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Behavioural Neuroscience > Chapter 7 > Flashcards

Chapter 7 Flashcards

1
Q

What kind of animals have something that interefere with neurotransmitter signaling? What is it?

A

Primairly snakes and spiders
The venom

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2
Q

Where do our knowledge of drugs and neurotransmitter signaling come from?
What do many of them do? How?

A

Studying the compounds of snakes and spiders venom.
They can cause paralysis or spasms through the intereference of neurotransmitter signaling at the neuromuscular junction.

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3
Q

What does acetylcholine do in the CNS? WHere?

A

Acts as a neuromodulator.
At axoaxonic synapses

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4
Q

What does acetylcholine do in the PNS? Where? What does it activate?

A

Acetylcholine is released by motor neurons at the neuromuscular junction.
It activates the fast excitatory ionotropic receptors on muscle cells that cause mucle contraction

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5
Q

What do motor neurons use as their main neurotransmitter?

A

acetylcholine

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6
Q

What do sensory neurons use as their main neurotransmitter?

A

Glutamate

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7
Q

What is black widow spider venom? What does it cause?

A

Poison produced by the black widow spider.
Triggers the release of acetylcholine.

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8
Q

What is botulinum toxic (botox)? What does it do? What produces it?

A

It is an acetylcholine system antagonist,.
It prevents the release of acetylcholine causing muscle paralysis.
It is produced by bacteria that grow in improperly canned food.

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9
Q

What is an neostigmine?
Which is?

A

A drug that inhibits activity of acetylcholinesterase
Which is the enzyme that breaks down acetylcholine in the synaptic cleft.

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10
Q

What does neostigmine cause?

A

It causes acetylcholine to hang around in the synapses for a longer period of time

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11
Q

What is Myasthenia Graves?
What is a symptom of this disorder?

A

A hereditary autoimmune disorder in which the person’s own immune system attacks their healthy acetylcholine receptors.
People with this disorder become noticeably weaker and weaker over time (fatigability)

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12
Q

What is a drug?

A

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

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13
Q

What is psychopharmacology?

A

Study of effects of drugs on the nervous system and behaviour

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14
Q

What is drug effect?

A

The changes a drug produces on physiological processes and behaviour.

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15
Q

What is 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 cells.

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16
Q

What is psychosis?
Symptoms?

A

Psychosis is an abnormal condition of the mind that results in difficulties determining what is real and what is not real.
Symptoms: delusions, hallucinations, incoherent speech and behaviour that is innapropiate for the situation

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17
Q

What are antypsychotics?
What do they treat?
What’s special about how they bind to receptors?

A

Neuroleptics : direct dopamine receptor antagonists
They treat psychosis
They bind to more than one

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18
Q

What kind of drugs cause hallucinations?
What’s special about this?
What are they?

A

Ones that directly activate serontonin 2A receptors.
Other direct serontonin 2A receptor antagonists do not cause hallucinations at all.
They are inhibitory metabotropic receptors expressed by neurons all over the brain

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19
Q

What are the 4 drugs that directly activate serontonin 2A receptors?
Which ones are hallucinogens?
Which ones aren’t?

A

mescaline, psilocybin, LSD, lisuride
mescaline, psilocybin and LSD
lsiuride

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20
Q

What’s the difference between halluninogens and non hallucinonengens?

A

When these agonists bind and activate a metabotropic receptors, they launch an intracellular signaling cascade that starts with protein Gq/11.
Hallucinogenic drugs activate an additional g protein know as Gi/o.
It is the 5HT2A receptor-induced activation of Gi/0 proteins that cause hallucinations

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21
Q

What is a biased agonism?

A

When a metabotropic receptor ligand causes the receptor to preferentially activate one type of intracellular g protein, whereas another ligand at the same receptor might preferentially activate a different g protein.

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22
Q

How can drugs affect postsynaptic receptor activity?

A

Directly or indirectly

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23
Q

What are direct agonists/antagonists?

A

Drugs that affect postsynaptic receptor activity by directly binding to post synaptic receptors

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24
Q

What are indirect agonists/antagonists?

A

Drugs that affect receptor activity in an indirect manner (the proteins they bind to are not post synaptic receptors)

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25
Q

What is the difference between indirect and direct agonists/antagonists?

A

Direct: directly binds to a post synaptic receptor proteins where indirectly does not bind to one.

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26
Q

What is a receptor agonist?

A

A drug that directly or indirectly increases the activity of post synaptic receptor proteins

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27
Q

What is a receptor antagonist?

A

A drug that directly or indirectly decreases the activity of post synaptic receptor proteins

28
Q

How can drugs be categorizd?

A
  1. according to behavioural affects
  2. according to their physiological effects
  3. according to their actions on specific proteins
  4. according to their effects on postsynaptic receptor activity
29
Q

How can direct agonist and antagonist be classified?

A

Competitive or non competitive

30
Q

What is a competive agonist?
Similar to?

A

It activates the receptor by binding where the neurotransmitter normally binds.
Similar to the endogenous neurotransmitter

31
Q

What can direct receptor agonists be?

