Brainscape's Knowledge GenomeTM

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


See full index

Psych 211 (neuro) > Drugs > Flashcards

Drugs Flashcards

You may prefer our related Brainscape-certified flashcards:
Psychology 101 flashcards GRE® Psychology flashcards
1
Q

What is acetylcholine?

A
  • neuromodulator in the CNS, often at axoaxonic synapses
  • primary neurotransmitter released by motor neurons at the neuromuscular junction
  • activates excitatory ionotropic receptors on muscle cells, causing fast EPSPs and muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do motor neurons generally release as their main neurotransmitter?

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

What do sensory neurons generally release as their main neurotransmitter?

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

What is black widow spider venom?

A
  • Poison produced by the black widow spider that triggers the release of acetylcholine from motor neurons
  • causes muscle cramps, spasms, pain, nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is botulunim toxin?

A
  • botox
  • Produced by bacteria that grow in improperly canned food
  • prevents acetylcholine release from motor neurons, causing muscle paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do many natural toxins target?

A
  • the vesicle release machinery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is neostigmine?

A
  • Drug that inhibits acetylcholinesterase, which is the enzyme that breaks down acetylcholine in the synapse
  • causes acetylcholine to stay around longer in the synapse, causing prolonged muscle contraction, spams
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Myasthenia Gravis?

A
  • autoimmune disorder in which a person’s immune system attacks healthy acetylcholine receptors
  • weaker over time
  • neostigmine keep acetylcholine in the synapse for longer periods of time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a receptor agonist?

A
  • drug that directly or indirectly increases the activity of postsynaptic receptor proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a receptor antagonist?

A
  • drug that directly or indirectly decreases the activity of postsynaptic receptor proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are direct agonists/antagonists?

A
  • bind directly to postsynaptic receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are indirect agonists/antagonists?

A
  • affect the activity of postsynaptic receptors in an indirect manner
  • agonist: neostigmine, black widow venom
  • antagonist: botox
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are antipsychotics (neuroleptics)?

A
  • Class of drugs used to treat psychosis
  • mostly dirty drugs, which means they bind to more than one type of receptor
  • the one action they all have in common is they directly block the dopamine D2 receptor, which is an inhibitory metabotropic receptor expressed by neurons all over the brain
  • direct dopamine receptor antagonists (dopamine receptor blockers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are drugs that cause hallucinations?

A
  • most popular ones directly activate serotonin 2A receptors, which are expressed by neurons all over the brain
  • Direct serotonin receptor agonists (serotonin receptor activators)
  • not all serotonin 2A receptor agonists cause hallucinations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What 4 drugs directly activate the serotonin receptor 5HT-2A?

A
  • mescaline
  • psilocybin
  • LSD
  • lisuride
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which serotonin receptor activators are not hallucinogens?

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

How do hallucinogens work?

A
  • the drugs activate the 5HT-2A receptor, which is metabotropic, they launch an intracellular signaling cascade that starts with the g protein Gq/11
  • also trigger the receptor to activate a different g protein: Gi/o
  • Hallucinations seem to result from 5HT-2A receptor activation of Gi/o proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is biased agonism?

A
  • when a ligand causes a metabotropic receptor to preferentially activate one type of intracellular g protein, whereas another ligand at the same receptor might preferentially activate a different g protein
  • way receptor activates biases which g protein inside cell gets turned on
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can direct agonists/antagonists be classified?

A
  • competitive binding
  • non competitive binding
20
Q

What is a competitive agonist?

A
  • acts similarly to the endogenous neurotransmitter
  • activates the receptor by binding where the neurotransmitter normally binds
  • can be full (activate as much as neurotransmitter) or partial agonists (half activate)
21
Q

What is a competitive antagonist?

A
  • attaches to the same binding where the neurotransmitter normally binds
  • it doesn’t activate the receptor
  • always full
22
Q

What is affinity?

A
  • probability and tightness of ligand receptor binding
  • competition for a binding site between an endogenous neurotransmitter and an exogenous drug will depend on their relative concentrations and their affinity for the binding site
23
Q

What is a non competitive agonist?

A
  • drug binds to a receptor at a site that does not interfere with the binding site of the normal ligand
  • neurotransmitter to bind on one site of a receptor while a drug binds on another
  • fully or partially activates the receptor
24
Q

What is a non competitive antagonist?

A
  • drug binds to a receptor at a site that does not interfere with the binding site of the normal ligand
  • neurotransmitter to bind on one site of a receptor while a drug binds on another
  • fully blocks receptor activation
  • “wins” without competing by binding to an alternative site
25
Q

What are allosteric modulators?

