Neurotransmitters Flashcards
1
Q
What are the two main classical neurotransmitters?
A
- Glutamate
-GABA
2
Q
What type of information do the main classical neurotransmitters deal with?
A
sensory information
3
Q
What is the basic effect of glutamate on brain chemical and electrostatic activity?
A
- It is an excitatory neurotransmitter
- Fast EPSP
4
Q
What do all ionotropic glutamate receptors have in common?
A
let sodium in
5
Q
What do all ionotropic GABA receptors have in common?
A
Let in chloride
6
Q
What is the basic effect of GABA on brain chemical and electrostatic activity?
A
- inhobitory neurotransmitter
- fast IPSP
7
Q
What is the main difference between neuromodulators and neurotransmitters?
A
Neuromodulators cannot affect ionotropic receptors. They only affect metabotropic receptors
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
9
Q
what is the action of ionotropic glutamate receptors?
A
let in sodium ions (EPSP and depolarization)
10
Q
What are the effects of glutamate agonists?
A
Seizures
Excitotoxicity
11
Q
what are the effects of glutamate antagonists?
A
dissociative anesthetics
12
Q
What is the action of ionotropic GABA receptors?
A
- let in chloride ions
- cause IPSP
- hyperpolarization
13
Q
What are the neuromodulators?
A
- acetylcholine
- dopamine
- serotonine
- norepinephrine
14
Q
What type of effects do neuromodulators have?
A
- subtle effects: not visible EPSPs or IPSPs
15
Q
Where do the neuromodulators diffuse?
A
short distances outside of the synapse
16
Q
Where are the conventional neurotransmitters released?
A
inside the synapse
17
Q
Where are neuromodulators produced?
A
In some specialized neurons
18
Q
Where are GABA and Glutamate produced?
A
Pretty much every neuron produces one or the other
19
Q
Are neuromodulators present only in the brain?
A
No, they are present as hormones inside the blood
20
Q
What is the structure of conventional neurotransmitters?
A
- amino acid derivatives
- single amino acids
21
Q
What are the conventional neurotransmitters?
A
- Gaba
- Glutamate
- dopamine
- serotonine
-acetylcholine - norepinephrine
22
Q
Where are the conventional neurotransmitters synthetized?
A
in the axon terminal
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
24
Q
What happens to the classical neurotransmitters after they have their effect?
A
- recaptured and reused
25
Where is the effect of classical neurotransmitters?
- binds to receptor directly across the synapse (GABA and Glutamate)
- can go to neighbouring neurons (neuromodulators)
26
What is the structure of neuropeptides?
Small chain of amino acids (baby sized proteins)
27
Where are neuropeptides synthetized?
In the soma
28
Why are neuropeptides necessarily made in the soma?
necessitate DNA transcription and translation
29
What happens to neuropeptides after they have been secreted?
They are destroyed (only used once)
30
how are neuropeptides secreted?
secreted from large dense core vesicles
these will be secreted after the vesicles containing conventional neurotransmitters
31
What type of receptors do the neuropeptides activate?
ONLY metabotropic receptors
32
Where do the neuropeptides diffuse?
- can diffuse long distance
- non synaptic communication
33
What is non synaptic communication?
When a neuropeptide diffuses away from the axon terminal that has released it to and then has an effect on a much further neuron
34
What type of neurotransmitter is associated with non synaptic communication?
Neuropeptide
35
How are lipid-based signaling molecules synthetized and released?
On demand
That is all we know
36
How are lipid-based signaling molecules secreted?
In a non vesicular manner
By post-synaptic neurons
37
What type of receptors are affected by lipid-based signaling molecules?
- metabotropic receptors on the pre-synaptic neuron
38
Where is the effect of lipid-based signaling molecules?
typically: on pre-synaptic neurons
39
What is the typical effect of lipid-based signaling molecules?
- hyperpolarize the pre-synaptic neuron
- stops the signal (there is too much signal being sent)
40
What type of neurotransmitter is cannabinoid?
lipid-based signaling molecule
41
what are lipid-based signaling molecules made of?
pieces of cell membraine that are clipped off
42
What happens to lipid-based signaling molecules after they have their effect?
Destroyed
43
What are the only neurotransmitters that are recycled?
