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PSYC211 > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What are the two main classical neurotransmitters?

A
  • Glutamate
    -GABA
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2
Q

What type of information do the main classical neurotransmitters deal with?

A

sensory information

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3
Q

What is the basic effect of glutamate on brain chemical and electrostatic activity?

A
  • It is an excitatory neurotransmitter
  • Fast EPSP
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4
Q

What do all ionotropic glutamate receptors have in common?

A

let sodium in

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5
Q

What do all ionotropic GABA receptors have in common?

A

Let in chloride

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6
Q

What is the basic effect of GABA on brain chemical and electrostatic activity?

A
  • inhobitory neurotransmitter
  • fast IPSP
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7
Q

What is the main difference between neuromodulators and neurotransmitters?

A

Neuromodulators cannot affect ionotropic receptors. They only affect metabotropic receptors

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8
Q

What is the difference between the effect of neuromodulators and that of neurotransmitters?

A
  • neuromodulators will tend to alter the postsynaptic activity to modulate it, but they do not generally cause fast EPSPs or IPSPs
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9
Q

what is the action of ionotropic glutamate receptors?

A

let in sodium ions (EPSP and depolarization)

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10
Q

What are the effects of glutamate agonists?

A

Seizures
Excitotoxicity

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11
Q

what are the effects of glutamate antagonists?

A

dissociative anesthetics

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12
Q

What is the action of ionotropic GABA receptors?

A
  • let in chloride ions
  • cause IPSP
  • hyperpolarization
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13
Q

What are the neuromodulators?

A
  • acetylcholine
  • dopamine
  • serotonine
  • norepinephrine
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14
Q

What type of effects do neuromodulators have?

A
  • subtle effects: not visible EPSPs or IPSPs
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15
Q

Where do the neuromodulators diffuse?

A

short distances outside of the synapse

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16
Q

Where are the conventional neurotransmitters released?

A

inside the synapse

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17
Q

Where are neuromodulators produced?

A

In some specialized neurons

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18
Q

Where are GABA and Glutamate produced?

A

Pretty much every neuron produces one or the other

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19
Q

Are neuromodulators present only in the brain?

A

No, they are present as hormones inside the blood

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20
Q

What is the structure of conventional neurotransmitters?

A
  • amino acid derivatives
  • single amino acids
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21
Q

What are the conventional neurotransmitters?

A
  • Gaba
  • Glutamate
  • dopamine
  • serotonine
    -acetylcholine
  • norepinephrine
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22
Q

Where are the conventional neurotransmitters synthetized?

A

in the axon terminal

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23
Q

How are the conventional neurotransmitters secreted?

A
  • through small synaptic vesicles
  • the synaptic vesicles will dock very close to the site of Ca entry in the axon terminal
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24
Q

What happens to the classical neurotransmitters after they have their effect?

A
  • recaptured and reused
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25
Q

Where is the effect of classical neurotransmitters?

A
  • binds to receptor directly across the synapse (GABA and Glutamate)
  • can go to neighbouring neurons (neuromodulators)
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26
Q

What is the structure of neuropeptides?

A

Small chain of amino acids (baby sized proteins)

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27
Q

Where are neuropeptides synthetized?

A

In the soma

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28
Q

Why are neuropeptides necessarily made in the soma?

A

necessitate DNA transcription and translation

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29
Q

What happens to neuropeptides after they have been secreted?

A

They are destroyed (only used once)

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30
Q

how are neuropeptides secreted?

A

secreted from large dense core vesicles
these will be secreted after the vesicles containing conventional neurotransmitters

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31
Q

What type of receptors do the neuropeptides activate?

A

ONLY metabotropic receptors

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32
Q

Where do the neuropeptides diffuse?

A
  • can diffuse long distance
  • non synaptic communication
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33
Q

What is non synaptic communication?

A

When a neuropeptide diffuses away from the axon terminal that has released it to and then has an effect on a much further neuron

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34
Q

What type of neurotransmitter is associated with non synaptic communication?

