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U1 Behavioural Neurological Psychology 211 > Lecture 6 > Flashcards

Lecture 6 Flashcards

Chapter 4

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1
Q

define Drug

A

An exogenous chemical that at relatively low doses significantly alters the function of certain cells

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2
Q

define Psychopharmacology

A

Study of effects of drugs on the nervous system and behavior

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3
Q

define Drug effect

A

The changes a drug produces on physiological processes and behavior

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4
Q

define Site of action

A

Location at which molecules of a drug interact with molecules located on or in cells of body, affecting some biochemical processes of these cels

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5
Q

how to CATEGORIZING DRUGS

A

Many drugs directly or indirectly alter the activity of receptor proteins.

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6
Q

A receptor agonist is what

A

a drug that (through any means) increases the activity of the receptor protein.

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7
Q

A receptor antagonist is what

A

a drug that (through any means) decreases the activity of the receptor protein

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8
Q

A partial agonist is what

A

a drug that partially activates a given receptor (relative to a fullagonist)

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9
Q

A partial antagonist is what

A

a drug that partially decreases the activity of the receptor protein (relative to a full antagonist).

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10
Q

These classes of drugs can bind one of 2 ways:

A

competitively or non-competitively

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11
Q

wha are the different categorizing of drugs

A

A receptor agonist

A receptor antagonist

A partial agonist
A partial antagonist

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12
Q

what does A direct agonist d

A

acts similarly to the endogenous neurotransmitter. It activates the receptor by attaching itself to the binding site where the neurotransmitter would normally bind.

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13
Q

what does A direct antagonist do

A

attaches to the binding site but it prevents the receptor from being activated.

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14
Q

The competition for a receptor binding site between an endogenous neurotransmitter and an exogenous drug will depend on what

A

their relative concentrations and their affinity for the binding site

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15
Q

The competition for a receptor binding site between an endogenous neurotransmitter and an exogenous drug will depend on their relative concentrations and their affinity for the binding site. The likelihood or strength of ligand-receptor binding is called what

A

affinity

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16
Q

If a receptor is highly active to begin (e.g., due to endogenous neurotransmitter signaling), then a competitive partial agonist with very high affinity for the binding site can produce what

A

the same effect as a partial antagonist

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17
Q

what is non-competitive binding

A

When a drug binds to a receptor at a site that does not interfere with the binding site of the principal ligand it is called non-competitive binding

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18
Q

is it possible for a neurotransmitter to bind on one site of a receptor while a drug binds on another in non-competitive binding

A

It is

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19
Q

how does An indirect agonist do noncompetitive binding

A

does so in a manner that facilitates activation of the receptor

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20
Q

how does An indirect antagonist do noncompetitive binding

A

does so in a manner that prevents activation of the receptor

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21
Q

A non-competitive antagonist doesn’t compete with an endogenous signaling molecule for a particular binding site. It wins how

A

by binding to an alternative site.

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22
Q

define Allosteric Modulator

A

Drug that binds non-competitively and influences (modulates) the effect of a primaryligand. Positive allosteric modulators amplify the effect of the primary ligand. Negative allosteric modulators reduce the effect of the primary ligand.

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23
Q

what are The Conventional Neurotransmitters

A

Glutamate

GABA

Dopamine
Norepinephrine
Acetylcholine
Serotonin

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24
Q

what is Glutamate

A

Main excitatory neurotransmitter in the brain

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25
Q

wha is GABA

A

Main inhibitory neurotransmitter in the brain

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26
Q 
what are Dopamine
Norepinephrine
Acetylcholine
Serotonin
 considered
A

Main neuromodulators in the brain

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27
Q

what is different about neuromodulators

A

Although these neuromodulators are indeed conventional (classic) neurotransmitters like glutamate and GABA, most of their receptors are metabotropic (as opposed ionotropic) and they tend to produce a more modulatory influence on postsynaptic cell activity (instead of causing a fast EPSP or IPSP).

