Psychopharmacology Flashcards

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1
Q

1 ) Which of the following represents a possible treatment for Parkinson’s disease?

A) neurosurgery to separate the corpus callosum

B) adminstration of MPTP

C) co-administration of amphetamine and meperidine

D) administration of L-DOPA

E) None of the above are correct.

A

D) administration of L-DOPA

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2
Q

2 ) Which of the following is a characteristic of a drug?

A) effective only at high doses

B) can include essential nutrients

C) must be an endogenous chemical

D) can be abused or misused by humans

E) an exogenous chemical

A

E) an exogenous chemical

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3
Q

3 ) Drugs that block or inhibit the postsynaptic receptor effects are termed

A) agonists.

B) ligands.

C) synergists.

D) antagonists.

E) pheromones.

A

D) antagonists.

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4
Q

4 ) Which pair of transmitters are most involved in synaptic neurotransmission in the brain?

A) glutamate; acetylcholine

B) GABA; glycine

C) glutamate; GABA

D) glycine; acetylcholine

E) acetylcholine; dopamine

A

C) glutamate; GABA

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5
Q

5) Match up the transmitter substance below with the appropriate behavioral role or action of that transmitter.

A) acetylcholine; facilitation of learning

B) dopamine; suppresses certain species-typical behaviors

C) norepinephrine; facilitation of learning

D) serotonin; increases vigilance

E) GABA; generally activates voluntary movements

A

A) acetylcholine; facilitation of learning

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6
Q

6) Parkinson’s disease involves degeneration of neurons within the ________ DA system.

A) nigrostriatal

B) mesocortical

C) hypothalamocortical

D) mesolimbic

E) retinal-suprachiasmatic

A
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7
Q

What are the 2 types of receptors?

A

ionotropic and metabotropic

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8
Q

Ionotropic

A

site for neurotransmitters to bind is on neuron

Faster and short lived

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9
Q

Metabotropic

A

receptor site is at another location separate from the channel

Operates a G protein which activated the channel

Long and slow

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10
Q

What does it take to be a neurotransmitter?

A

Exists pre-synaptically.

Released in response to action potential.
- Ca enters cell , vesicles bind with presynaptic membrane

Application at synapse produces response.

  • post-synaptic membrane has receptors which bind with neurotransmitter and has effect
  • Can be EPSP or IPSP

Blocking release stops synaptic function.

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11
Q

Psychopharmacology

A

The study of the effects of drugs on the nervous system and on behavior.

How are drugs influencing our nervous system and in turn how does that influence our behavior
Drugs we take, drugs naturally existing in brain,

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12
Q

Drug effects

A

The changes a drug produces in an animal’s physiological processes and behavior.

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13
Q

What is a ‘drug’?

A

a very vague term.

all ingested substances alter bodily function.
- We don’t say bananas are drugs cause when we eat them they alter our bodily functions

‘drug’ is reserved for things that have pronounced effects when ingested in small quantities but has a significant effect on our behavior and physiological behvaiour

Tiny pills or plants

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14
Q

Sites of Action

A

The locations at which drugs interact with cells of the body, thus affecting some biochemical processes of these cells

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15
Q

What can drugs be classified as?

A

Agonist or Antagonist
THESE ARE NOT LIKE IPSP AND EPSP

Neurotransmitter determines if exicitory or inhibitory

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16
Q

Agonist

A

A drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell.

Increase the chances of whatever effect

If neurotransmitter usually has inhibitory effect the agonist makes it easier for that effect to happen

Agonist drug binds at same sites as neurotransmitter and produces same effects and this will free up neurotransmitter to bind at more sites so you have enhanced cellular activity

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17
Q

Antagonist

A

A drug that opposes or inhibits the effects of a particular neurotransmitter on the postsynaptic cell.