Classical neurotransmitters
44
What are the only neurotransmitters that can activate ionotropic receptors?
GABA and Glutamate
45
How are classical neurotransmitters produced and used?
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
46
What are monoamine neuromodulators?
The four common neuromodulators
47
What is the structure of monoamine neuromodulators?
Composed of just one amino acid
they all have a relatively similar structure
48
What is the protein that packages monoamine neuromodulators in vesicles?
VMAT
49
What are catecholamines?
- dopamine
- norepinephrine
- epinephrine
50
Why are the catecholamines classified together, as one family?
They have an extremely similar molecular structure
51
What are neuropinephrine and epinephrine synthetized from?
Dopamine
52
What is a dirty drug?
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.
53
Where do botulinum toxin and black widow spider venom take effect?
in the PNS (cannot cross blood-brain barrier)
54
What is the effect of black widow spider venom?
- triggers the release of acetylcholine
- causes spasms (extreme muscular activity), cramps, pain, nausea
55
What is the effect of botulinum toxin?
- acetylcholine system antagonist
- prevents the release of acetylcholine
- causes muscle paralysis
56
What is the function of acetylcholine in the CNS?
neuromodulator
57
What is the function of acetylcholine in the PNS?
activates the fast excitatory ionotropic receptors on muscle cells that cause muscle contraction
58
In general, what is the main neurotransmitter of motor neurons?
acetylcholine
59
In general, what is the main neurotransmitter of sensory neurons?
glutamate
60
What is the chemical mechanism of the black widow venom?
- acts like calcium
- constantly forces the axon terminal to release acetylcholine
61
What is the chemical mechanism of the botulinum toxin?
- 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
What is neostigmine?
- 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
What is a receptor agonist?
- drug that increases (directly or not) the activity of post-synaptic receptor proteins
64
What is a receptor antagonist?
- drug that decreseases (directly or not) the activity of post-synaptic receptor proteins
65
What are direct agonists/antagonists?
- affects postsynaptic receptor activity by directly binding to the post-synaptic receptors
66
What are indirect agonists/antagonists?
- affect postsynaptic receptor activity in an indirect manner, by binding to proteins that are not postsynaptic receptors
67
What type of drugs are antipsychotics?
direct dopamine receptor antagonists
68
What are neuroleptics used for?
treatment of psychosis
69
What is the mode of action of neuroleptics?
- dirty drugs
- will all directly block the dopamine D2 receptor
70
What is the dopamine D2 receptor?
inhibitory metabotropic receptos
71
What type of drugs are hallucinogenics?
direct serotonin receptor agonists
72
What is the chemical mode of effect of hallucinogenics?
- activate serotonin 2A receptors
73
What are serotonin 2A receptors?
inhibitory metabotropic receptors expressed by neurons all over the brain
74
Do all drugs that affect the serotonine 2A receptor cause hallucinations?
no
75
Name hallucinogenics
- Mescaline
- Psilocybin
- LSD
76
What are the 2 g-protein that are responsible for hallucinations?
it is the COMBINATION of the Gi/o and Gq/10 protein
77
What is biased agonism?
The process by which a metabotropic receptor ligand causes the receptor to activate one type of g-protein
78
What is a competitive agonist?
- acts similarly to the endogenous neurotransmitter
- activates the receptor by binding where the neurotransmitter normally does
79
What is a competitive antagonist?
- binds to the binding site of a receptor
- does not activate the receptor
80
Is a competitive antagonist a full antagonist or a partial antagonist?
Full antagonist
81
What is a partial agonist?
- NECESSARILY A COMPETITIVE AGONIST
- half activates the binding site.
82
What does affinity refer to?
- Probability and tightness of ligand-receptor binding
83
What will the outcome of an endogenous neurotransmitter-exogenous drug depend on?
Affinity for the binding site
84
What is non-competitive binding?
- drug binds to a receptor at a site that does not interfere with he binding site of the natural ligand
85
What is the effect of a non-competitive agonist?
fully or partially activates the receptor
86
What is the effect of a non-competitive antagonist?
Fully blocks receptor activation
87
What is an allosteric modulator?
- non-competitive drug that will have an effect on receptor activity only if the neurotransmitter is also bound to the receptor
88
What is the effect of a negative allosteric modulator?