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28
Q

More than 99% of neurons release one of these two neurotransmitters:

A

Glutamate

GABA

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29
Q

is Glutamate excitatory or inhibitory

A

Typically excitatory (the gas pedal)

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30
Q

is GABA excitatory or inhibitory

A

Typically inhibitory (the brakes)

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31
Q

Ionotropic glutamate receptors induce what

A

Ionotropic glutamate receptors induce excitatory post-synaptic currents (EPSCs) and membrane depolarization, perhaps an action potential

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32
Q

Ionotropic GABA receptors induce what

A

Ionotropic GABA receptors induce inhibitory post-synaptic currents (IPSCs) and membrane hyperpolarization

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33
Q

Glutamate agonists do what

A

Agonists: often cause seizures and excitotoxicity (kainic acid, NMDA)

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34
Q

GABA agonists do what

A

Antagonists: often cause seizures

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35
Q

Glutamate Antagonists do what

A

Antagonists: dissociative anesthetics (ketamine, PCP)

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36
Q

GABA Antagonists do what

A

Agonists: anesthetics, anticonvulsants, muscle relaxants, sleeping pills, anti-anxiety (alcohol, barbiturates, benzodiazepines)

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37
Q

In addition to glutamate or GABA, many neurons also co-release what

A

neuromodulators and/or neuropeptides.

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38
Q

The Neuromodulators are made of what

A

These neurotransmitters are made in a small collection of neurons that send their axons out widely

39
Q

Neuromodulators are distinguished as neuromodulators because

A

they don’t typically produce simple excitatory or inhibitory effects in the CNS
most of their receptors are G-protein coupled receptors, not ion channels
they often diffuse short distances outside of the synapse and can influence activity of neighboring neurons

40
Q

Serotonin, dopamine, and norepinephrine all have a similar chemical structure and are known as what

A

monoamines

41
Q

Within the monoamine category of neurotransmitters, there are what

A

catecholamines (dopamine and norepinephrine) and indolamines (serotonin).

42
Q

what re the 3 categories of Neurotransmitters

A

Conventional neurotransmitters
Neuropeptides
Lipid-based signaling molecules

43
Q

give characteristics of Conventional neurotransmitters

A

mostly amino acid derivatives
The main players: glutamate, GABA, dopamine, serotonin, norepinephrine, acetylcholine
are synthesized locally in axon terminals
are usually secreted from small synaptic vesicles that dock very close to the site of Ca2+entry in the axon terminal
generally activate ionotropic and metabotropic receptors
are typically recaptured after secretion and reused
usually bind receptors directly across the synapse. Even when neurotransmitters diffuse, they only act over distances of tens to hundreds of micrometers.

44
Q

give characteristics of Neuropeptides

A

short string of amino acids (i.e., a protein formed with only ~ 10-30 amino acids)
Examples from the list of >70: oxytocin, vasopressin, enkephalin, prolactin, NPY, ghrelin, CRH
are synthesized in the cell soma, transported down the axon while undergoing additional processing, and released just once.
are usually secreted from large dense core vesicles that dock a ways back from the site of Ca2+entry in the axon terminal
only activate metabotropic receptors (neuropeptides do not activate ionotropic receptors)
no synaptic recylcing occurs of either the neuropeptides or their immediate precursors.
may diffuse long distances and exert action at a distance (non-synaptic communication)

45
Q

give characteristics of Lipid-based signaling molecules

A

(e.g., the cannabinoids anandamide and arachidonoylglycerol)
are synthesized and released on demand (as needed; the details remain murky)
are secreted in an unknown, non-vesicular manner typically from postsynaptic neurons
activate metabotropic receptors typically located on the presynaptic axon terminal

46
Q

who is the Godfather of Molly

A

Sasha Shulgin

47
Q

What are the similarities of Heroin, morphine and Imodium Anti-Diarreal

A

They are all very strong opiates

48
Q

What are the differences of Heroin, morphine and Imodium Anti-Diarreal

A

heroin– crosses the blood-brain barrier quickly because it is very lipid (fat) soluble.

morphine– crosses the blood-brain barrier a bit slower because it is less lipid soluble.

imodium– does not cross the blood-brain barrier.

49
Q

define Pharmacokinetics

A

Process by which drugs are absorbed, distributed within the body, metabolized, and excreted

50
Q

Drugs have to reach their site of action which is what

A

the point where drug molecules interact with molecules located on or in cells of the body.