Makes it harder for effect

  • plugging up receptor sites and not opening channels causing the natural neurotransmitter to not bind at those sites so your blocking neural activity
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18
Q

List some ways that drugs can agonize

A
  • precursor to neurotransmitter
    In parkinsons your cells arent produing enough dopamine but you cant give a person a dopamine pill because it won’t cross the blood brain barrier instead you give L-Dopa which is able to cross blodd brain barrier and turn into dopamine
    L-Dopa is providing building blocks so that the brain can get more dopamine

stimulate release

  • More neurotransmitter you have released into the synapse the more likely the effect will happen on post synaptic membrane
  • Ex- emphadimine

receptor binding
- Imitate a neurotransmitter and bind at the channel….

block auto receptors

  • Auto receptors are metabotropic receptors at pre synaptic membrane
  • If these are blocked the cell keeps on pumping neurotransmitter
  • More neurotransmitter released more in synapse more effect

inhibition of reuptake
- Ex if we add cocaine we block the reuptake meaning the neurotransmitter can keep operating at the synapse

inhibition of deactivation

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19
Q

List Ways that drugs can antagonize

A

prevent synthesis
- Stop conversion of precursor into neurotransmitter meaning less is avaible preventing the neurotransmitter from doing its job

prevents storage
- Interfere with storage then that reduces amount of neurotransmitter to be released

block release

receptor blocker
- Imitate neurotransmitter bind at site but not activate

stimulates auto receptors
- Reuptake neurotransmitter making it harder for it to have effect on post synaptic membrane

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20
Q

Direct agonist

A

Binds at same site neurotransmitter would- competitive binding
- keeps channels open

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21
Q

Direct antagonist

A

binds at the same site as the neurotransmitter but keeps the ion channel close

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22
Q

Indirect antagonist

A

drug keeps ion channels closed
Binds at different site.
- noncompetitive binding

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23
Q

Indirect agonist

A

drug keeps ion channels open

- noncompetiive binding

24
Q

List the four major neurotransmitter systems

A

Acetylcholine- thought to play a role in memory, part of Alzheimer disease

Dopamine- movement, Parkinson’s disease, to much l- dopa to much dopamine= schizophrenic symptoms
- Substantia nigra

Norepinephrine- emotional regulatory, to little= depression to much= maniac

Serotonin- walking cycles, obsessive compulsive disorder

25
Q

Amines

A

Modulatory effect on systems

26
Q

Monoamines

A

catecholamines (dopamine, norepinephrine)

indoleamines (serotonin)

27
Q

Quaternary amines

A

Acetylcholine

28
Q

Information transmitters

A

amino acids (glutamate, GABA)

Learning, info transfer

29
Q

Acetylcholine

A

muscular movement

high during REM sleep- rapid eye movements

  • learning
  • Memories
  • Forgettting

Cholinergic pathways in the brain - basal forebrain, dorsolateral pons.

30
Q

Dopamine

A

related to movement

metabotropic receptors

Amphetamines alter dopamine uptake and produce schizophrenic-like delusions.

can see similar effects with cocaine use.

Parkinson’s disease – degeneration of the nigrostriatial dopamine system.

31
Q

Norepinephrine

A

These are modulatory effects so they aren’t responsible for appetite but changes in the drug level can make you hungry or full- modifies things

  • increase in vigilance
  • attention
  • sexual behavior
  • appetite

Noradrenergic pathways in the brain - locus coeruleus

32
Q

Serotonin

A

regulation of mood

control of eating, sleeping and arousal

regulation of pain

dreaming

Serotonergic pathways in the brain – raphe nuclei

33
Q

Glutamate

A

the primary excitatory neurotransmitter

34
Q

GABA

A

the primary inhibitory neurotransmitter

35
Q

Amino acids:

A

The workhorses of the neurotransmitter family

Other neurotransmitters have more of a modulatory effect – rather than an information transmitting effect

Information that is learned and remembered is transmitted by neurons secreting glutamate and GABA

36
Q

The glutamate receptor

A

Activation of NMDA receptor can cause entry of calcium and changes in the numbers of AMPA receptors – a mechanism for learning? Building blocks of a newly formed memory?