A

Neuropeptide

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35
Q

How are lipid-based signaling molecules synthetized and released?

A

On demand
That is all we know

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36
Q

How are lipid-based signaling molecules secreted?

A

In a non vesicular manner
By post-synaptic neurons

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37
Q

What type of receptors are affected by lipid-based signaling molecules?

A
  • metabotropic receptors on the pre-synaptic neuron
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38
Q

Where is the effect of lipid-based signaling molecules?

A

typically: on pre-synaptic neurons

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39
Q

What is the typical effect of lipid-based signaling molecules?

A
  • hyperpolarize the pre-synaptic neuron
  • stops the signal (there is too much signal being sent)
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40
Q

What type of neurotransmitter is cannabinoid?

A

lipid-based signaling molecule

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41
Q

what are lipid-based signaling molecules made of?

A

pieces of cell membraine that are clipped off

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42
Q

What happens to lipid-based signaling molecules after they have their effect?

A

Destroyed

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43
Q

What are the only neurotransmitters that are recycled?

A

Classical neurotransmitters

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44
Q

What are the only neurotransmitters that can activate ionotropic receptors?

A

GABA and Glutamate

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45
Q

How are classical neurotransmitters produced and used?

A

1) free-floating amino acids in axonic terminal
2) an enzyme finds a loose amino acid and turns it into an NT
3) NT floats around
4) NT put into a vesicle
5) influx of calcium ions
6) vesicle fuses with membrane
7) the vesicle releases nerutransmitters into the synaptic cleft

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46
Q

What are monoamine neuromodulators?

A

The four common neuromodulators

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47
Q

What is the structure of monoamine neuromodulators?

A

Composed of just one amino acid
they all have a relatively similar structure

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48
Q

What is the protein that packages monoamine neuromodulators in vesicles?

A

VMAT

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49
Q

What are catecholamines?

A
  • dopamine
  • norepinephrine
  • epinephrine
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50
Q

Why are the catecholamines classified together, as one family?

A

They have an extremely similar molecular structure

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51
Q

What are neuropinephrine and epinephrine synthetized from?

A

Dopamine

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52
Q

What is a dirty drug?

A

Affects more than one receptor of the monoamies, as they are very similar. Most drugs are dirty drugs. It is extremely hard to synthetize a molecule that will affect only one of the types of neuromodulator receptors.

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53
Q

Where do botulinum toxin and black widow spider venom take effect?

A

in the PNS (cannot cross blood-brain barrier)

54
Q

What is the effect of black widow spider venom?

A
  • triggers the release of acetylcholine
  • causes spasms (extreme muscular activity), cramps, pain, nausea
55
Q

What is the effect of botulinum toxin?

A
  • acetylcholine system antagonist
  • prevents the release of acetylcholine
  • causes muscle paralysis
56
Q

What is the function of acetylcholine in the CNS?

A

neuromodulator

57
Q

What is the function of acetylcholine in the PNS?

A

activates the fast excitatory ionotropic receptors on muscle cells that cause muscle contraction

58
Q

In general, what is the main neurotransmitter of motor neurons?

A

acetylcholine

59
Q

In general, what is the main neurotransmitter of sensory neurons?

60
Q

What is the chemical mechanism of the black widow venom?

A
  • acts like calcium
  • constantly forces the axon terminal to release acetylcholine
61
Q

What is the chemical mechanism of the botulinum toxin?

A
  • blocks the site of entry for calcium on the axon terminal
  • calcium being unable to bind itself, there is no release of the neurotransmittor, even when there is an action potential
62
Q

What is neostigmine?

A
  • drug that inhibits the activity of acetylcholenesterase
  • since it is nbot broken down, acetylcholine will stay longer in the synaptoc cleft and cause more muscle contraction
63
Q

What is a receptor agonist?

A
  • drug that increases (directly or not) the activity of post-synaptic receptor proteins
64
Q

What is a receptor antagonist?