51
Q

what is Intravenous (i.v.) injection

A

into the vein

52
Q

what is Intraperitoneal (i.p.) injection -

A

into the abdominal wall (peritoneal cavity)

53
Q

what is Intramuscular (i.m.) injection -

A

into the muscle

54
Q

what is Subcutaneous (s.c.) injection -

A

into the space between the skin

55
Q

what is Oral administration

A
  • by mouth
56
Q

what is Sublingual administration -

A

under the tongue

57
Q

what is Intrarectal administration –

A

in the rectum as a suppository

58
Q

what is Inhalation -

A

by smoking

59
Q

what is Topical administration –

A

on the skin

60
Q

what is Intracerebral administration -

A

directly into the brain

61
Q

what is Intracerebroventricular (ICV) –

A

into a cerebral ventricle

62
Q

what is Intrathecal (epidural) –

A

into the cerebrospinal fluid of the spinal cord

63
Q

The speed of drug absorption into the blood and the extent to which the drug might be metabolized before getting to the blood or to the brain are heavily influenced by what

A

the route of administration

64
Q

what are Principles of PsychopharmacologyInactivation and Excretion

A

Drugs do not remain in body indefinitely
Many drugs are deactivated by enzymes in the liver and blood, and all are eventually excreted, primarily by kidneys
The brain also contains enzymes that destroy some drugs

65
Q

what is A dose response curve

A

is a graph of the magnitude of an effect of a drug as a function of the amount that is administered. It is obtained by giving subjects various doses of drug (typically according to weight).

66
Q

Higher doses cause larger effects until when

A

the point of maximum effect

67
Q

what is the margin of safety

A

The difference between the two curves is the drugs margin of safety – often conveyed as therapeutic index: the ratio between the dose that produces desired effect in 50 percent of animals and the dose that produces toxic effects in 50 percent of animals

68
Q

Drugs that fully activate (or inactivate) the same receptor can vary in effectiveness because:

A

They have different sites of action (competitive vs non-competitive).

They have different pharmacokinetics (heroin vs morphine).

They have different affinities for the molecules to which they attach. The affinity of a drug is the readiness with which two molecules join together.

a) A drug with a high affinity will produce an effect at low doses whereas a drug with a low affinity may have to be administered at a high dose.
b) A single drug can have a high affinity at one site of action and a low affinity at a different site of action.

69
Q

what is Tolerance

A

when the effect of drug diminishes because of repeated administration. It is the body’s attempt to compensate for the effects of the drug.

 E.g., a regular heroin user must take larger and larger amounts of the drug to keep feeling the same effect. Having developed tolerance to heroin, the user will suffer withdrawal symptoms which are opposite effects of the drug (i.e. euphoria vs dysphoria).

 E.g., barbiturates have sedative and depressive effects. The sedative effect shows tolerance but the depressive effect does not. Thus, if larger doses of barbiturates are taken to achieve a sedative effect, you run the risk of taking a dangerously high dose of the drug.

70
Q

what is Sensitization

A

occurs when a drug becomes more and more effective through repeated use.

71
Q

what is placebo

A

A placebo is an inert substance that has no direct physiological effect. It is given to subjects to control the effects of mere administration of a drug

72
Q

what are the Effects of Repeated Administration

A

Tolerance
Sensitization
placebo

73
Q

what re the Effects on Production of Neurotransmitters (from drugs)

A

Neurotransmitters are synthesized from precursor molecules

Steps in synthesis of neurotransmitters are controlled by enzymes

The packaging of neurotransmitter into synaptic vesicles can be blocked by a drug

Some drugs act as antagonists by preventing release of synaptic vesicles from the axon terminal

Other drugs have just the opposite effect:
They act as agonists by binding with vesicle

The clearance of neurotransmitters is controlled by proteins

74
Q

define Neurotransmitters are synthesized from precursor molecules

A

In some cases the rate of synthesis and release of a neurotransmitter is increased when a precursor is administered
In these cases, the precursor itself serves as an agonist

75
Q

explain Steps in synthesis of neurotransmitters are controlled by enzymes

A

Therefore, if a drug inactivates one of these enzymes, it will prevent the neurotransmitter from being produced.
Such a drug serves as an antagonist