37
Q

The GABA receptor

A

inhibitory synapses

necessary for brain stability

Epilepsy - an abnormality in this process

38
Q

Barbiturates

A

gaba agonists

  • anxiety drugs
  • sleep medication
  • seizure treatments
39
Q

Peptides

A

produced in minute quantities.

often substances that are also found in areas of body other than brain (vasoactive intestinal polypeptide).

tremendously potent and long-acting (neuromodulatory).

Opiates

40
Q

The opiate story

A

Opiates have been used for centuries to relieve pain.

It wasn’t until 1975 that we discovered endogenous (produced from within, naturally occuring) opioids.

Like runners high where they feel better after run

several varieties of receptors.

41
Q

Incentive sensitization model

A

the wanting and liking theory.

wanting – equivalent to craving a drug

liking – pleasure from drug taking

repeated use:

tolerance for liking

wanting becomes sensitized

42
Q

Acetylcholine how it’s made

A

Acetyl-CoA & Choline mix & ChAT transfers acetate ion from acetyl-CoA to choline - all together form CoA & ACh

43
Q

Which drugs are the most addictive?

A

fast-acting drugs are most addictive

e.g., cocaine, heroin

44
Q

Why are slow-acting drugs addictive?

A

the effect of the drug is paired with the memory of taking the drug

e.g. alcohol- I was nervous before I went to a party and took shots and was amazing so next time you think you need to drink next time or you have a presentation and know alcohol calms you down so you drink

45
Q

Do animals get addicted to drugs?

A

difficult to addict animals to slow-acting drugs.

Monkey in Caribbean have become addicted to alcohol

Liking in alcohol is determined by our genes

46
Q

Most effective:

A

stimulus —-> immediate response

hence the high addictiveness of fast-acting drugs

preference for heroin over morphine

Heroine was developed to get soldiers off morphine

47
Q

Neural Mechanism

A

addictive drugs (and other reinforcers) cause the release of DA in the nucleus accumbens.

48
Q

What are the 2 types of actions for neural mechanism?

A

two types of actions:

dopamine agonist

IMITATING DOPAMINE SITE SO YOU AHVE MORE DOPAMINE AVAILABLE

reuptake inhibitor

Like what cocaine does

49
Q

Schizophrenia

A

Affects about 1/100 people.

Begins in 20’s.

Often triggered by stress and illness but there’s also a genetic predisposition.

Amanda bynes

50
Q

Symptoms of schizophrenia

A

Positive symptoms

  • hallucinations, delusions, paranoia

Negative symptoms

  • lack of emotion, energy, directedness
51
Q

The dopamine theory of schizophrenia

A

Dopamine antagonist
Over activity in the mesolimbic dopamine pathway is thought to mediate the positive symptoms of schizophrenia such as delusions and hallucinations (Figure 1).

More recently, under activity in the mesocortical dopamine pathway has been hypothesized to be the mediator of negative symptoms of schizophrenia (Figure 2).

52
Q

Beyond dopamine

A

New generation antipsychotics affect serotonin as well

Glutamate agonists can help with negative symptoms.

  • But they can cause seizures.
  • Glycine (amino acid) agonists are usually given that facilitate glutamate but don’t have the dangerous side-effects.

Schizophrenia likely affects a host of systems perhaps by disturbing a fundamental balance among neurotransmitters

53
Q

Alzheimer’s Disease

A

First described by Alois Alzheimer in 1907.

Course of disease:

initially, some memory loss (new memories and disorientation).

relentlessly progressive until one loses identity.

54
Q

Neuropathology in Alzheimer’s disease

A

amyloid plaques neurofibrillary tangles

55
Q

What are treatments of AD?

A
  1. ‘Cognitive enhancers’
    - Acetylcholinesterase inhibitors to offset loss of cholinergic neurons.
    - stops ACE from destroying synaptic ACH
  2. NMDA receptor antagonists
    - Cells damaged by AD release a large amount of glutamate, which over-excites NMDA receptors, which in turn speed up cell damage. Partially blocking NMDA receptors prevents this destructive chain.
56
Q

i

A

Nucleus basalis of Meynert – cell loss seen in AD