A
  • drug that decreseases (directly or not) the activity of post-synaptic receptor proteins
65
Q

What are direct agonists/antagonists?

A
  • affects postsynaptic receptor activity by directly binding to the post-synaptic receptors
66
Q

What are indirect agonists/antagonists?

A
  • affect postsynaptic receptor activity in an indirect manner, by binding to proteins that are not postsynaptic receptors
67
Q

What type of drugs are antipsychotics?

A

direct dopamine receptor antagonists

68
Q

What are neuroleptics used for?

A

treatment of psychosis

69
Q

What is the mode of action of neuroleptics?

A
  • dirty drugs
  • will all directly block the dopamine D2 receptor
70
Q

What is the dopamine D2 receptor?

A

inhibitory metabotropic receptos

71
Q

What type of drugs are hallucinogenics?

A

direct serotonin receptor agonists

72
Q

What is the chemical mode of effect of hallucinogenics?

A
  • activate serotonin 2A receptors
73
Q

What are serotonin 2A receptors?

A

inhibitory metabotropic receptors expressed by neurons all over the brain

74
Q

Do all drugs that affect the serotonine 2A receptor cause hallucinations?

75
Q

Name hallucinogenics

A
  • Mescaline
  • Psilocybin
  • LSD
76
Q

What are the 2 g-protein that are responsible for hallucinations?

A

it is the COMBINATION of the Gi/o and Gq/10 protein

77
Q

What is biased agonism?

A

The process by which a metabotropic receptor ligand causes the receptor to activate one type of g-protein

78
Q

What is a competitive agonist?

A
  • acts similarly to the endogenous neurotransmitter
  • activates the receptor by binding where the neurotransmitter normally does
79
Q

What is a competitive antagonist?

A
  • binds to the binding site of a receptor
  • does not activate the receptor
80
Q

Is a competitive antagonist a full antagonist or a partial antagonist?

A

Full antagonist

81
Q

What is a partial agonist?

A
  • NECESSARILY A COMPETITIVE AGONIST
  • half activates the binding site.
82
Q

What does affinity refer to?

A
  • Probability and tightness of ligand-receptor binding
83
Q

What will the outcome of an endogenous neurotransmitter-exogenous drug depend on?

A

Affinity for the binding site

84
Q

What is non-competitive binding?

A
  • drug binds to a receptor at a site that does not interfere with he binding site of the natural ligand
85
Q

What is the effect of a non-competitive agonist?

A

fully or partially activates the receptor

86
Q

What is the effect of a non-competitive antagonist?

A

Fully blocks receptor activation

87
Q

What is an allosteric modulator?

A
  • non-competitive drug that will have an effect on receptor activity only if the neurotransmitter is also bound to the receptor
88
Q

What is the effect of a negative allosteric modulator?

A
  • reduces the effect of the primary ligand
89
Q

What is the effect of a positive allosteric modulator?

A

amplifies the effect of the primary ligand

90
Q

What is the difference between an allosteric modulator and antagonists/agonists?

A

Allosteric modulators only have their effect if the neurotransmitter binds itself to the receptor. Not the antagonists/agonists

91
Q

What caracterises Parkinson’s disease?

A
  • tremor
  • rigidity of limbs
  • poor balance
  • difficulty initiating movement
92
Q

What causes parkinson’s disease?

A
  • Death of dopamine neurons in the brain
93
Q

Why can L-DOPA be used to treat Parkinson’s disease?

A
  • small enough to pass through the blood-brain barrier
  • it is proto-dopamine, so it gets pulled in the brain and the dopamine reuptake system confuses it for dopamine. It is uptook and then transformed back into dopamine
93
Q

What molecule is used to treat parkinson’s?

94
Q

What are the effects of L-DOPA?

A
  • increases dopamine production in the brain
  • acts as an indirectopamine receptor agonist
95
Q

What is the principle upon which psychopharmacology is based?

A

There are many ways to influence receptor activity besides directly binding to receptor proteins

96
Q

What is the concept of using presursor molecules as drugs?

