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Brain & Behaviour > Lecture 6 - Psychopharmacology > Flashcards

Lecture 6 - Psychopharmacology Flashcards

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1
Q

What are the 2 receptor types for synaptic action? List & briefly describe

A
  1. Ionotropic
    - n.t.’s bind RIGHT ON the channel & that opens up an ion channel; allowing ions to come in
  2. Metabotropic
    - receptor site for n.t. is off site; operating through a 2nd messenger system, which will open for a foreign channel
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2
Q

Being a neurotransmitter: What does it take?

A
  • Exists pre-synaptically.
  • Released in response to action potential.
  • Application at synapse produces response.
  • post-synaptic membrane has receptors. (excit. or inhib.)
  • Blocking release stops synaptic function. (stop activity @ synapse)
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3
Q

Psychopharmacology:

A

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

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4
Q

Drug effects:

A

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

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5
Q

What is a ‘drug’?

A
  • a very vague term.
  • all ingested substances alter bodily function.
  • ‘drug’ is reserved for things that have pronounced effects when ingested in small quantities.
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6
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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7
Q

What is the basic classification of drug actions?

A
  1. Agonist

2. Antagonist

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8
Q

Agonist:

A

A drug that facilitates the effects of a particular neurotransmitter (excit. or inhib.) on the postsynaptic cell.

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9
Q

Antagonist:

A

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

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10
Q

What is the difference in the role of n.t. & the drug?

A

n. t. will determine if there’s an excit. or inhib. effect on the cell, the drug will make it easier (agonist) or harder (antagonist) for that drug to have its effect
ex) if a n.t. normally has an inhib. effect, an agonist would make it easier for that inhib. effect to happen & an antagonist would make it harder for that inhib. effect to happen

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11
Q

Agonist drug effect

A
  • agonist drug binds to the receptor site

- enhanced cellular activity
more receptors being activated, more channels being open, it increases the effect

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12
Q

Antagonist drug effect

A
  • plugging receptor sites, but not opening the channels & causing natural n.t. to not be able to bind at those sites
  • block or reduce cellular activity b/c you’re letting n.t. act at fewer receptor sites
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13
Q

Ways that drugs can agonize

A
  1. precursor to neurotransmitter
    - L-DOPA is a precursor to dopamine that can cross BBB, that convert to dopamine in brain
  2. stimulate release
    - more n.t. released in synapse, more likely the effect on PS membrane & increased effect of that n.t.
  3. receptor binding
    - & open channels
  4. block autoreceptors
    - cells keeps pumping out n.t. - acting like an agonist (b/c signal to slow down doesn’t happen)
  5. inhibition of reuptake
    - n.t. can keep operating at synapse - having an agonist effect
  6. inhibition of deactivation
    - acetylcholinesterase breaks down ACh
    - if we inhibit, we allow n.t. to act longer in the synapse
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14
Q

What are autoreceptors?

A
  • receptors on pre-synaptic membrane
  • monitor amount of n.t. in synapse
  • normally when things bind to them, they’ll cause slow down of release of n.t. b/c it will be a sign there’s enough n.t. b/c its feeding back on itself
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15
Q

Ways that drugs can antagonize

A
  1. prevent synthesis
    - have a drug that blocks synthesis of L-DOPA –> dopamine
  2. prevents storage
    - less n.t. released into synaptic cleft
  3. block release
    - can’t do it’s job if it’s not being released in the pre synaptic
  4. receptor blocker
    - plugs imitate preventing a possible binding site for n.t.
  5. stimulates autoreceptors
    - starts reuptake too early, presynaptic cell is getting a signal theres so much n.t. in synapse that its binding to me (artificially fooling)
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16
Q

What are 2 different Drug Actions at Binding Sites

A
  1. Competitive Binding
    - Binds at same site neurotransmitter would.
  2. Noncompetitive Binding
    - Binds at different site.

BOTH can have agonist & antagonist effects

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17
Q

What are the four major neurotransmitter systems?

A
  1. Acetylcholine
  2. Dopamine
  3. Norepinephrine
  4. Serotonin
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18
Q

Acetylcholine

A
  • active in maintaining waking electroencephalographic (EEG) patterns of the neocortex
  • thought to play a role in MEMORY by maintaining neuron excitability
  • death of acetylcholine neurons & decrease in acetylcholine in the neocortex are thought to be related to ALZHEIMER’S DISEASE
  • produced in the BASAL FOREBRAIN NUCLEI & MIDBRAIN NUCLEI
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19
Q

Where is Acetylcholine produced?

A

produced in the BASAL FOREBRAIN NUCLEI & MIDBRAIN NUCLEI

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20
Q

Dopamine

A
  • active in maintaining normal MOTOR behaviour
  • loss of dopamine is related to PARKINSON’S DISEASE, in which muscles are rigid & movements are difficult to make
  • increases in dopamine activity may be related to SCHIZOPHRENIA
  • produced in the SUBSTANTIA NIGRA
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21
Q

Where is Dopamine produced?

