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Psychopharmacology Flashcards

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1
Q

Which of the following is a compensatory mechanism that would result in drug tolerance?

A

Reduced the number of drug receptors

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2
Q

A drug that binds at a postsynaptic site that is different from that of the neurotransmitter binding site and prevents the opening of ion channels would be termed a(n)

A

Indirect antagonist

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3
Q

Stimulation of a presynaptic auto-receptor

A

Reduces the release of neurotransmitters from the axon to the terminal buttons

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4
Q

________ is the primary efferent (motor neuron) neurotransmitter secreted by efferent axons of the CNS (muscle fiber).

A

Acetylcholine (ACh)

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5
Q

________ is the enzyme that accepts an acetate ion from coenzyme A and transfers it to a choline molecule, thereby producing acetylcholine.

A

Choline acetyltransferase

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6
Q

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

A

Nigrostriatal

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7
Q

Which pair of transmitter substances are most involved in synaptic neurotransmission in the brain?

A

Glutamate : GABA

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8
Q

Directly into a vein

A

Intravenous Injection

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9
Q

The most common route used for animals goes into the peritoneal cavity (stomach, abdomen, etc). What are the drawbacks?

A

Intraperitoneal Injection. It is administered laterally, which can hit major organs and it also takes 30 minutes for effectiveness.

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10
Q

Used for vaccines and injected into the muscles. What happens when it is mixed with ephedrine?

A

Intramuscular. When mixed it speeds up the absorption rate.

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11
Q

Less stressful for animals and requires small dosages beneath the skin.

A

Subcutaneous Injections

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12
Q

The effects of a small dose of an effective drug?

A

Minimize side effects and equal or exceed the effects of a larger dosage of an ineffective drug that creates more or negative side effects.

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13
Q

Why can’t insulin be used in ________ administration?

A

Oral. Digestive enzymes will break it down before it can be absorbed into the body.

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14
Q

Fastest effectiveness and administered beneath the tongue.

A

Sublingual administration

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15
Q

Fast effectiveness, not used with rats, and administered through the rectum.

A

Intrarectal administration

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16
Q

Why can’t cocaine be administered _______ ? What can be?

A

Topical. Can not be absorbed through the skin due to the mucus lining of the nose (can’t get into the lungs). Nicotine patches and steroid screams can be absorbed.

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17
Q

_______ is site-specific and _______ circulates throughout the brain ventricles, expect for the PNS.

A

Intracerebral : Intracerebroventricular

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18
Q

The blood-brain barrier is not water-soluble

A

False. It is water-soluble as water molecules can enter. Lipids can only pass through capillaries in the CNS that distribute throughout the brain.

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19
Q

________ is when a drug provides no more relief/ a stronger effect, therefore, it is maxed out and increasing doses will still have no impact. (a.k.a it plateaus)

A

Ceiling effect

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20
Q

The difference between the usual dose (effective) and the dosage that causes severe side effects (lethal) is _______

A

The margin of safety. A wide margin is needed because it indicates less risk of exceeding the therapeutic index (the estimated margin —> overdose)

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21
Q

How well a drug binds to a receptor is _____ . To be high in this means the drug binds well and creates low dosages/concentrations.

A

Affinity

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22
Q

______ Is when the drugs decrease in their effectiveness due to repeated use and can become very addictive. If a drug is needed for an injury then you won’t develop this.

A

Tolerance

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23
Q

An increase in the effectiveness of a drug that is used repeatedly and the individual becomes dependent on the drug (cravings)

A

Sensitization

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24
Q

_______ is when a drug used to be administered and is no longer taken, therefore, having addiction symptoms.

A

Withdrawal

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25
Q

2 possible compensatory mechanisms for both tolerance and withdrawal are

A

Decrease in the effectiveness of drug binding (Affinity decreases & receptors move-not getting rid of The drug will travel further which will cause deactivation enzymes to destroy it or cause the drug to be less effective.

And alteration to a receptor and ion channel processes. ( Ion channel won’t open since communication is broken down )

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26
Q

Taking a sip of coffee (caffeine) and feeling energized after is an example of a?

A

A placebo effect because it takes about 30 minutes for it takes effect.

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27
Q

Neurotransmitters can only be ______ or _____ .

A

Excitatory (AP) or Inhibitory (No AP)

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28
Q

Drugs can only be _____ or ______

A

Antagonist or Agonist

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29
Q

A drug that prevents a neurotransmitter from opening ion channels on the postsynaptic cell (Sites 1,2a,2b, & 3a)

A

Antagonist

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30
Q

A drug that helps or mimics a neurotransmitter opens ion channels in the postsynaptic cell. It can also severe as a precursor (Sites 1,2a,2b, & 3a)

A

Agonist

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31
Q
  1. Cell Body
A

Antagonists decrease/block the production of NT to be ineffective. Agonist increase/help production of NT to be effective

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32
Q

2a. Storage of Neurotransmitters

A

Under normal conditions, NT goes from the axon to the terminal button prior to an action potential.

Antagonists will block/decrease storage (10 to 8 NTs in the future)

Agonists will help/increase storage to release (8 to 10 NTs in the future).

