Chapter 4: Neurochemistry and Drug Abuse Flashcards

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
Receptors are specific to
Ligands
26
There is a ____ between action potential and neurotransmitter binding
delay of 10 microseconds
27
How many receptors does each neurotransmitter can bind to?
Several
28
2 receptor sub types for acetylcholine
Muscarinic and nicotinic
29
5 dopamine receptor subtypes
D1-D5
30
4 serotonin receptor subtypes
5-HT(1-4)
31
The message conveyed to the postsynaptic cell depends on the ____
receptor sub-type that is activated
32
Ionotropic effect
NT binding causes immediate opening of an ion channel
33
Ionotropic channels are
chemically-gated ion channels
34
Duration of ionotoppic effect
Very fast and short
35
Excitatory NT in ionotropic effect
Glutamate
36
Channel involved in iontropic effect
Ionophore
37
Inhibitory NT in ionotropic effect
GABA
38
What happens when glutamate binds to its receptor?
It opens up sodium channels to allow sodium influx which produces EPSP in postsynaptic cell
39
What happens when GABA binds to its receptor?
It opens up Cl- channels allowing for Cl- inlfux which produces IPSP
40
Metabotropic effect
- NT binding activates a second messenger system | - Slower action; longer duration
41
6 steps in second messenger systems
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
Two mechanisms for inactivation
Enzymatic breakdown and re-uptake
43
MAO or monoamine oxidase
Breaks down monoamines such as serotonin and the catecholamines
44
This enzyme breaks down ACh into choline and acetate
AChE or acetylcholinesterase
45
This enzyme is involved in acetylcholine metabolism
AChE; acetylcholinesterase
46
Monoamine oxidase inhibitors or MAOIs
Antidepressants
47
Acetylcholinesterase inhibitors
- Treatment for Alzheimer's disease - Pesticides - Chemical warfare
48
Re-uptake
- Neuron recyles NT | - Repackaged into vesicles (endocytosis) - re-uptake transporter
49
Psychopharmacology
All drugs that affect behavior do so by altering neural communication
50
Endogenous CHEMICALS
- naturally found in body | - NT, neuromodulators, enzymes, hormones
51
Exogenous DRUGS
Introduced from the outside
52
5 effects of drugs
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
Agonist
Any drug that increases NT effect
54
Direct agonist
Attaches to same receptor as NT (has same action as NT)
55
Indirect agonist
Increase NT activity by other means (increase synthesis, increase release, prevent degradation of NT)
56
Antagonist
Any drug that decreases NT effect
57
Direct antagonist
Attaches to and blocks NT receptor
58
Indirect antagonist
Decreases NT effects in another way (decrease synthesis, prevent release, increase rate of degradation)
59
Agonists and antagonists can both be treatments to
Psychological disorders/ disorder of movement
60
Agonists for GABA are
anti-anxiety drugs
61
Agonists for Serotonin are
anti-depressant drugs
62
Antagonists for dopamine are
Anti-psychotic drugs
63
Substance Abuse
A maladaptive pattern of substance use leading to clinically significant impairment or distress
64
Olds & Milner experiment
Reinforcement from electircal stimulation...same behabior when administered heroin or cocaine
65
Reward pathway
Dopamine cell bodies in ventral tegmental area (VTA) - Release DA in nucleus accumbens - - DA Inhibitory - - N. accumbens decreases activity = reward/pleasure
66
Addictions release
Dopamine in nucleus accumbens
67
Addictive potential
- Reinforcement/reward | - Reward: an individual will work to get it
68
Stimulant drugs
- Increase activity, arousal, alertness, elevate mood, decrease fatigue
69
Stimulants cause release of
Dopamine and norepinephrine
70
Stimulants ____ transporter (re-uptake mechanims)
reverse or block
71
Reward
More dopamine
72
Arousal and alertness
More norepinephrine
73
What type of drug is MDMA or ecstasy?
It is a stimulant
74
How does MDMA work?
It stimulates DA release and revereses DA transporter. It also reverses 5-HT transporter and stiumlates 5-HT release.
75
MDMA Hallucinogenic effects may be due to
increased 5-HT release
76
At high doses, MDMA or ecstasy can
destroy serotonin cells
77
MDMA or ecstasy also release
oxytocin
78
Oxytocin is involved in
love, attachment, and bonding
79
Stimulants increase DA activity in ______ and where
In nucleus accumbens and where DA is released from cell bodies in VTA
80
How are narcotic analgesics produced?
Derived from opium poppy and synthesized to resemble natural derivatives
81
States associated with opiates
Pleasant states, withdrawal reality, anlgesia (decreased pain)
82
What type of drug is heroin?
Opiate
83
How does heroin work?
It crosses blood brain barrier more readily and gives a faster "high". Converted into morphines in the brain
84
Opiate drugs act on
opiate receptors
85
Endogenous opiates
endorphins/enkephalins
86
Endorphins
endogenous morphine | - pain relief and euphoria
87
3 types of opiate receptors
u-mu, k-kappa, delta
88
Opiate receptor agonists
Bind to receptor, act like endogenous chemical
89
Opiates's effect on reward system
They increase DA release in nucleus accumbens by activating cell bodies in the VTA
90
Where are opiate receptors?
They are on axon terminal of a GABA neuron
91
Opiate drugs inhibit an
inhibitor; presynaptic inhibition
92
2 subtypes of hallucinogenic drugs
Psychedlics and dissociative anesthetics
93
States associated with hallucinogens
- Reality distortion - Hallucinations - Disordered thought - Loss of emotional response - Memory loss
94
LSD
A psychedelic - similar to 5-HT - Hallucinogneic mechanisms unknown - appears to have no effect on dopamine release - most potent need 100 micrograms
95
Synesthesia
Mixing of sense
96
Dissociative anesthetics
- used in anesthetic cocktail | - produce feelings of detachment (dissociation) from environment
97
3 examples of dissociative anesthetics
PCP, Ketamine, Destromethorphan or Robitussin