A

Full agonists or partial agonists

32
Q

What is a competitive antagonist?

A

A full antagonist

33
Q

Where does a competive antagonist bind?

A

To the same binding where the neurotransmitter normally binds but DOESN’T activate the receptor

34
Q

What is affinity?

A

Affinity refers to the probability and tightness of ligand receptor binding

35
Q

What does the competition for a binding site between an endogenous neurotransmitter and an exogenous drug depend on?

A

They will depend on their relative concentrations and their affinity for the binding site

36
Q

What is non competitive binding?
What is possible?

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 possible for a neurotransmitter to bind one site of a receptor while a drug binds on another

37
Q

What does a non competitive agonist do?

A

It fully or partially activates the receptor.

38
Q

What does a non competitive antagonist do? What’s special about it?

A

It fully blocks the receptor activation.
It DOESN’T compete for the neurotransmitter binding site, it “wins” without competing by binding to an alternative site

39
Q

What are allosteric modulators?

A

Non competive drugs that only influence receptor activity when the neurotransmitter is also bound to the receptors

40
Q

What do negative allosteric modulators do?

A

reduce the primary effect of the primary ligand

41
Q

What do positive allosteric modulators do?

A

Amplify the effect of the primary ligand

42
Q

What is parkinson’s disease?

A

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

43
Q

What causes parkinsons?

A

The degeneration of dopamine neurons in the midbrain

44
Q

What is used to treat parkinsons? Why?

A

The amino acid L-Dopa, because it increases dopamine production in the brain and thus acts as an indirct dopamine receptor agonist

45
Q

Where are conventional neurotransmitters made? From what?

A

They are made in axon terminals.
They are made from precurosor molcules (generally from amino acids)

46
Q

What happens in some cases in regards to precursor molecules? Why? What happens in such cases?

A

They can be adminstered as drugs.
Because they can increase the amount of neurotransmitter that is made and released.
The precursors acts as receptor agonists

47
Q

What controls the synthesis of neurotransmitter from precursor molecules?
Why?

A

Enzymes
Some antagonists work by blocking these enzymes, thus reducing production of the neurotransmitter so there is less in each vesicle

48
Q

What happens once neurotransmitters are made?

A

Neurotransmitters are packaged into synaptic vesicles

49
Q

How do some antagonists work? What happens when this occurs?

A

They work by blocking the transporter proteins that package neurotransmitter into vesicles.
When this occurs, synaptic vesicles can remain empty, so nothing is released when they fuse with the presynaptic membrane

50
Q

What regulates synaptic vesicle exocytosis?

A

Many proteins in the axon terminal

51
Q

What is synaptic vesicle exocytosis?

A

The vesicle fusion with the presynaptic membrane

52
Q

How do some antagonists such as botox work?

A

By blocking the vesicular release machinery, so no transmitter is released.

53
Q

How do some agonist such as black widow spider venom work?

A

By binding and activating the vesicular release machinery to directly cause the release of neurotransmitter

54
Q

What controls the clearance of neurotransmitters from the syanpse?

A

Reuptake transporter proteins and enzymatic deactivation

55
Q

What do some agonist such as neostigmine do?

A

Block the enzymatic deactivation of neurotransmitter in the synaptic cleft.

56
Q

What do some agonists block?

A

Neurotransmitter reuptake proteins, some even reverse the reuptake proteins, so that they start to traffic neurotransmitter into the synpases as soon as it is made and before it is packaged into the synaptic vesicle

57
Q

What are drugs that block the reuptake of catecholamine neurotransmitters? What do they block?

A

Methylphenidate and cocaine
They block the dopamine norepinephrine reuptake transporters

58
Q

What are drugs that reverse catecholamine transporters? What does it cause? What type of release?

A

Adderall and Crystal meth
It causes dopamine and norepinephrine molecules to flow directly out of the presynaptic terminal (non - vesicular release)

59
Q

What is a dose response curve? How is it obtained?

A

A graph of magnitude of an effct of a drug as a function of the amount that is administered.
It is obtained by giving subjects various doses of drug

60
Q

What is a margin of safety/thereapeutic index?

A

The ration between the dose that produces a toxic effecr in 50 percent of animals and the dose that produces the desired effect in 50 percent of animals

61
Q

What is pharmacockinetics?

A

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

62
Q

What does the route of administration effect?

A

Where the drug goes, in what quantity and for how long?

63
Q

What are the 3 key consideration when choosing a route of administration?

A
  1. Does the drug naturally cross the blood-brain barrier
  2. Is it better to have a high concentration of drug for a shirt time or a low concentration of drug for a short time or low concentration of drug for a long time?
  3. Where in the body are the enzymes that break down that drug?
64
Q

What is tolerance? What is it the body’s attempt to do?

A

When a effect of the drug diminishes because of repeated administration.
To compensate for the effects of the drug

65
Q

What does sensitization do?

A

A drug becomes more and more effective through repeated use

66
Q

What is a placebo?

A

An inert substance that has no direct physiological effect. It is given to subject to control the effects of mere administration of a drug

Behavioural Neuroscience (15 decks)

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