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Brain and Behaviour > 4) Neurotransmitters & Psychopharmacology > Flashcards

4) Neurotransmitters & Psychopharmacology Flashcards

1
Q

Which 2 neurotransmitters carry out most synaptic communication

A

Glutamate- excitatory
GABA/ glycine (in spinal cord)- inhibitory
Both secreted by terminal buttons

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2
Q

What is psychopharmacology

A

The study of drug effects on the nervous system

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3
Q

What is an antagonist drug

A

A drug that opposes/inhibits the effect of a neurotransmitter on a postsynaptic cell

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4
Q

What is an agonist drug

A

A drug that facilitates the effect of a neurotransmitter on a postsynaptic cell.

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5
Q

How can the rate of neurotransmitter synthesis be increased

A

Administering a precursor, so acts as an agonist

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6
Q

What controls neurotransmitter synthesis

A

Enzymes. So drugs that inactivate an enzyme serve as antagonists

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7
Q

How do drugs effect storage and release of neurotransmitters?

A

A drug molecule binds to a site on a transporter and inactivates it, as it is occupying the same where enzymes usually work. Since nothing can be synthesised, the vesicle is empty and nothing is released when the vesicle fuses with the presynaptic membrane (Serves as an antagonist)

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8
Q

Once some drugs bind to the postsynaptic receptor, what 2 effects can it have?

A

Serve as a:
direct agonist/antagonist =
> drug that binds directly onto the receptor of interest
Indirect agonist/antagonist=
drug attaches to a binding site on a different postsynaptic receptor, which facilitates/inactivates action of the receptor of interest.

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9
Q

In what 2 ways can drugs effect reuptake/neurotransmitter destruction

A

1) Interfere with the action of transporter molecules responsible for reuptake of neurotrans molecules back into the terminal buttons of the presynaptic molecule. It does so by blocking and inactivating them
2) Binds with enzyme activation sites which prevents the process of destroying excess neurotransmitters molecules in the cleft, since the binding sites have been occupied with the drug

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10
Q

What do both ways of effecting reuptake/destruction of neurotransmitter have in common?

A

BOTH of them prolong the presence of neurotransmitter in the synaptic cleft, so serve as AGONISTS

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11
Q

Placebo is..

A

an inert substance instead of the physiologically active drug, used as an experimental control for an administered drug

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12
Q

Placebo effect is..

A

The behavioural effects observed of taking/not taking a drug (feelings of getting better on the placebo).
Helps to conclude if any actual changes are caused by the drug.

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13
Q

Nocebo effect is..

A

Patient feeling worse after even when no effect should have occurred.

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14
Q

Where is the neurotran ACh (Acetylcholine) secreted from?

A

By the EFFerent nerves axons in the CNS.

Also found in parasympathetic branch of ANS

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15
Q

What is ACh’s key roles?

A
  • ALL muscular movement accomplished by ACh release.

- Involved in REM sleep regulation, memory, perceptual learning

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16
Q

Who discovered ACh

A

Otto Loewi

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17
Q

Describe the 2 types of ACh receptors, what stimulates them and what blocks them

A

1) Nicotinic receptor:
ionotropic (direct), stimulated by nicotine
It is blocked by curare (poison serves as muscle relaxant/paralysis).
It acts at the neuromuscular junction between nerve cells and muscles
2) Muscarinic receptor:
Metabotropic (indirect), produces the parasympathetic nerve effects of heart, smooth muscles, glands
Stimulated by muscarine, blocked by atropine (prevents ACh from depolarising the post-synaptic membrane, stops impulse generation to this cell)

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18
Q

Explain the first 3 stages of transmission across a cholinergic synapse (ACh present at these types of synapses)

A

1) AP arrives at the presynaptic membrane, Ca2+ channels open and calcium ions enter the presynaptic neuron
2) Calcium ions cause vesicles to fuse to the presynaptic membrane and then release ACh into the cleft
3) ACh diffuses across the cleft and binds to neuroreceptor sites in post-synaptic membrane

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19
Q

Explain the last 2 stages of cholinergic synapse transmissions

A

4) Sodium channels open and ions diffuse into post synaptic membrane, causing depolarisation and an AP to fire
5) Ach- ase (enzyme) breaks down ACh, with leftover products diffusing back into presynaptic neuron where ACh is resynthesises using ATP for next transmission

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20
Q

What is the name of the post synaptic membrane at a neuromuscular junction

A

The muscle fibre membrane is called the sarcolemma.

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21
Q

What does depolarisation of the sarcolemma lead to?

A

Muscle contraction

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22
Q

Which neurotransmitters belong to the compound family The Monoamines?

A

Dopamine, serotonin, noradrenaline (norepinephrine) , adrenaline (epinephrine)

23
Q

They all primarily effect mood and anxiety. What is dopamine more specifically involved with?