A
  • produced in the SUBSTANTIA NIGRA
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22
Q

Norephinephrine

A
  • active in maintaining EMOTIONAL tone
  • decreases in norepinephrine activity are thought to be related to DEPRESSION, whereas increases in it are thought to be related to MANIA (overexcited behaviour)
  • produced in the LOCUS COERULEUS
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23
Q

Where is Norepinephrine produced?

A
  • produced in the LOCUS COERULEUS
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24
Q

Serotonin

A
  • active in maintaining waking EEG patterns
  • increases in serotonin activity are related to OBSESSIVE-COMPULSIVE DISORDER, TICS, & SCHIZOPHRENIA
  • decreases in serotonin activity are related to DEPRESSION
  • produced in the RAPHE NUCELI
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25
Q

Where is Serotonin produced?

A
  • produced in the RAPHE NUCELI
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26
Q

Amines

A

Modulatory effect on systems

Monoamines

  • catecholamines (dopamine, norepinephrine)
  • indoleamines (serotonin)

Quaternary amines
- Acetylcholine

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27
Q

Information transmitters

A

amino acids (glutamate, GABA)

learning - info transfer

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28
Q

Acetylcholine functions

A
  • muscular movement
  • high during REM sleep
  • learning
  • memories
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29
Q

Acetylcholine produced

A

Cholinergic pathways in the brain - basal forebrain, dorsolateral pons. (producing ACh)

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30
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

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31
Q

Dopamine description

A
  • 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.
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32
Q

Amphetamines

A

alter dopamine uptake and produce schizophrenic-like delusions.

  • stimulant
  • cause release of n.t. dopamine - activates receptor molecules
  • may also interfere with reuptake process (blocks)
  • but continues to activate it’s receptors
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33
Q

Cocaine

A
  • blocks reuptake of dopamine
  • dopamine continues to activate its receptors
  • constant use can lead to large amounts of dopamine in synaptic cleft
  • esp. paranoia
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34
Q

Parkinson’s disease

A

degeneration of the nigrostriatial dopamine system.

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35
Q

Norepinephrine functions

A
  • increase in vigilance
  • attention
  • sexual behaviour
  • appetite
    (modify last 3)
36
Q

Norepinephrine how it’s made

A

Tyrosine –> L-DOPA –> Dopamine –> Norepinephrine

each arrow is an enzyme

37
Q

Norepinephrine produced

A

Noradrenergic pathways in the brain - locus coeruleus

38
Q

Serotonin functions

A
  • regulation of mood
  • control of eating, sleeping and arousal
  • regulation of pain
  • dreaming
39
Q

Serotonin how it’s made

A

Tryptophan –> 5-hydroxytrytophan (5-HTP) –> 5-hydroxytryptamine (5-HT, or serotonin)

(each arrow is an enzyme)

40
Q

Serotonin produced

A

Serotonergic pathways in the brain – raphe nuclei

41
Q

Amino acids are the…

A

workhorses of the neurotransmitter family

42
Q

Which AA’s are the workhorses of the neurotransmitter family?

A
  1. Glutamate

2. GABA

43
Q

Glutamate

A

the primary excitatory neurotransmitter

44
Q

GABA

A

the primary inhibitory neurotransmitter (calming effects)

45
Q

Other neurotransmitters (not the workhorses) have more of a…

A

modulatory effect – rather than an information transmitting effect.

46
Q

Information that is learned and remembered is transmitted by…

A

neurons secreting glutamate and GABA

47
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 new formed memory?

  • allowing more AMPA receptors, strengthening that synaptic connection, giving more opportunity for binding - by having that learning process you’re allowing more receptors to be formed
48
Q

The GABA receptor

A
  • inhibitory synapses
  • necessary for brain stability
  • Epilepsy - an abnormality in this process

Barbiturates: gaba agonists

INFLUX OF CL- IONS

49
Q

Epilepsy is an abnormality in which process?

A

GABA receptor

50
Q

Barbiturates

A

gaba agonists

  • anxiety drugs
  • sleep medication
  • seizure treatments

bind to GABA receptors & may also lead to influx of Cl- ions

51
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
52
Q

The opiate story

A
  • Opiates have been used for centuries to relieve pain. (& increase mood)
  • It wasn’t until 1975 that we discovered endogenous (produced from within) opioids.
  • naturally occurring
  • several varieties of receptors.
53
Q

Opioids

A
  • runner’s high - feels good after run even if you didn’t want to run
  • causes hyperpolarizing effects
  • opium, morphine, heronin, naloxone
54
Q

Theories of addiction

A

Incentive sensitization model – the wanting and liking theory.

  • wanting – equivalent to craving a drug
  • liking – pleasure from drug taking

repeated use:

  • TOLERANCE for liking
  • wanting becomes SENSITIZED

(becomes a vicious cycle where you aren’t taking the drug to feel high, but to not feel low crashes when you’re off drug - just to feel normal)

55
Q

Incentive sensitization model

A

the wanting & liking theory

56
Q

Wanting

A

equivalent to craving a drug

57
Q

Liking

A

pleasure from drug taking

58
Q

What does repeated use do?