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33
Q

Vesicles (2a)

A

Neurotransmitters attach to vesicles, but those that do not attach are destroyed by enzymes. When molecules are blocked by the drugs it can fire an AP, but not release NTs and the vesicles will remain empty.

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34
Q

2b. Release of neurotransmitters

A

Antagonists prevent the release of NTs by deactivating calcium channels that help fuse vesicles together.

Agonists help the release of NTs by opening calcium channels to fuse vesicles together.

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35
Q

3a. Postsynaptic

A

Antagonists will prevent ion channels from opening.

Agonists will open ion channels.

36
Q

3a. Indirect (Noncompetitive)

A

Agonist attaches to the binding site on a receptor that is not the NT receptor and helps.

Antagonists will bind to a site on a receptor that is not the NT receptor and interfere.

37
Q

3a. Direct (Competitive)

A

Agonists will bind to the NT receptor and mimic it.

Antagonists will bind to the NT receptor and block NT from binding.

38
Q

3b. Presynaptic autoreceptors (Inhibitory)

A

Monitors neurotransmitters in the synaptic cleft and sends signals to presynapse in the future to send fewer NTs.

Agonists will block presynaptic receptors (reduce what will be sent in the future): Leaving leftover NTs in the synaptic cleft to be used.

Antagonist will stimulate presynaptic receptors (continuing to release a normal amount or more): Reducing the number of NTs, when this happens nothing will bind autoreceptor.

39
Q

4a. Reuptake (Synaptic Cleft - Inhibatory)

A

Agonists will block reuptake and enzymes to keep the neurotransmitter alive as it will bind to an autoreceptor someday.

Antagonists will stimulate reuptake and allow enzymes to destroy the neurotransmitter.

40
Q

4b. Deactivation Enzymes (Synaptic Cleft - Inhibitory)

A

Agonists block enzymes.

Antagonists will help enzymes.

41
Q

Two effects that neurotransmitters have on postsynaptic membranes are _______ (EPSP) or ______ (IPSP).

A

Depolarization: Hyperpolarization

42
Q

________ prime certain areas of the brain for neurotransmitters. modulating (modifying or controlling influence) effects

A

Neuromodulators

43
Q

What are two important neurotransmitters that makeup 90% of synaptic communication? Information-transmitting effects

A

Glutamate - Excitatory effects

GABA - Inhibitory effects

44
Q

Acetylcholine is involved in

A
  • Muscular movement
  • Regulating REM sleep (body paralysis, eyes only move)
  • Perceptual learning
  • Memory
  • Electrical rhythms of the hippocampus ( converting short-term memory to long-term memory)
45
Q

Acetyl-CoA

A

A cofactor (protein) that helps/assists acetate (ion) attach to choline (enzyme) because acetate can not be directly attached to choline. CoA falls off when they connect and go to another ion.

46
Q

Choline acetyltransferase (ChAT)

A

The enzyme that converts acetate (ion) from Acetyl-CoA to choline to make acetylcholine.

47
Q

An acetylcholine _____ prevents the release of terminal buttons.

A

Site 2b, Antagonist, decreases Ach.
(e.g. Botox and muscle contractions)

48
Q

A poison (____) that triggers the release of acetylcholine

A

Site 2b, Agonist, increase Ach
(e.g. Black widow venom)

49
Q

A drug that inhibits the activity of acetylcholinesterase (enzyme).

A

Site 4b, Agonist
(e.g. Neostigmine)

50
Q

_______ and ______ are two types of ACh receptors

A

Ionotropic (receptor and ion together)

Metabotropic (receptor and ion separate)

51
Q

A nictotinic receptor is ______

A

Ionotropic because the response and effects are quick and the receptor closes quickly.

52
Q

A muscarinic receptor is ______

A

Metabotropic because the response and effects are low but the receptor closes slowly, hence giving a longer effect.

53
Q

Dopamine, norepinephrine, epinephrine, and serotonin are _______

A

Monoamines

54
Q

Catecholamines

A

Dopamine, norepinephrine, and epinephrine come from the same precursor tyrosine. Responsible for “fight-or-flight” responses.

55
Q

Dopamine

A

Functions for the fluidity of movement, attention, learning, and reinforcing effects of drug abuse.

Tyrosine converts to L-Dopa by tyrosine hydroxylase (enzyme)

L-Dopa (Site 1): Often used for Parkinson’s disease because it is a dopamine agonist.
** Crosses the BBB to change into dopamine with help of another enzyme**

56
Q

One of the three important systems of dopaminergic neurons that control the fluidity of movement

A

Nigrostriatal system:
Origin: Caudate nucleus (learning movement)
Terminate: Putamen of the basal ganglia (performing movement)

57
Q

One of the three important systems of dopaminergic neurons is studied more, especially addiction because it reinforces the effects of drugs that are abused.

A

Mesolimbic system:
Origin: Ventral tegmental area
Terminate:
- Nucleus accumbens: Pleasure feeling
- Amygdala: Emotions **Drugs overexcite which increases activity, and causes the body to try to get to normal baseline b/c the baseline is altered — withdrawals)
- Hippocampus: Memory Thinking of how the drug makes the individual feel

58
Q

One of the three important systems of dopaminergic neurons influences short-term memory, planning, problem-solving, also attention/learning.

