Recreational Drugs and Synaptic Transmission

Question 1

What are drugs?

Answer 1

they are chemicals that can have an adverse effect on humanity

Question 2

What are recreational drugs?

Answer 2

drugs that are taken for pleasure

Question 3

what are some examples of recreational drugs?

Answer 3

caffeine and/or nicotine

Question 4

What effect do recreational drugs have on the CNS?

Answer 4

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

Question 5

what are legal highs?

Answer 5

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

Question 6

What are some popular legal high drugs?

Answer 6

cannabinoids

Question 7

What does alcohol do?

Answer 7

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

Question 8

are many drugs like alcohol?

Answer 8

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

Question 9

Why do people do things?

Answer 9

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

Question 10

What is the name of one of the reward centres?

Answer 10

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

Question 11

what does the mesolimbic pathway include?

Answer 11

dopaminergic, GABAergic and glutamatergic neurons

Question 12

How does nicotine affect the reward pathway?

Answer 12

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

Question 13

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

Answer 13

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

Question 14

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

Answer 14

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

Question 15

how does nicotine lead to addiction?

Answer 15

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

Question 16

is nicotine addictive?

Answer 16

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

Question 17

How does marijuana/cannabis work on the brain?

Answer 17

they act by binding to cannabinoid receptors

Question 18

where are cannabinoid receptors?

Answer 18

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

Question 19

What is the cannabis receptor on the brain?

Answer 19

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

Question 20

How does dopamine fit into the cannabis process?

Answer 20

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

Question 21

How does dopamine fit into drug activity and the synapse?

Answer 21

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

Question 22

what are the two types of recreational drugs?

Answer 22

agonists and antagonists

Question 23

what are agonists?

Answer 23

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

Question 24

what are some examples of agonists?

Answer 24

nicotine, cannabis and heroin

Question 25

what are antagonists?

Answer 25

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

Question 26

what are some examples of antagonists?

Answer 26

amphetamines

Question 27

Why is dopamine released with the use of cannabis?

Answer 27

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

Question 28

How does cannabis affect attention and cause memory loss?

Answer 28

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

Question 29

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

Answer 29

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

Question 30

What are some symptoms of taking heroin?

Answer 30

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

Question 31

What does long term use of heroin do?

Answer 31

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

Question 32

How does cocaine affect dopamine?

Answer 32

it is a reuptake inhibitor

Question 33

how is cocaine a reuptake inhibitor?

Answer 33

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

Question 34

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

Answer 34

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

Question 35

is cocaine an amphetamine?

Answer 35

yes

Question 36

What does long term cocaine use do?

Answer 36

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

Question 37

What is the normal process of the reward pathway?

Answer 37

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

Question 38

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

Answer 38

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

Question 39

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

Answer 39

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

Question 40

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

Answer 40

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

Question 41

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

Answer 41

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

Question 42

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

Answer 42

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

Question 43

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

Answer 43

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

Question 44

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

Answer 44

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

Question 45

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

Answer 45

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

Question 46

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

Answer 46

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

Question 47

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

Answer 47

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

Question 48

What are the weaknesses of recreational drugs and synaptic transmission?

Answer 48

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

Question 49

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

Answer 49

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.

Question 50

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

Answer 50

Laboratory experiments & Studies using animal models

Question 51

define drug

Answer 51

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

Question 52

define psychoactive drug

Answer 52

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

Question 53

define recreational drug

Answer 53

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

Question 54

define agonist

Answer 54

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

Question 55

define antagonist

Answer 55

any drug that decreases activity at a specific type of synapse

Question 56

define tolerance

Answer 56

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

Question 57

define dependance

Answer 57

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