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Brain, Biology and Behaviour > Week 3 - Synaptic Transmission & Psychopharmacology > Flashcards

Week 3 - Synaptic Transmission & Psychopharmacology Flashcards

1
Q

What are the basic functions and properties of a relfex arc?

A

Reflexes are automatic muscular responses to stimuli.

The CIRCUIT from SENSORY NEURON to MUSCLE RESPONSE is called a reflex arc.

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2
Q

Are reflexes slower or faster than conduction along an axon?

A

SLOWER.

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3
Q

Do several weak stimuli presented at nearby places or times produce a stronger or weaker reflex than one stimulus alone?

A

STRONGER.

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4
Q

What was Sherringtons’s evidence for synaptic delay?

A

The speed of conduction long an axon is about 40m/s, but the speed of conduction through a reflex arc is slower and more variable, sometimes 15m/s or less. He presumed the delay occurs at the synapse.

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5
Q

What is the term used to describe the cumulative effect of repeated stimuli within a brief window?

A

Temporal (over time) Summation.

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6
Q

Are action potentials always depolarisations?

A

Yes.

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7
Q

Are graded potentials either depolarisations (excitatory) or hyperpolarisations (inhibitory)?

A

They can be either.

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8
Q

What is a graded depolarisation known as?

A

An Excitatory postsynaptic potential (ESPS). It results from a flow of sodium ions into the neuron.

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9
Q

What is known as summation over space?

A

Spatial summation.

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10
Q

Do temporal and spatial summation occur together or separately?

A

They normally occur together.

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11
Q

Can summation effects depend on the order of stimuli along a dendrite?

A

Yes! Greater depolarisation would occur if signals begin at the furthest distance along the dendrite and signals continued to be sent at closer and closer points along the dendrite. The opposite is true for signals beginning closest to the soma and moving away, down the dendrite.

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12
Q

What does hyperpolarisation within a cell produce?

A

An inhibition. It increases the negative charge within the cell, moving it farther from the threshold and decreasing the probability of an action potential.

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13
Q

What is the temporary hyperpolarisation of a cell called?

A

An Inhibitory Postsynaptic Potential (IPSP)

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14
Q

Is the speed and strength of all synapses the same?

A

No, they can vary in speed, strength, their combined effects can equal more (or less) than the sum of their signals, and certain combinations of synapses summate with one another more strongly than others do.

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15
Q

Most neurons have a ….., which is a periodic production of action potentials even without synaptic input.

A

Spontaneous firing rate.

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16
Q

What was Sherrington’s false assumption regarding transmission of signal through a neuron?

A

He assumed it was too fast to be chemical, and thought it must be electrical.

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17
Q

What happens at the presynaptic terminal that allows the release of neurotransmitters into the synaptic cleft?

A

Calcium enters the presynaptic terminal via an action potential, releasing neurotransmitters from the terminals into the cleft.

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18
Q

What happens to neurotransmitters after they have separated from their receptors?

A

They may be taken back into the presynaptic neuron for recycling or they may diffuse away.

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19
Q

Which neurotransmitters are those within the Amino Acid group?

A

Glutamate, GABA, Glycine, Aspartate, others.

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20
Q

Which neurotransmitter is a modified amino acid?

A

Acetylcholine

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21
Q

Which are the monoamines?

A

Serotonin, dopamine, norepinephrine, epinephrine

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22
Q

Which are the neuropeptides?

A

Endorphins, substance P, neuropeptide Y, many others

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23
Q

Which are the Purines?

A

ATP, adenosine, maybe others.

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24
Q

Which are the Gases?

A

NO (nitric oxide), maybe others

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25
Q

What is a neurotransmitter?

A

A chemical.

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26
Q

What does nitric oxide do?

A

As a neurotransmitter, it dilates blood vessels nearby increasing bloodflow to the brain and influences other neurons.

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27
Q

How do neurons synthesise neurotransmitters?

A

Nearly all neurotransmitters are synthesised from amino acids, which the body obtains from proteins in the diet.

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28
Q

What are vesicles?

A

Tiny spherical packets for neurotransmitter molecule storage in the pre-synaptic terminal.

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29
Q

Where does neurotransmitter synthesis occur?

A

Mostly at the presynaptic terminal.

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30
Q

Is there any neurotransmitter outside the vesicle?

A

Yes, the presynaptic terminal also maintains much neurotransmitter outside the vesicles.

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31
Q

What does Monoamine Oxidase (MAO) do?

A

It breaks down neurotransmitters into inactive chemicals, thereby preventing the transmitters from accumulating to harmful levels.

32
Q

How does calcium get into the presynaptic terminal?

A

Depolarisation opens voltage-dependant calcium gates in the presynaptic terminal. Wtihin 1-2ms after calcium enters, it causes EXOCYTOSIS.

33
Q

What is exocytosis?

A

Bursts of release of neurotransmitter from the presynaptic neuron.

34
Q

How long does it take for a neurotransmitter to diffuse across the cleft?

A

No more than .01ms.

35
Q

How wide is the cleft?

A

20 to 30 nanometres wide.

36
Q

Do neurons release just the one neurotransmitter?

A

No. Many, if not most, release a combination of two or more transmitters at a time. Some release two transmitters at the same time.

37
Q

Which is faster and which is slower out of ionotropic and metabotropic effects?