A

Mesocortical system:
Origin: Ventral tegmental area
Terminate: Pre-frontal cortex

59
Q

A drug that interferes with the storage of monoamines in the synaptic vesicles.

A

Monoamine antagonist (2a)
(e.g. Reserpine - High blood pressure)

60
Q

A drug that reduces the symptoms of schizophrenia by blocking dopamine D2 receptors.

A

Antagonist (3a)

61
Q

Serotonin

A

Plays a role in the regulation of mood, the control of eating, sleeping, dreaming, and arousal.

Thought to regulate pain

Tryptophan is the precursor

62
Q

A drug that stimulates the release of serotonin and also inhibits reuptake.

A

2b and 4a
(e.g. Fenfluramine)

63
Q

An ionotropic glutamate receptor that controls calcium channels (depolarizes charges). Mg2+will stay blocking the channel until a stimulus removes it (voltage removes it and ligand opens the channel).

A

NMDA receptor

If PCP (a drug) is involved: It is an indirect antagonist because it is not bound to the glutamate receptor.

This receptor is also responsible for operant and classical conditioning: Learning.

64
Q

An ionotropic glutamate receptor that controls sodium channels and produces EPSPs. It is also the most common receptor.

A

AMPA receptor

65
Q

An ionotropic glutamate receptor that controls sodium channels, it has similar effects to the most common receptor and the only difference is that there is less of this receptor.

A

Kainate receptor

66
Q

A drug that blocks glutamate binding sites on NMDA receptors and impairs synaptic plasticity (less calcium) and certain forms of learning.

A

Direct antagonist

67
Q

A drug that binds with the PCP binding site of the NMDA.

A

Indirect antagonist

68
Q

GABA (A) Drugs

A

ionotropic and ligand-gated. Involves chloride channels. Keeps individual at rest -70mv.

4 binding sites:
- Benzodiazepine (tranquilizing effect, highly addictive & quick tolerance)
- Barbiturates (Anti-anxiety, frequent overdose, small margin, less addictive)
- Steroids (Anesthesia)
- Picrotoxin (Pain)

69
Q

GABA (B) Drugs

A

Metabotropic receptor and opens potassium channels.
- Hyperpolarization
- Uses a G-Protein

70
Q

A neuromodulator that plays a primary role in the initiation of sleep.
As glycogen levels decrease this neuromodulator’s levels increases causing the individual to sleep.

A

Adenosine

71
Q

Plays a primary role in awakeness. This burns throughout the day and peaks when an individual wakes in the morning.
As adenosine levels decrease then this increases causing the individual to be awake.

A

Glycogen

72
Q

Two groups of ACh neurons that are involved in arousal are located:

A

Dorsal pons and basal forebrain

73
Q

Norepinephrine neurons that are involved in arousal are located in:

A

Locus coerulus

74
Q

Serotonin neurons that are involved in arousal are located in:

A

Raphe nuclei

75
Q

Histamine neurons that are involved in arousal are located in:

A

Hypothalamus

76
Q

Orexin neurons that are involved in wakefulness are located in:

A

Lateral hypothalamus & have an excitatory effect
- Degeneration causes narcolepsy

77
Q

The majority of sleep neurons are located in

A

the ventrolateral preoptic area (vIPOA)
- Anterior hypothalamus

78
Q

The term for reciprocal (mutual) inhibition and what does it mean?

A

Flip-Flop. When the vIPOA receives inhibitory signals from the inactive area and vice versa (forebrain to vIPOA).

Meaning:
- Sleep neurons are more active than the arousal system off: high in adenosine [OFF-SLEEP]

  • Arousal system active (Excitatory signals sent to the 4 NTs) then sleep neurons off: low in adenosine [ON-AWAKE]
79
Q

What role does orexin do for wakefulness?

A

It keeps the arousal system (alert-waking state) active by boosting the arousal system with an excitatory response. It also plays a role in alertness throughout the day and stabilizes the ‘flip-flop’ by preventing us from falling asleep during the day.

80
Q

Factors that stabilize/control the activity of orexin

A
  • Biological clock (Time of day): Excitatory
  • Hunger: Excitatory
  • Satiety (Comfort level – e.g. full from a meal = dozing off): Inhibitory
81
Q

Caffeine is an ___________

A

Adenosine antagonist

82
Q

What is the sublaterodorsal nucleus (SLD)?

A

Contains REM-ON neurons.
- Brain regions controlling components of REM sleep
- Paralysis

83
Q

What is the ventrolateral periaqueductal gray mater (vIPAG)?

A

Contains REM-OFF neurons
- Awake

84
Q

REM-On and REM-OFF are ________

A

Mutal means one is on while the other is off.

85
Q

What is the suprachiasmatic nucleus (SCN) and where is it located?

A

Located in the hypothalamus and plays a role in organizing the body’s circadian rhythms.

Psych (6 decks)

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