76
Q

explain The packaging of neurotransmitter into synaptic vesicles can be blocked by a drug

A

These drugs act as antagonists because the synaptic vesicles remain empty and nothing is released when they eventually fuse with the presynaptic membrane

77
Q

explain Some drugs act as antagonists by preventing release of synaptic vesicles from the axon terminal

A

They do so by deactivating proteins that cause synaptic vesicles to fuse with presynaptic membrane and expel their contents into synaptic cleft

78
Q

explain Other drugs have just the opposite effect:

A

They act as agonists by binding with vesicle release machinery or reuptake transporters and directly trigger the release of neurotransmitter

79
Q

explain The clearance of neurotransmitters is controlled by proteins

A

Drugs that affect neurotransmitter clearance can act as agonists or antagonists.
The clearance of neurotransmitters is achieved by reuptake into the axon terminal, enzymatic destruction, or diffusion.

80
Q

what is Acetylcholine

A

In the central nervous system acetylcholine is often classified as a neuromodulator. (It is made in a small collection of neurons that send their axons out widely. It typically acts to regulate the efficacy of glutamatergic and GABAergic synapses.)

However, acetylcholine is also the primary neurotransmitter secreted by efferent axons that leave the central nervous system. All muscular movement is accomplished by the release of acetylcholine.

81
Q

All motor neurons release what as their main neurotransmitter

A

acetylcholine

82
Q

Most sensory neurons release what as their main neurotransmitter.

A

glutamate

83
Q

what does Black widow spider venom

do

A

Poison produced by the black widow spider that triggers the release of acetylcholine

84
Q

what does Botulinum toxin (botox

do

A

Produced by a baterium that can grow in improperly canned food. It is a acetylcholine system antagonist, because it prevents the release acetylcholine causing muscle paralysis

85
Q

The synaptic vesicle recycling machinery (i.e., endocytosis-driven synaptic vesicle reformation) is another target for what

A

drugs and toxins

86
Q

what is Neostigmine

A

Drug that inhibits activity of acetylcholinesterase, which is the enzyme that breaks down acetylcholine in the synaptic cleft. Neostigmine causes acetylcholine to hang around in the synapses for a longer period of time.

87
Q

what is Myasthenia Gravis

A

hereditary disorder in which the person’s own immune system attacks healthy acetylcholine receptors.

People with this disorder become noticeably weaker and weaker over time (fatigability).

We don’t yet have a good way to give these people back functional receptors, but with drugs like Neostigmine we can make the released acetylcholine stay around for longer periods of time

88
Q

what is Parkinson’s disease

A

a neurological disorder that is often characterized by tremors, rigidity of limbs, poor balance, and difficulty initiating movements.

It is caused by the degeneration (death) of dopamine neurons in the midbrain.

L-Dopa is often used to treat Parkinson’s disease because it increases dopamine production in the brain and thus acts as a dopamine agonist.

89
Q

what do Methylphenidate,
Cocaine
do

A

Drugs that inhibit the reuptake of catecholamine neurotransmitters (dopamine & norepinephrine) by blocking their synaptic transporters.
Tylenol (acetaminophen) does the same thing to one of the cannabinoid reuptake transporters. Elevating synaptic endocannabinoids levels may result in pain relief

90
Q

what do Adderall,
Crystal meth
do

A

Drugs that reverse catecholamine transporters, causing dopamine and norepinephrine molecules to flow directly out of the presynaptic terminal (non-vesicular release).
Ecstasy (MDMA) does a similar thing to all of the monoamine transporters (i.e. causes them to run backwards).

91
Q

what is an example of Receptor blockers

A

Antipsychotics

(neuroleptics

92
Q

what do Antipsychotics
(neuroleptics
do

A

Class of drugs used to treat psychosis (schizophrenia). They are typically dirty drugs (i.e. they have many sites of actions), but most prominently they block one of the dopamine receptors, the D2 receptor.

93
Q

define allosteric modulator

A

Drug that binds non-competitively and influences (modulates) the effect of a primaryligand. Positive allosteric modulators amplify the effect of the primary ligand. Negative allosteric modulators reduce the effect of the primary ligand.

U1 Behavioural Neurological Psychology 211 (22 decks)

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