Recreational Drugs and Synaptic Transmission Flashcards

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1
Q

What are drugs?

A

they are chemicals that can have an adverse effect on humanity

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2
Q

What are recreational drugs?

A

drugs that are taken for pleasure

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3
Q

what are some examples of recreational drugs?

A

caffeine and/or nicotine

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4
Q

What effect do recreational drugs have on the CNS?

A

a ‘psychoactive’ effect which may be beneficial to the individual e.g. medical marijuana

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5
Q

what are legal highs?

A

drugs that have legal purpose but can also be used recreationally - they are not yet made illegal by the Misuse of Drugs 1971 Act

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6
Q

What are some popular legal high drugs?

A

cannabinoids

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7
Q

What does alcohol do?

A

it is a drug that doesn’t have a single effect, but many as it affects the connection between the amygdala and the prefrontal cortex

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8
Q

are many drugs like alcohol?

A

mainly they’re taken for a single effect, a single mode of action at the synapse

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9
Q

Why do people do things?

A

the brain has a reward pathway or ‘pleasure centre’ which means we do things to recieve pleasure through a surge of dopamine

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10
Q

What is the name of one of the reward centres?

A

the mesolimbic pathway- includes the ventral tegmental in the midbrain)

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11
Q

what does the mesolimbic pathway include?

A

dopaminergic, GABAergic and glutamatergic neurons

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12
Q

How does nicotine affect the reward pathway?

A

it mimics acetylcholine and bind to its receptors, exciting the neuron, causing it to release dopamine which ten excites neurons in the reward pathway - this produces a pleasure feeling

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13
Q

What is the process of nicotine’s activity within the brain?

A

if nicotine binds to the acetylcholine receptor, the receptor causes an impulse, ‘exciting’ the neuron which causes an action potential down the axon of the neuron in question to release more of the neurotransmitter in question e.g. dopamine

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14
Q

What is the effect of nicotine within the brain over time?

A

it affects the acetylcholine receptors and decreases the size of the dopamine receptors, which means that when nicotine isn’t present as there aren’t many post-synaptic neuron receptors, more dopamine is require to stimulate the receptor to a normal level known as desensitisation

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15
Q

how does nicotine lead to addiction?

A

nicotine is needed to maintain what was before normal functioning due to its effect over time, and cells have begun to change due to the nicotine bind to the acetylcholine receptors

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16
Q

is nicotine addictive?

A

there may be genetic factors that make nicotine more addictive - some may have the allei, resulting in them having less receptors in the first place

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17
Q

How does marijuana/cannabis work on the brain?

A

they act by binding to cannabinoid receptors

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18
Q

where are cannabinoid receptors?

A

one type is found in many regions of the brain but the other only found within the immune system - most are found in the hippocampus which is why cannabis can sometimes affect your memory

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19
Q

What is the cannabis receptor on the brain?

A

they bind to cannabinoid receptors, blocking them so there is less neuron activity in the hippocampus and thus affecting memories

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20
Q

How does dopamine fit into the cannabis process?

A

more dopamine is released as a result of the blocking of the cannabinoid receptors,

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21
Q

How does dopamine fit into drug activity and the synapse?

A

it’s a neurotransmitter associated with reward, creating feelings of pleasure and a desire to repeat activities - it’s naturally generated within the brain when we do certain activities

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22
Q

what are the two types of recreational drugs?

A

agonists and antagonists

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23
Q

what are agonists?

A

some drugs imitate natural neurotransmitters, ‘fooling’ the brain into activating the pleasure centres but they are much more powerful than most naturally occurring neurotransmitters

24
Q

what are some examples of agonists?

A

nicotine, cannabis and heroin

25
Q

what are antagonists?

A

they massively boost the amount of normal neurotransmitters, triggering the brain’s pleasure centre

26
Q

what are some examples of antagonists?

A

amphetamines

27
Q

Why is dopamine released with the use of cannabis?

A

cannabis inhibits the GABAergic neurons, which have cannabinoid receptors, causing them to remove their inhibitors so that the dopamine neurons can be activated to release dopamine to a higher extent

28
Q

How does cannabis affect attention and cause memory loss?

A

it affects CBI receptors, affecting the blood flow and reducing oxygen to the brain

29
Q

What is the process of heroin once it enters the brain?

A

it converts to morphine and binds and activates mu-opioid receptors (MORs) which are typically used to regulate pain, hormone release and feelings of well being, causing then to stimulate the release of dopamine

30
Q

What are some symptoms of taking heroin?

A

warm flushing of the skin, drug mouth and heavy feeling in the extremities with possible effects such as nausea, vomiting and severe itchiness.

31
Q

What does long term use of heroin do?

A

it changes the physical structure of the brain, causing long-term imbalances in neuronal and hormonal systems that aren’t easily reversed e.g. deterioration of white matter which may affect decision-making capabilities

32
Q

How does cocaine affect dopamine?

A

it is a reuptake inhibitor

33
Q

how is cocaine a reuptake inhibitor?

A

Cocaine attaches to the reuptake receptor, ‘blocking it’ so that dopamine cannot be reabsorbed into the neuron

34
Q

Why does cocaine inhibiting dopamine from being reabsorbed cause a ‘high’?

A

The levels of dopamine in the synaptic gap keeps building, and the dopamine receptors get overstimulated

35
Q

is cocaine an amphetamine?

