5 - GPCR’s

51
Q

Loss of dopaminergic neurons in ______ pathway leads to Parkinson’s Disease

A

Loss of dopaminergic neurons in nigral-striatal (substantia nigra) pathway leads to Parkinson’s Disease

52
Q

Which pathway is dopamine involved in in the ventral tegmental area?

A

mesolimbic pathway

53
Q

What is the pathway of dopamine in the substantia nigra?

A

Nigrostriatal pathway

54
Q

The ________ pathway (DA) is involved in addiction and reward

A

The Mesolimbic (ventral tegmental area) pathway (DA) is involved in addiction and reward

55
Q

dopamine receptor _______ are used to treat psychosis - act in ______ pathway

A

dopamine receptor antagonists are used to treat psychosis - act in mesolimbic (ventral tegmental area) pathway

56
Q

How does cocaine potentiate dopamine?

A

Blocks its uptake - contributes to its euphoric effect in mesolimbic pathway (ventral tegmental area)

57
Q

What are the four serotonin (5-HT) receptors. What type of receptors are they?

A
  • 5-HT1
  • 5-HT2
  • 5HT4
  • 5-HT7

G-protein coupled (metabotropic)

58
Q

Which dopamine receptor is a cation channel?

A

5-HT3

59
Q

Serotonin cell bodies in ______

A

Serotonin cell bodies in Raphe nuclei

60
Q

Serotonin has a peripheral role in _________

A

Serotonin has a peripheral role in enteric nervous system

61
Q

Pharmacology aspect of serotonin (5-HT)

A

Selective serotinin reuptake inhibitors (SSRIs) such as fluoxetine (prozac) used in depression

62
Q

GABA is a major ______ neurotransmitter

A

GABA is a major inhibitory neurotransmitter

63
Q

Inhibition of effects of GABA (with ______) produce _______

A

Inhibition of effects of GABA (with bicuculline) produce convulsant effects

64
Q

GABAa - _______ channel

A

GABAa - Cl- channel (ionotropic)

65
Q

GABAb - _______ receptor

A

GABAb - G-protein coupled receptor (metabotropic)

66
Q

GABAa receptor channel has binding sites for _______, ______, certain _____ and other ________ drugs (potentiate GABA action)

A

GABAa receptor channel has binding sites for benzodiazepines (diazepam etc), barbiturates, certain steroids and other sedative-hypnotic, anxiolytic or anticonvulsant drugs (potentiate GABA action - calm things down)

*EtOH acts on gaba receptors

67
Q

______ activates Cl- channels to act as an inhibitory neurotransmitter esp in spinal cord

A

glycine activates Cl- channels to act as an inhibitory neurotransmitter esp in spinal cord

68
Q

Effects of glycine are blocked by ______

A

Effects of glycine are blocked by strychnine

Strychnine interacts with an ionotropic receptor (Cl-) to cause painful convulsions (laxative effect)

69
Q

Glutamate is an _____ neurotransmittor

A

Glutamate is an excitatory (acidic) aminoacid neurotransmittor

70
Q

What three ionotropic receptors does glutamate act on?

A

NMDA

AMPA

Kainate

71
Q

What metabotropic receptors does glutamate act on?

A

G-protein coupled

72
Q

NMDA receptors require ______ or _____ for activation

A

NMDA receptors require glycine or D-serine for activation

73
Q

NMDA receptors are blocked by _____

A

NMDA receptors are blocked by Mg2+

74
Q

NMDA receptors have a binding site for _________

A

NMDA receptors have a binding site for dissociative anesthetics (NMDA antagonists) eg ketamine

75
Q

Neuropeptide Y controls:

A

appetite and blood pressure

76
Q

Two endogenous peptides that mimic opioids

A

Enkephalins and Endorphins

77
Q

Which neuropeptide is involved in pain transmission?

A

Substance P

78
Q

All neuropeptides interact with ______ receptors

A

All neuropeptides interact with G-protein receptors

79
Q

Activation of GABAa receptors:

a) leads to G-protein activation
b) produces a change in membrane potential by the opening chloride channels
c) Produces responses that can be blocked by benzodiazepines
d) Produces responses that are blocked by low concentrations of strychnine
e) Potentiates the action of glutamate at NMDA receptors

A

Activation of GABAa receoptors:

a) leads to G-protein activation (Cl- channel)

b) produces a change in membrane potential by the opening chloride channels

c) Produces responses that can be blocked by benzodiazepines (potentiates GABA action)
d) Produces responses that are blocked by low concentrations of strychnine (glycine effects blocked by strychnine)
e) Potentiates the action of glutamate at NMDA receptors (glycine or D-serine allow NMDA receptors to be activated)

80
Q

Which of the following enzymes would be found in noradrenergic nerve terminals but not in dopaminergic nerve terminals?

a) Tyrosine hydroxylase
b) Dopa decarboxylase
c) Dopamine beta hydroxylase
d) Choline acetyl transferase
e) Phenylethanolamine N methyl transferase

A

Which of the following enzymes would be found in noradrenergic nerve terminals but not in dopaminergic nerve terminals?

a) Tyrosine hydroxylase
b) Dopa decarboxylase

c) Dopamine beta hydroxylase - converts dopamine to norepinephrine

d) Choline acetyl transferase
e) Phenylethanolamine N methyl transferase

81
Q

Which of the following statements is true?

a) Administration of cocaine to a patient with Parkinson’s disease could theoretically worsen their symptoms
b) Atropine might be useful in reducing some of the effects of nerve gas poisoning
c) Serotonin is exclusively a CNS NT and has no important actions outside of the brain
d) Atropine is of great value in the tx of Alzheimer’s disease
e) All glycine receptors are g-protein coupled

A

Which of the following statements is true?

a) Administration of cocaine to a patient with Parkinson’s disease could theoretically worsen their symptoms - cocaine potentiates dopamine - loss of dopaminergic neurons in nigral-striatal pathway leads to parkinsons

b) Atropine might be useful in reducing some of the effects of nerve gas poisoning - blocks muscarinic receptors of ACh - excess ACh involved in nerve gas poisoning

c) Serotonin is exclusively a CNS NT and has no important actions outside of the brain - serotinin acts in enteric nervous system
d) Atropine is of great value in the tx of Alzheimer’s disease - cholinergic neurons are lost - atropine blocks muscarinic receptors (ACh)
e) All glycine receptors are g-protein coupled - glycine acts on Cl- receptors

82
Q

Which of the following neurotransmitters interacts with an ion channel coupled receptor:

a) NPY
b) Noradrenaline
c) serotonin
d) Dopamine
e) Substance P

A

Which of the following neurotransmitters interacts with an ion channel coupled receptor:

a) NPY - GPCR
b) Noradrenaline - alpha and beta adrenergic receptors (GPCR)

c) serotonin

d) Dopamine - (GPCR)
e) Substance P - (GPCR)

PMCOL 371 - Cellular Neuroscience (19 decks)

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