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Physiological Psychology > Chapter 4: Neurochemistry and Drug Abuse > Flashcards

Chapter 4: Neurochemistry and Drug Abuse Flashcards

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1
Q

Sherrington

A
  • proposed concept of synapse
  • Believed communication is too fast for chemicals
  • Favors electrical communication
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2
Q

Loewi’s experiment

A
  • With CN-X; vagus nerve;parasympathetic nervous system
  • Heart #1 in solution connected to an electrical stimulator
  • Heart#2 placed in solution that Heart #1 bathed in but without electrical stimulation
  • It must be chemical
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3
Q

Neurotransmitter in Loewi’s experiment

A

Acetylcholine

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4
Q

Presynaptic cell

A

The sender

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5
Q

Length of synaptic cleft

A

10 micrometers

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6
Q

Postsynaptic cell

A

The receiver

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7
Q

The four broad chemicals involved in neurons communication

A

Neurotransmitters, neuromodulators, peptides, hormones

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8
Q

5 major categories of neurotransmitters

A

Biogenic amines, Amino acids, pepetides (modulators), purines, gases

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9
Q

Name 5 biogenic amines

A

Acetylcholine, serotonin, dopamine, norepinephrine, epinephrine

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10
Q

Name 2 amino acid neurotransmitters

A

GABA and glutamate

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11
Q

5 events in chemical transmission

A
  1. Synthesis
  2. Transport to axon terminal
  3. Release
  4. Receptor binding
  5. Inactivation
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12
Q

What are neurotransmitters made from?

A

From compounds obtained in diet and enzymes present in cell

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13
Q

Do all neurons have all the enzymes needed to synthesize all neurotransmitters?

A

Only neurons that release a specific neurotransmitter will have necessary enzymes to synthesize that neurotransmitter

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14
Q

2 reactants in acetylcholine synthesis

A

Acetyl co-enzyme A and choline

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15
Q

Where do you get acetyl co-enzyme A?

A

It is made in the mitochondria

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16
Q

Where do you get choline?

A

From diet

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17
Q

Name of enzyme that facilitates production of acetylcholine

A

CAT; choline acetyltransferase

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18
Q

Order of synthesis of dopamine, norepinephrine, and epinephrine

A

dopamine, norepinephrine, and epinephrine

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19
Q

Where are neurotransmitters released from?

A

The presynaptic terminal region

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20
Q

What facilitates transport of neurotransmitters or other compounds such as choline?

A

Microtubules

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21
Q

What are opened when action potential arrives at axon terminal?

A

Voltage gated calcium channels are opened

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22
Q

What enters cell when action potential reaches axon terminal?

A

Ca++

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23
Q

What does the inlfux of Ca++ cause at the axoxn terminal?

A

Vesicle membrane to fuse with cell membrane and exocytosis

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24
Q

What happens to neurotransmitters once they are released by exocytosis?

A

They diffuse (passive process) and then attach to receptors (binding).

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25
Q

Receptors are specific to

A

Ligands

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26
Q

There is a ____ between action potential and neurotransmitter binding

A

delay of 10 microseconds

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27
Q

How many receptors does each neurotransmitter can bind to?

A

Several

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28
Q

2 receptor sub types for acetylcholine

A

Muscarinic and nicotinic

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29
Q

5 dopamine receptor subtypes

A

D1-D5

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30
Q

4 serotonin receptor subtypes

A

5-HT(1-4)

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31
Q

The message conveyed to the postsynaptic cell depends on the ____

A

receptor sub-type that is activated

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32
Q

Ionotropic effect

A

NT binding causes immediate opening of an ion channel

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33
Q

Ionotropic channels are

A

chemically-gated ion channels

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34
Q

Duration of ionotoppic effect

A

Very fast and short

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35
Q

Excitatory NT in ionotropic effect

A

Glutamate

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36
Q

Channel involved in iontropic effect

A

Ionophore

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37
Q

Inhibitory NT in ionotropic effect

A

GABA

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38
Q

What happens when glutamate binds to its receptor?

A

It opens up sodium channels to allow sodium influx which produces EPSP in postsynaptic cell

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39
Q

What happens when GABA binds to its receptor?

A

It opens up Cl- channels allowing for Cl- inlfux which produces IPSP

40
Q

Metabotropic effect

A
  • NT binding activates a second messenger system

- Slower action; longer duration

41
Q

6 steps in second messenger systems

A
  1. NT (1st messenger) binds to receptor
  2. Change in configuration of receptor proteins
  3. Release G-protein
  4. Activates adenylyl cyclase
  5. produces 2nd messenger or cAMP
  6. 2nd messenger activates other proteins that open/close ion channels, alter production of proteins, activates genes
42
Q