- reduces the effect of the primary ligand
89
What is the effect of a positive allosteric modulator?
amplifies the effect of the primary ligand
90
What is the difference between an allosteric modulator and antagonists/agonists?
Allosteric modulators only have their effect if the neurotransmitter binds itself to the receptor. Not the antagonists/agonists
91
What caracterises Parkinson's disease?
- tremor
- rigidity of limbs
- poor balance
- difficulty initiating movement
92
What causes parkinson's disease?
- Death of dopamine neurons in the brain
93
Why can L-DOPA be used to treat Parkinson's disease?
- 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
What molecule is used to treat parkinson's?
L-DOPA
94
What are the effects of L-DOPA?
- increases dopamine production in the brain
- acts as an indirectopamine receptor agonist
95
What is the principle upon which psychopharmacology is based?
There are many ways to influence receptor activity besides directly binding to receptor proteins
96
What is the concept of using presursor molecules as drugs?
- they can increase the number of neurotransmitters that are made and released
- precursor acts as a receptor agonist
97
What controls the synthesis of neurotransmitters from precursor molecules?
Enzymes
98
How can you use a drug to reduce the production of neurotransmitters?
- block enzymes
- antagonist
99
How can you use drugs that affect protein transporters?
- as antagonists
- prevent the transporter proteins from putting the neurotransmitter into vesicles
100
How do antagonists act on the vesicular release machinery?
Block the vesicular release machinery (botox)
101
How do agonists act on the vesicular release machinery?
activate the vesicular release machinery (black widow spider venom)
102
Would a drug that blocks the enzymatic deactiation of a neurotransmitter in the synaptic cleft be an antagonist or an agonist?
agonist
103
Would a drug that blocks the neurotransmitter reuptake protein be an agonist or an antagonist?
agonist
104
What is the effect of cocaine and methylphenidate?
- blocks the reuptake of catecholamines (dopamine and neuropinephrine)
105
What is the effect of adderall and crystal meth?
- reverse catecholamine reuptake transporters. Dopamine and neuropinephrineflow out of the axon terminal beforeing packaged into a vesicle.
106
Are drugs that serve as precursos agonists or antagonists?
agonist
107
are drugs that prevent storage of neurotransmitters in vesicles agonists or antagonists?
antagonists
108
Are drugs that stimulate the release of NTs by vesicles agonists or antagonists?
Agonists
109
Are drugs that inhibit the release of vesicles agonists or antagonists?
antagonists
110
Are drugs that stimulate postsynaptic receptors agonists or antagonists?
agonists
111
Are drugs that block postsynaptic receptors agonists or antagonists?
Antagonists
112
Are drugs that act as synthetic enzymes and inhibit the synthesis of neurotransmitters agonists or antagonists?
Antagonist
113
Are drugs that stimulate autoreceptors agonists or antagonists?
Antagonists
114
Are drugs that block autoreceptors agonists or antagonists?
Agonists
115
Are drugs that block reuptake agonists or antagonists?
Agonists
116
Are drugs that inactivate acetylcholinesteras agonists or antagonists?
Agonists
117
What type of drugs are heroin, morphin and imodium anti-diarrheal?
opiates
118
What differenciates different drugs' efficiency?
the drugs' efficiency in passing the blood-brain barrier
119
How can drugs pass the blood-brain barrier?
If they are lipid-soluble
120
What are withdrawal syndrome?
- The opposite of the effect of the drug that used to be consumed
- caused by the absence of the drug in the system
121
How do the barbiturates effect cerebral activity?
- GABA receptors agonists
122
What are the effects of barbiturates?
- calming effect
- reduce breathing and heart rate
123
What is the particularity of the development of tolerance to barbiturates?
- tolerance to the calming effect develops more rapidly than that to the depressing on breathing and heart rate
124
What is tolerance?
A drug becomes less effective the more you use it
125
What is sensitization?
Occurs when a drug effect becomes larger with repeated use
126
What is a placebo?
Inert substance that has no direct physiological effect
127
What is the effect of a partial agonist?
partially increases or decreases the activity of the cell
128
What determines the impact of a neurotransmitter?
The receptor to which it binds
129
What is the difference between direct and indirect drugs?
- 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
What is the particularity of an allosteric modulator?
The neurotransmitter needs to be bound to the receptor for the modulator to have an effect
