How Drugs Affect our Behavior Flashcards

1
Q

Receptor agonist vs agonist

A
  • agonist is endogenous, receptor agonist is exogenous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Competitive vs noncompetitive antagonists

A
  • Competitive antaagonist: blocks agonists from binding to the receptors
  • Noncompetitve antaagonist: bind to target receptors at a site that is different from where the endogenous ligand binds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does it mean to have a low affinity for a receptor?

A
  • If a particular drug has a low affinity for a receptor, then it will quickly uncouple from the receptor
  • To bind half the receptors at any given time, a higher concentration of the drug is needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does it mean if a drug has a high affinity?

A
  • the receptor and the drug will stay together for a longer time, and a lower concentration of drug will be sufficient to bind half the receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens when there are equal concentrations of a low affinity and a high affinity drug?

A
  • the high affinity drug will be bound to more receptors at any given time
  • if the drugs have an equivalent effect on the receptors, then the higher affinity drug will be more potent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is an effective dose?

A
  • The basic dose-response curve plots increasing drug doses against increasing strength of the response being studied.
  • An effective dose is the dose at which the drug shows half of its maximal effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is potency?

A
  • Relative potencies are assessed by comparing the ED50 values
  • In the example, both drugs have comparable effects, but one of the drugs has the effects at lower doses, and therefore is more potent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is efficacy?

A
  • Drug efficacies are compared by evaluating maximal responses, rather than doses
  • drug with greater maximal effect has higher efficacy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a partial agonist/antagonist?

A

A drug of only moderate efficacy

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

Phencyclidine

A
  • PCP or Angel Dust
  • NMDA receptor antagonist
  • Mind altering drug that may lead to hallucinations
  • Ketamine has similar effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

NMDA Antagonists symptoms

A
  • Loss of responsiveness (not consciousness)
  • Loss of sense of self/identity
  • Dissociation
  • Psychotic thoughts
  • Sensory aberrations
  • Aggression and agitation (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

NMDA and Schizophrenia

A
  • Because NMDA receptor antagonists, such as PCP, are psychotomimetic (elicit psychotic symptoms in people), it may be reasonable to assume that NMDA receptors are naturally sub-functional in people with psychotic disorders
  • If that is true, may drugs that enhance NMDA receptor function be of benefit to them?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

GABA-A Receptor

A
  • Cl- channel
  • Has multiple binding sites for other substances
  • These are inbolved in allosteric (enzyme) regulation/modulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Positive allosteric modulators examples

A
  • Valium
  • Lunesta
  • Clonazepam
  • Ambiem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ethanol

A
  • beverage alcohol
  • Calming, anxiolytic, and sedative/hypnotic effects of alcohol depend upon GABA-A receptor positive modulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the dark side of positive modulators?

A
  • drugs violate homeostasis
  • receptor desensitization (down-regulation): fewer functional receptors=less drug-induced imhibition, doesn’t always involve fewer receptors
  • tolerance
17
Q

Norepinephrine/Dopamine and ADHD

A
  • All medications for ADHD influence the norepinephrine and dopamine systems
  • Some block NE and/or DA reuptake via the transporter (Ritalin, Focalin, Strattera)
  • Some cause NE and/or DA release (Adderall, dexedrine, vyvanse)
18
Q

Serotonine reuptake inhibitors

A
  • Enable serotonin to stay in the synapse for longer
  • Prozac, paxil, celexa, zoloft, luvox
19
Q

What are opioids?

A
  • Ex. morphine, heroin, oxycodone, fentanyl
  • Analgesic and addictive properties
20
Q

What are the three opioid receptors?

A
  • delta
  • kappa
  • mu
  • All opioids have a high affinity for mu receptors but will also bind to the others
21
Q

What are the three endogenous opioids?

A

enkephalins, endorphins, and dynorphins

22
Q

What are naloxone and naltrexone?

A

opioid antagonists used to treat alcohol use disorder

23
Q

How do opioids increase dopamine release?

A
  • indirectly
  • opiods bind to mu opioid receptor on GABA neuron
  • when GABA is released on the GABA-A receptors on the dopamine neuron, the dopamine neuron will not fire
  • When opiod is binding to GABA (blocking), GABA is not released. So, dopamine can be released easier (with no inhibition)
24
Q

What type of drug is nicotine?

A

A stimulant

25
Q

What receptor does nicotine bind to?

A

nicotinic acetylcholine receptors (nACh), calcium and sodium ion channel

26
Q

What does nicotine increase the release of?

A
  • increases dopamine release
  • when nicotine binds, acetylcholine is also released, leading to increased dopamine release

may also affect other neurotransmitters like norepinephrine

27
Q

What does a positive allosteric modulator do?

A
  • the allosteric modification may result in enhancement in the binding affinity of the ligand with the orthosteric site causing boosting of a signal or increased activity
28
Q

What type of drug is cocaine and what does it do?

A
  • stimulant
  • blocks the dopamine transporter to increase the amount of dopamine available in the postsynaptic cleft (prevents dopamine reuptake, also norepinephrine and serotonin)
  • allows for longer activation of the postsynaptic cell
29
Q

How do amphetamines work/what do they do?

A
  • Enters presynaptic terminal via DA transporter
  • Packaged into vesicles in place of dopamine
  • Excess dopamine pumped out of cell via DA transporter
  • Increased dopamine release into synaptic cleft (also norepinephrine and 5-HT)

reverses function of transporters allowing them to push out dopamine instead of bringing it inwards

30
Q

What type of drug is alcohol?

A

initial stimulant, prolonged depressant, sedative (unique in this range of effects)

31
Q

What receptors does alcohol act on and what does it do?

A
  • Enhances GABA-A receptor activity
  • reduces NMDA (glutamate receptor) activity
32
Q

Low dose alc vs High dose

A
  • Low dose alcohol stimulates dopamine release- neurons are allowed to fire due to disinhibition
  • At high doses, more ubiquitous action that suppresses the overall system leading to sedative effects