A
  • Non-competitive drugs that only influence receptor activity when the neurotransmitter is also bound to the receptor
  • negative allosteric modulators reduce the effect of the primary ligand
  • positive amplify the effect of the primary ligand
26
Q

What is Parkinson’s disease?

A
  • neurological disorder
  • tremors, rigidity of limbs, poor balance, and difficulty initiating movements
  • caused by the degeneration (death) of dopamine neurons in the midbrain
27
Q

How is Parkinson’s treated?

A
  • amino acid L-Dopa is used as a drug to treat Parkinson’s disease
  • it increases dopamine production in the brain and thus acts as an indirect dopamine receptor agonist
28
Q

How do indirect agonists work?

A
  • Conventional neurotransmitters are made in axon terminals, where an enzyme converts a precursor molecule (typically an amino acid) into a neurotransmitter
  • the precursor molecule can be given as a drug, since it can increase the amount of neurotransmitter that is made and released
  • the precursor molecule is an indirect receptor agonist
29
Q

How do indirect antagonists work?

A
  • Enzymes synthesize neurotransmitter from precursor molecules
  • Some antagonists work by blocking these enzymes, thus reducing production of the neurotransmitter so there is less in each synaptic vesicle
    OR
  • Once made, neurotransmitters are packaged into synaptic vesicles
  • Some antagonists work by blocking the transporter proteins that package neurotransmitter into vesicles
  • the synaptic vesicles can remain empty, so nothing is released when they fuse with the presynaptic membrane
30
Q

How do drugs affect neurotransmitter release?

A
  • Some antagonists work by blocking the vesicular release machinery, so no neurotransmitter is ever released (botox)
  • Some agonists work by activating the vesicular release machinery, causing neurotransmitter release (black widow venom)
31
Q

How do drugs affect enzymatic deactivation?

A
  • Some agonists block the enzymatic deactivation of neurotransmitter in the synaptic cleft (neostigmine)
  • stays longer in synapse
32
Q

How do drugs affect reuptake transporter proteins?

A
  • Some agonists block neurotransmitter reuptake transporters (stays longer)
  • Some agonists can even reverse the direction of reuptake transporters, so they push neurotransmitter into the synapse as soon as it is made (without being packaged into a synaptic vesicle)
33
Q

What is Methylphenidate/cocaine?

A
  • Drugs that block catecholamine reuptake transporters, meaning they block the reuptake of dopamine & norepinephrine
34
Q

What is Adderall/crystal meth?

A
  • Drugs that reverse catecholamine reuptake transporters, causing dopamine and norepinephrine to flow out of the axon terminal before being packaged into a vesicle
  • action potential-independent, non-vesicular release
  • Ecstasy (MDMA) has a similar effect on all the monoamine reuptake transporters (causing them to run backwards)
35
Q

What are the ways agonists affect synaptic transmission?

A
  • drug serves as precursor
  • drug stimulates release of neurotransmitter
  • drug stimulates postsynaptic receptors
  • drug blocks autoreceptors, increases synthesis/release of NT
  • drug blocks reuptake
  • drug inactivates acetylcholinesterase
36
Q

What are the ways antagonists affect synaptic transmission?

A
  • drug inactivates synthesis enzyme, inhibits synthesis of NT
  • drug prevents storage of NT in vesicles
  • drug inhibits release of NT
  • drug blocks postsynaptic receptors
  • drug stimulates autoreceptors, inhibits synthesis/release of NT
37
Q

How can drugs be categorized?

A
  • according to their effects on postsynaptic receptor activity
  • according to their behavioural effects
  • according to their physiological effects
  • according to their actions on specific proteins
38
Q

Can heroin enter the brain?

A
  • very easily crosses the blood-brain barrier (because an enzyme in the blood makes it very lipid/fat soluble)
39
Q

Can morphine enter the brain?

A
  • less easily crosses the blood-brain barrier (it is less lipid soluble than heroin
40
Q

Can imodium anti-diarrheal enter the brain?

A
  • does not cross the blood-brain barrier
41
Q

What do heroin, morphine, and imodium anti-diarrheal have in common?

A
  • They are all very strong opiates (opioids) that cause constipation
42
Q

What are opioid receptors?

A
  • inhibitory metabotropic receptors
  • found throughout the body and brain
  • normally get activated by endogenous opioid peptides that function as hormones in the body and as neuropeptides in the CNS
43
Q

What is tolerance?

A
  • when a drug effect gets smaller with repeated administration
  • body becomes used to the drug and actively counteracts its effects
44
Q

What are withdrawal symptoms?

A
  • opposite the effects of the drug
45
Q

What is sensitization?

A
  • when a drug effect becomes larger with repeated use

Psych 211 (neuro) (22 decks)

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