A 
Ionotropic = FAST
Metabotropic = S L O W
38
Q

Why is metabotropic slow?

A

It is using a metabolic process, often with several steps, as part of the “secondary messenger” system. Can be as short as 30ms and as long as several minutes. Used for messages that aren’t super time-sensitive (such as sight or hearing).

39
Q

What do stimulants do?

A

Increasing behavioural activity, either by increasing motor activity, or by counteracting fatigue.

40
Q

Stimulants such as cocaine or amphetamines augment the release of…

A

dopamine from the presynaptic membrane and block reputake mechanism that reabsorbs dopamine.

41
Q

So briefly, what do stimulants do?

A

Increase the amount of dopamine in the cleft.

42
Q

What does nicotine do?

A

Stimulates the acetylcholine receptors at nerve muscle junctions. One type of receptor (nicotinic receptor).

43
Q

Where does nicotine increase the release of dopamine?

A

The nucleus accumbens.

44
Q

Which are opiates?

A

Morphine & Heroin

45
Q

What do opiates do?

A

Relieve pain, relax & induce euphoria, by mimicking brain’s natural opiates at post-synaptic (endorphin) receptors.

46
Q

What neurotransmitter do opiates release?

A

Endorphins.

47
Q

What do endorphin receptors do?

A

Endorphin receptors inhibit the release of GABA, which otherwise inhibits the release of dopamine (it restricts gatekeeping on dopamine).

48
Q

What does marijuana do?

A

It stimulates norepinephrine post-synaptic receptors and can reduce glutamate and GABA.

49
Q

What does LSD do?

A

Mimicks serotonin at post-synaptic receptors, or blocks activity of serotonin neurons.

50
Q

What does alcohol do?

A

It is biphasic. Initial stimulant phase, followed by second depressant phase. Can facilitate response at GABA receptors, blocks glutamate receptors - leading to decrease in brain activity. Can also increase activity of dopamine receptors in nucleus accumbens.

51
Q

Which drugs can increase activity in nucleus accumbens?

A

Nicotine and Alcohol.

52
Q

What are the characteristics of ionotropic receptors?

A

Fast acting
Short-lived effects (mseconds)
Local effects - open/shut gates/channels receptors are attached to.
Useful for situations in situations when message needs to be quick.

53
Q

What are characteristics of metabotropic receptors?

A

Slow acting
Long-lasting effects (seconds-minutes)
Effects may be widespread
Uses ‘second messenger’ - DOES NOT directly open channel.

54
Q

What is a drug?

A

A chemical substance that effects mood or behaviour or both, or substances that are used in the management of the neurological or psychiatric disorders. Nearly all drugs act on synapses - attach to receptors.

55
Q

What is a drug that blocks or takes away from the effects of the neurotransmitter?

A

Antagonist.

56
Q

What is a drug that mimics or increases the effects of a neurotransmitter?

A

Agonist.

57
Q

Which is affinity, and which is efficacy?

A

Affinity - ability of a drug to bind to a receptor (lock/key)
Efficacy - degree to which the drug activates the receptor once bound

58
Q

Why is a drug with high affinity and low efficacy an antagonist?

A

Because by occupying the receptor, it prevents the normal effects of the neurotransmitter.

59
Q

Which drugs are stimulants?

A

Cocaine, amphetamines.

60
Q

What do stimulants do?

A

Increase motor activity or counteract fatigue.

61
Q

How does tolerance occur?

A

Either because the body improves in ability to metabolise drug, or because nervous system becomes less responsive to it.

62
Q

Where are nicotinic receptors abundant?

A

On neurons that release dopamine in the nucleus accumbens.

63
Q

What effects do nicotine have?

A

increased blood pressure, secretion of hyrochloric acid in stomach, boosts motor activity of bowels.

64
Q

What class of drug are morphine and heroin?

A

Opiates.

65
Q

How do opiates work?

A

They mimic post-synaptic stimulation of neurotransmitters.

66
Q

What do opiates do?

A

Decrease sensitivity to pain.

67
Q

How do opiates act?

A

They inhibit GABA, which in turn, prevents inhibition of dopamine, thus uptick in DOPAMINE.

68
Q

What is the genetic link for alcoholism?

A

One gene responsible for producing less acetaldehyde dehydrogenaise metabolise acetaldehyde more slowly. Metabolising acetaldehyde more slowly means negative effects of alcohol are more prominent. If you don’t have this gene, you produce the dehydrogenase more quickly, and get fewer negative effects of alcohol, making you more prone to drink faster.

Serotonin synapses are also affected. Mechanism isn’t known but associated with alcoholism.

69
Q

Which area of the brain was being stimulated in rats?

A

The septum.

70
Q

How often per hour were rats self-stimulating?

A

Up to 2000 times per hour.

71
Q

Where was dopamine being released specifically

A

The nucleus accumbens, directly or indirectly.

72
Q

Where does stimulation from sexual excitement, music, gambling and videogames result in dopamine activity?

A

the nucleus accumbens!

73
Q

What does the rat stimulation results suggest regarding all addiction and all substance abuse?

A

That dopamine release might be essential in these, although initial research may have overrepresented the importance of dopamine.

74
Q

How do we define addiction?

A

A person may be said to be addicted if they persist in doing a behvaiour due to a physical/psychological NEED, even though it causes them harm.

75
Q

How do we define substance abuse?

A

it is an addiction that involves taking a substance, such as a drug.

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