A

Pleasure, with more of this reward chemical sent to the decision making area of the brain, in order to help feed our pleasurable behaviours i.e. food, sex, water

24
Q

Define addiction

A

state of engaging in excessive compulsive behaviours, reinforcing a certain behaviour, since it’s pleasurable. Tends to be followed with a loss of control of intake

25
Q

Define tolerance

A

state of no longer responding to a drug, so a higher dose in needed in order to achieve the same effect

26
Q

Define dependence

A

normal functioning is only achieved through presence of the drug , with physical disturbance apparent when drug is withdrawn

27
Q

Where in the brain are the addiction/dependence pathways found?

A

In the mid brain region, just above the start of the spinal cord

28
Q

Is it possible to have a dependence without an addiction?

A

Yes, for example needing to take prescribed drugs for a condition otherwise normally functioning can’t be achieved

29
Q

What is dopamine’s involvement in Parkinson’s disease?

A

It is a neurological disease affected by a lack of dopamine production + degeneration of the nigrostriatal system.
Effects include tremors, rigid limbs, poor balance

30
Q

What can treat Parkinson’s ?

A

L- DOPA amino acid, a direct precursor to dopamine, that facilitates dopamine production

31
Q

What system does the pleasure chemical Dopamine follow and what structures are involved?

A

Follows a process in the MESOLIMBIC system

starts at the VTA > ends in nuccleus accumbens, amygdala, hippocampus - all of mid brain

32
Q

Where is cocaine’s binding site?

A

The nuccleus accumbens, in basal forebrain

33
Q

What effect does cocaine have on dopamine ?

A

Inhibition of dopamine reuptake, by attaching to the binding site and blocking the reuptake pump.
Therefore increased amount of dopamine transmission across the synaptic gap leading to more nerve impulse to the reward system = excitatory behavioural response

34
Q

What have PET activation scans of metabolic activity in cocaine users shown?

A

Blood sugar levels reduce dramatically when using cocaine

35
Q

Which neurotransmitter is responsible for a whole range of things like mood, eating, sleeping, dreaming, pain and arousal.

A

Serotonin (5-HT)

36
Q

Describe the rough pathway serotonin takes in the brain

A

Spread out and across the brain from the raphe nuclei (base of spinal cord in mid brain region).

37
Q

How does the LSD drug work?

A

Stimulates the SNS centre and has a serotonin-blocking effect

38
Q

What common drug serves as noradrenergic and serotinergic AGONIST

A

MDMA (facilitates adrenaline/serotonin transmission across neurons)

39
Q

What are some effects of MDMA

A

Excitatory behavioural/hallucinogenic response, such as elevated mood, heightened perception, reduced appetite

40
Q

Outline the effect of MD of serotonin neurotransmitters

A

It blocks the transporter reuptake binding site, so more 5-HT sent to the psot-synaptic receptor binding sites.
(serotonin-enhacing effect)

41
Q

Aside from depression like feelings and irritability, what are some other adverse effects of ecstasy

A

Clouded thinking, hypothermia, disturbed behaviour, jaw clenching (gurn)

42
Q

What long term effects of MD are there?

A

Degeneration of serotonin nerve terminals, and impairment to verbal and visual memory

43
Q

Explain the typical cause of mild depression

A

Low levels of serotonin, leading to feelings of anxiety, insomnia, feelings of worthlessness, fatigue, apathy

44
Q

How do pharmaceutical drugs like Prozac help with depression?

A

Increases the amount of serotonin in the brain’s synapses by blocking the reuptake of serotonin into presynaptic cell. Thus, more serotonin crosses to bind to serotonin receptor sites on the postsynaptic membrane in order to activate them and decrease depression like symptoms

45
Q

Where is Noradrenaline (norepinephrine) found and what does it do?

A

NE secreted by the adrenal gland in kidney, working alongside adrenaline to give the body energy in stressful situations ‘fight or flight’.
NE inhibiting medication also helps with depression

46
Q

Where is the neurotransmitter adrenaline (epinephrine) found ?

A

Hormone secreted in adrenal medulla (of brain)

47
Q

Which are the most common neurotransmitters (amino acids) in the CNS

A

Glutamate, GABA and glycine

48
Q

Which amino acid is the most important excitatory neurotransmitter in brain?

A

Glutamate

49
Q

What is the specialised glutamate receptor called?

A

NMDA- ionotropic (direct)

50
Q

Which is the most important inhibitory neurotransmitter in brain/ different form in the spinal cord

A

GABA (in brain), glycine (in spinal cord)

51
Q

What analogy helps explain GABA’s role

A

The brake system, with GABA as the brakes. When driving, you need an accelerator but you also need brakes. GABA does this

52
Q

Why is GABA’s inhibitory effect good?

A

It blocks out excessive and unneccessary brain activity i.e. like avoiding negative thinking in depression

53
Q

Tranquilizer drugs like benzos (anxiolytic drugs) work in what way toward GABA receptors?

A

Works as an indirect agonist, used for it’s sedative, relaxing effects i.e. Valium

Brain and Behaviour (18 decks)

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