A
  • they can increase the number of neurotransmitters that are made and released
  • precursor acts as a receptor agonist
97
Q

What controls the synthesis of neurotransmitters from precursor molecules?

98
Q

How can you use a drug to reduce the production of neurotransmitters?

A
  • block enzymes
  • antagonist
99
Q

How can you use drugs that affect protein transporters?

A
  • as antagonists
  • prevent the transporter proteins from putting the neurotransmitter into vesicles
100
Q

How do antagonists act on the vesicular release machinery?

A

Block the vesicular release machinery (botox)

101
Q

How do agonists act on the vesicular release machinery?

A

activate the vesicular release machinery (black widow spider venom)

102
Q

Would a drug that blocks the enzymatic deactiation of a neurotransmitter in the synaptic cleft be an antagonist or an agonist?

103
Q

Would a drug that blocks the neurotransmitter reuptake protein be an agonist or an antagonist?

104
Q

What is the effect of cocaine and methylphenidate?

A
  • blocks the reuptake of catecholamines (dopamine and neuropinephrine)
105
Q

What is the effect of adderall and crystal meth?

A
  • reverse catecholamine reuptake transporters. Dopamine and neuropinephrineflow out of the axon terminal beforeing packaged into a vesicle.
106
Q

Are drugs that serve as precursos agonists or antagonists?

107
Q

are drugs that prevent storage of neurotransmitters in vesicles agonists or antagonists?

A

antagonists

108
Q

Are drugs that stimulate the release of NTs by vesicles agonists or antagonists?

109
Q

Are drugs that inhibit the release of vesicles agonists or antagonists?

A

antagonists

110
Q

Are drugs that stimulate postsynaptic receptors agonists or antagonists?

111
Q

Are drugs that block postsynaptic receptors agonists or antagonists?

A

Antagonists

112
Q

Are drugs that act as synthetic enzymes and inhibit the synthesis of neurotransmitters agonists or antagonists?

A

Antagonist

113
Q

Are drugs that stimulate autoreceptors agonists or antagonists?

A

Antagonists

114
Q

Are drugs that block autoreceptors agonists or antagonists?

115
Q

Are drugs that block reuptake agonists or antagonists?

116
Q

Are drugs that inactivate acetylcholinesteras agonists or antagonists?

117
Q

What type of drugs are heroin, morphin and imodium anti-diarrheal?

118
Q

What differenciates different drugs’ efficiency?

A

the drugs’ efficiency in passing the blood-brain barrier

119
Q

How can drugs pass the blood-brain barrier?

A

If they are lipid-soluble

120
Q

What are withdrawal syndrome?

A
  • The opposite of the effect of the drug that used to be consumed
  • caused by the absence of the drug in the system
121
Q

How do the barbiturates effect cerebral activity?

A
  • GABA receptors agonists
122
Q

What are the effects of barbiturates?

A
  • calming effect
  • reduce breathing and heart rate
123
Q

What is the particularity of the development of tolerance to barbiturates?

A
  • tolerance to the calming effect develops more rapidly than that to the depressing on breathing and heart rate
124
Q

What is tolerance?

A

A drug becomes less effective the more you use it

125
Q

What is sensitization?

A

Occurs when a drug effect becomes larger with repeated use

126
Q

What is a placebo?

A

Inert substance that has no direct physiological effect

127
Q

What is the effect of a partial agonist?

A

partially increases or decreases the activity of the cell

128
Q

What determines the impact of a neurotransmitter?

A

The receptor to which it binds

129
Q

What is the difference between direct and indirect drugs?

A
  • direct drugs have an effect by binding directly to the postsynaptic receptor (not necessarily the binding site)
  • indirect drugs have an affect by binding to something other than the post synaptic receptor
130
Q

What is the particularity of an allosteric modulator?

A

The neurotransmitter needs to be bound to the receptor for the modulator to have an effect

PSYC211 (21 decks)

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