Two mechanisms for inactivation

A

Enzymatic breakdown and re-uptake

43
Q

MAO or monoamine oxidase

A

Breaks down monoamines such as serotonin and the catecholamines

44
Q

This enzyme breaks down ACh into choline and acetate

A

AChE or acetylcholinesterase

45
Q

This enzyme is involved in acetylcholine metabolism

A

AChE; acetylcholinesterase

46
Q

Monoamine oxidase inhibitors or MAOIs

A

Antidepressants

47
Q

Acetylcholinesterase inhibitors

A
  • Treatment for Alzheimer’s disease
  • Pesticides
  • Chemical warfare
48
Q

Re-uptake

A
  • Neuron recyles NT

- Repackaged into vesicles (endocytosis) - re-uptake transporter

49
Q

Psychopharmacology

A

All drugs that affect behavior do so by altering neural communication

50
Q

Endogenous CHEMICALS

A
  • naturally found in body

- NT, neuromodulators, enzymes, hormones

51
Q

Exogenous DRUGS

A

Introduced from the outside

52
Q

5 effects of drugs

A
  1. Change synthesis of NT
  2. Prevent packaging in vesicles
  3. Increase or decrease NT release
  4. Affect inactivation of a NT
  5. Directly affect NT receptors (agonist or antagonist)
53
Q

Agonist

A

Any drug that increases NT effect

54
Q

Direct agonist

A

Attaches to same receptor as NT (has same action as NT)

55
Q

Indirect agonist

A

Increase NT activity by other means (increase synthesis, increase release, prevent degradation of NT)

56
Q

Antagonist

A

Any drug that decreases NT effect

57
Q

Direct antagonist

A

Attaches to and blocks NT receptor

58
Q

Indirect antagonist

A

Decreases NT effects in another way (decrease synthesis, prevent release, increase rate of degradation)

59
Q

Agonists and antagonists can both be treatments to

A

Psychological disorders/ disorder of movement

60
Q

Agonists for GABA are

A

anti-anxiety drugs

61
Q

Agonists for Serotonin are

A

anti-depressant drugs

62
Q

Antagonists for dopamine are

A

Anti-psychotic drugs

63
Q

Substance Abuse

A

A maladaptive pattern of substance use leading to clinically significant impairment or distress

64
Q

Olds & Milner experiment

A

Reinforcement from electircal stimulation…same behabior when administered heroin or cocaine

65
Q

Reward pathway

A

Dopamine cell bodies in ventral tegmental area (VTA)

  • Release DA in nucleus accumbens
    • DA Inhibitory
    • N. accumbens decreases activity = reward/pleasure
66
Q

Addictions release

A

Dopamine in nucleus accumbens

67
Q

Addictive potential

A
  • Reinforcement/reward

- Reward: an individual will work to get it

68
Q

Stimulant drugs

A
  • Increase activity, arousal, alertness, elevate mood, decrease fatigue
69
Q

Stimulants cause release of

A

Dopamine and norepinephrine

70
Q

Stimulants ____ transporter (re-uptake mechanims)

A

reverse or block

71
Q

Reward

A

More dopamine

72
Q

Arousal and alertness

A

More norepinephrine

73
Q

What type of drug is MDMA or ecstasy?

A

It is a stimulant

74
Q

How does MDMA work?

A

It stimulates DA release and revereses DA transporter. It also reverses 5-HT transporter and stiumlates 5-HT release.

75
Q

MDMA Hallucinogenic effects may be due to

A

increased 5-HT release

76
Q

At high doses, MDMA or ecstasy can

A

destroy serotonin cells

77
Q

MDMA or ecstasy also release

A

oxytocin

78
Q

Oxytocin is involved in

A

love, attachment, and bonding

79
Q

Stimulants increase DA activity in ______ and where

A

In nucleus accumbens and where DA is released from cell bodies in VTA

80
Q

How are narcotic analgesics produced?

A

Derived from opium poppy and synthesized to resemble natural derivatives

81
Q

States associated with opiates

A

Pleasant states, withdrawal reality, anlgesia (decreased pain)

82
Q

What type of drug is heroin?

A

Opiate

83
Q

How does heroin work?

A

It crosses blood brain barrier more readily and gives a faster “high”. Converted into morphines in the brain

84
Q

Opiate drugs act on

A

opiate receptors

85
Q

Endogenous opiates

A

endorphins/enkephalins

86
Q

Endorphins

A

endogenous morphine

- pain relief and euphoria

87
Q

3 types of opiate receptors

A

u-mu, k-kappa, delta

88
Q

Opiate receptor agonists

A

Bind to receptor, act like endogenous chemical

89
Q

Opiates’s effect on reward system

A

They increase DA release in nucleus accumbens by activating cell bodies in the VTA

90
Q

Where are opiate receptors?

A

They are on axon terminal of a GABA neuron

91
Q

Opiate drugs inhibit an

A

inhibitor; presynaptic inhibition

92
Q

2 subtypes of hallucinogenic drugs

A

Psychedlics and dissociative anesthetics

93
Q

States associated with hallucinogens

A
  • Reality distortion
  • Hallucinations
  • Disordered thought
  • Loss of emotional response
  • Memory loss
94
Q

LSD

A

A psychedelic

  • similar to 5-HT
  • Hallucinogneic mechanisms unknown
  • appears to have no effect on dopamine release
  • most potent need 100 micrograms
95
Q

Synesthesia

A

Mixing of sense

96
Q

Dissociative anesthetics

A
  • used in anesthetic cocktail

- produce feelings of detachment (dissociation) from environment

97
Q

3 examples of dissociative anesthetics

A

PCP, Ketamine, Destromethorphan or Robitussin

Physiological Psychology (5 decks)

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