A
  • TOLERANCE for liking

- wanting becomes SENSITIZED

59
Q

Positive Reinforcement

A
  • fast-acting drugs are most addictive
    e. g., cocaine, heroin
  • slow-acting drugs are addictive because:
    • the EFFECT of the drug is paired with the MEMORY of taking the drug
      e. g. alcohol (makes you feel better & relaxed)
  • difficult to addict ANIMALS to slow-acting drugs.
  • drunk monkeys
  • Reinforcing behaviour
  • Most effective:
  • stimulus –> immediate response
  • hence the high addictiveness of fast-acting drugs
  • preference for heroin over morphine
60
Q

_____- acting drugs are MOST addictive

A

FAST

e.g., cocaine, heronin

61
Q

Slow-acting drugs are addictive because:

A
  • the EFFECT of the drug is paired with the MEMORY of taking the drug
  • e.g. alcohol (makes you feel better & relaxed)
62
Q

Difficult to addict animals to ____-acting drugs.

A

SLOW

- drunk monkeys

63
Q

Reinforcing behaviour

A

can get a stimulus & then an immediate response is what makes things so addictive
- fast-acting drugs

64
Q

Most effective (positive reinforcement):

A
  • stimulus –> immediate response
  • hence the high addictiveness of fast-acting drugs
  • preference for heroin (faster acting) over morphine
65
Q

Neural Mechanism

A
  • addictive drugs (and other reinforcers) cause the release of DA (dopamine) in the nucleus accumbens.
66
Q

What are the 2 types of actions for neural mechanism?

A
  1. dopamine agonist - imitating dopamine site so you have more dopamine available b/c the drug is imitating the dopamine at the binding site
  2. reuptake inhibitor - allowing n.t. to keep acting at the site for a longer amount of time

BOTH allowing dopamine to act longer at the synapse

67
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 - Hollywood teen actress
  • People with this have to stay on drugs v. imp
68
Q

POSITIVE Symptoms of schizophrenia

A
  • hallucinations, delusions, paranoia

adding these symptoms that we don’t have

69
Q

Negative Symptoms of schizophrenia

A
  • lack of emotion, energy, directedness

schizophrenia is taking these things away - subtracting/reducing

70
Q

The dopamine theory of schizophrenia

A

Dopamine antagonist

  • in 1956 they realized there was a link to dopamine
  • today most people just have to stay on meds

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).

71
Q

Over activity in the mesolimbic dopamine pathway is thought to…

A

mediate the positive symptoms of schizophrenia such as delusions and hallucinations (Figure 1).

72
Q

More recently, under activity in the mesocortical dopamine pathway has been hypothesized to be the…

A

mediator of negative symptoms of schizophrenia (Figure 2).

- cognitive, negative, & affective symptoms

73
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 (may be why we see a host of symptoms & systems being affected)

74
Q

Antipsychotics

A

affect serotonin as well

  • Risperdal - more effective in preventing relapse in patients with schizophrenia
  • it improves symptoms, & cuts the relapse rate in half
  • say benefits outweigh the risks
75
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.
76
Q

Alzheimer’s Disease (how it happens)

A
  • Nucleus Basalis - headquarter for neurons that run throughout the cortex, carry ACh that causes other neurons to fire
  • (tiny cluster of cells, near center of brain), seems to deteriorate & entire system of cells begins to dev. plaques & tangles that interfere with chemical transmission & then the cells begin to die - when the NB & its connections disappear, the cortex becomes starved for excitation & its cells in turn begin to die
77
Q

Neuropathology in Alzheimer’s disease

A

have neurofibrillary & amyloid plaques

  • brain changes that take place: plaque (formed when specific proteins in the neuron in cell membrane are processed differently) & tangles (made when a protein called tau is modified)
  • neurons in certain brain areas disconnect & eventually die, causing memory loss
  • as these processes continue, the brain shrinks & loses function
78
Q

Cholinergic involvementBasal forebrain

A

Nucleus basalis of Meynert – cell loss seen in AD

79
Q

Brain Atrophy in Advanced Alzheimer’s Disease

A
  • decay of tissue

- parts of brain dying away

80
Q

Treatments for Alzheimer’s Disease (describe both)

A
  1. ‘Cognitive enhancers’
    - Acetylcholinesterase inhibitors to offset loss of cholinergic neurons.
    • stops ACE from destroying synaptic ACH
      (so it can act longer in synapse & hopefully help eleviate some symptom)
  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.
81
Q

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

82
Q 
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

83
Q 
Drugs that block or inhibit the postsynaptic receptor effects are termed
A) agonists.
B) ligands.
C) synergists.
D) antagonists.
E) pheromones.
A

D) antagonists.

84
Q 
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

85
Q

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

86
Q 
Parkinson's disease involves degeneration of neurons within the \_\_\_\_\_\_\_\_ DA system.
A) nigrostriatal
B) mesocortical
C) hypothalamocortical
D) mesolimbic
E) retinal-suprachiasmatic
A

A) nigrostriatal

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