A

yes

36
Q

What does long term cocaine use do?

A

the number of dopamine receptors decrease in response to the excess of dopamine which means larger amounts of cocaine are needed to achieve the same ‘high’ (desensitisation) and therefore the brain’s reward pathways don’t work leading to unhappiness and cravings

37
Q

What is the normal process of the reward pathway?

A

When activated, the cell within the reward pathway relays an electrical signal to release dopamine from the presynaptic neuron into the synaptic gap to be picked up by receptors to carry on the signal→ dopamine is distributed into the synaptic gap before being picked up by transporter proteins

38
Q

Why is the reward pathway necessary (in evolutionary terms)?

A

this process helped humans learn and adapt behaviours to better suit our environment

39
Q

How plausible is the theory of reward pathways existing and their link to addiction?

A

Lots of evidence to support the existence of reward pathways/pleasure centres e.g. Olds and Milner (1954); Straiker and Mackie (2005); and Skinner’s theory of Operant Conditioning

Face validity in the observations of drug users and self-reports which match what the neurobiology of recreational drugs predict e.g. euphoric feeling followed by desensitisation and addiction with long-term use

40
Q

How does Straiker and Mackie (2005) support the existence of pleasure centres/reward pathways and their link to addiction?

A

Straiker and Mackie (2005) carried out a similar experiment to Olds and Milner (1954) on mice and found similar addictive behaviour to humans when dosed with cannabis

41
Q

How does Olds and Milner (1954) support the existence of pleasure centres/reward pathways and their link to addiction?

A

Olds and Milner (1954) studied rats and connected wires to their brain to trigger the pleasure centre in the septum area of the brain using electricity - the rats could give their brains a pleasurable electric shock by pressing a lever. They noticed that the rats would return to the lever over and over, ignoring other sources of pleasure e.g. food or the opposite sex - they behaved like drug addicts

42
Q

What is something that lessens the credibility of the existence of pleasure centres/reward pathway and their links to addiction?

A

Not all drugs work on dopamine e.g. PCP and ketamine produce intense euphoria by stimulating glutamate receptors called NMDA rather than dopamine receptors

43
Q

What are some objections to the link between synaptic transmission and recreational drugs?

A

Generalising from animals to human studies is problematic as it’s reductive explanation and the problem of the placebo effect

44
Q

Why is the ‘placebo effect’ detrimental to the explanations of the link between synaptic transmission and recreational drugs?

A

Jones and Stone (1990) gave regular cannabis user either marijuana (which contained cannabis) or placebo where the users couldn’t detect the difference.

If the effects of drugs was purely biological, the placebo group would experience no effect but they experienced a ‘high’, suggesting there to also be a cognitive element here

45
Q

Why is generalisation from animal to human studies detrimental to the explanations of the link between synaptic transmission and recreational drugs?

A

Humans have more complex cognition than animals and se drugs for reason e.g. to regulate mood, cope with stress, bond socially with friends or even out of curiosity - neurobiological explanations ignore all these other choices and motivations and so is reductive, placing drug users as slaves to their neurobiology

46
Q

How is the neurobiological view of recreational drugs similar to the learning approach?

A

They both involve the idea of euphoria as the main reason people take drugs and keep taking then - OC calls this positive reinforcement

Both explain addiction through unpleasant side-effects of not taking the drugs - OC calles this negative reinforcement

47
Q

What are the applications of the neurobiological view of recreational drugs?

A

led to biological treatments for addiction - DRT giving substitutes to try and ‘wean’ the addict off drugs, dealing with problems of desensitisation and addiction

48
Q

What are the weaknesses of recreational drugs and synaptic transmission?

A

The brain is a complex organism and there is more than one reward pathway and brain region: there should be more than one explanation

Hard to study the mode of action at the synapse -brain scanning has only helped marginally

Much of this has been found out through the analysis of the animal brain - hard to generalise and human brains are considered to be much more complex

49
Q

Why is Olds and Milner (1954) considered important to recreational drugs and synaptic transmission
?

A

Olds and Milner (1954) wired rats to an apparatus which, when the rat pressed a level, would deliver electrical stimulation to part of the rat’s brain (the septal area). They found that the rats would repeatedly press the button, ignoring other possible rewards (e.g. food and drink) until they collapsed from exhaustion. This led to the discovery of the reward pathway, which we now know to be involved in why people take recreational drugs. Much of the reward system relies on dopamine as its main neurotransmitter.

50
Q

what research methods are used in recreational drugs and synaptic transmission?

A

Laboratory experiments & Studies using animal models

51
Q

define drug

A

a substance put into the body deliberately in order to change its functioning.

52
Q

define psychoactive drug

A

a substance that changes the functioning of the brain, bringing about changes in thinking, feeling and behaviour.

53
Q

define recreational drug

A

a psychoactive drug taken for non-medical reasons, because the user wants or needs to feel the effect

54
Q

define agonist

A

any drug that increases activity at a specific type of synapse (e.g. cocaine is a dopamine agonist)

55
Q

define antagonist

A

any drug that decreases activity at a specific type of synapse

56
Q

define tolerance

A

a process in which the brain becomes used to a drug, so more is needed to produce the same effect.

57
Q

define dependance

A

a state where a user is unable to function fully in their normal capacity unless they take a specific drug.