Recreational Drugs and Synaptic Transmission Flashcards
What are drugs?
they are chemicals that can have an adverse effect on humanity
What are recreational drugs?
drugs that are taken for pleasure
what are some examples of recreational drugs?
caffeine and/or nicotine
What effect do recreational drugs have on the CNS?
a ‘psychoactive’ effect which may be beneficial to the individual e.g. medical marijuana
what are legal highs?
drugs that have legal purpose but can also be used recreationally - they are not yet made illegal by the Misuse of Drugs 1971 Act
What are some popular legal high drugs?
cannabinoids
What does alcohol do?
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
are many drugs like alcohol?
mainly they’re taken for a single effect, a single mode of action at the synapse
Why do people do things?
the brain has a reward pathway or ‘pleasure centre’ which means we do things to recieve pleasure through a surge of dopamine
What is the name of one of the reward centres?
the mesolimbic pathway- includes the ventral tegmental in the midbrain)
what does the mesolimbic pathway include?
dopaminergic, GABAergic and glutamatergic neurons
How does nicotine affect the reward pathway?
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
What is the process of nicotine’s activity within the brain?
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
What is the effect of nicotine within the brain over time?
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
how does nicotine lead to addiction?
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
is nicotine addictive?
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
How does marijuana/cannabis work on the brain?
they act by binding to cannabinoid receptors
where are cannabinoid receptors?
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
What is the cannabis receptor on the brain?
they bind to cannabinoid receptors, blocking them so there is less neuron activity in the hippocampus and thus affecting memories
How does dopamine fit into the cannabis process?
more dopamine is released as a result of the blocking of the cannabinoid receptors,
How does dopamine fit into drug activity and the synapse?
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
what are the two types of recreational drugs?
agonists and antagonists
what are agonists?
some drugs imitate natural neurotransmitters, ‘fooling’ the brain into activating the pleasure centres but they are much more powerful than most naturally occurring neurotransmitters
what are some examples of agonists?
nicotine, cannabis and heroin
what are antagonists?
they massively boost the amount of normal neurotransmitters, triggering the brain’s pleasure centre
what are some examples of antagonists?
amphetamines
Why is dopamine released with the use of cannabis?
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
How does cannabis affect attention and cause memory loss?
it affects CBI receptors, affecting the blood flow and reducing oxygen to the brain
What is the process of heroin once it enters the brain?
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
What are some symptoms of taking heroin?
warm flushing of the skin, drug mouth and heavy feeling in the extremities with possible effects such as nausea, vomiting and severe itchiness.
What does long term use of heroin do?
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
How does cocaine affect dopamine?
it is a reuptake inhibitor
how is cocaine a reuptake inhibitor?
Cocaine attaches to the reuptake receptor, ‘blocking it’ so that dopamine cannot be reabsorbed into the neuron
Why does cocaine inhibiting dopamine from being reabsorbed cause a ‘high’?
The levels of dopamine in the synaptic gap keeps building, and the dopamine receptors get overstimulated
is cocaine an amphetamine?
yes
What does long term cocaine use do?
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
What is the normal process of the reward pathway?
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
Why is the reward pathway necessary (in evolutionary terms)?
this process helped humans learn and adapt behaviours to better suit our environment
How plausible is the theory of reward pathways existing and their link to addiction?
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
How does Straiker and Mackie (2005) support the existence of pleasure centres/reward pathways and their link to addiction?
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
How does Olds and Milner (1954) support the existence of pleasure centres/reward pathways and their link to addiction?
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
What is something that lessens the credibility of the existence of pleasure centres/reward pathway and their links to addiction?
Not all drugs work on dopamine e.g. PCP and ketamine produce intense euphoria by stimulating glutamate receptors called NMDA rather than dopamine receptors
What are some objections to the link between synaptic transmission and recreational drugs?
Generalising from animals to human studies is problematic as it’s reductive explanation and the problem of the placebo effect
Why is the ‘placebo effect’ detrimental to the explanations of the link between synaptic transmission and recreational drugs?
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
Why is generalisation from animal to human studies detrimental to the explanations of the link between synaptic transmission and recreational drugs?
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
How is the neurobiological view of recreational drugs similar to the learning approach?
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
What are the applications of the neurobiological view of recreational drugs?
led to biological treatments for addiction - DRT giving substitutes to try and ‘wean’ the addict off drugs, dealing with problems of desensitisation and addiction
What are the weaknesses of recreational drugs and synaptic transmission?
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
Why is Olds and Milner (1954) considered important to recreational drugs and synaptic transmission
?
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.
what research methods are used in recreational drugs and synaptic transmission?
Laboratory experiments & Studies using animal models
define drug
a substance put into the body deliberately in order to change its functioning.
define psychoactive drug
a substance that changes the functioning of the brain, bringing about changes in thinking, feeling and behaviour.
define recreational drug
a psychoactive drug taken for non-medical reasons, because the user wants or needs to feel the effect
define agonist
any drug that increases activity at a specific type of synapse (e.g. cocaine is a dopamine agonist)
define antagonist
any drug that decreases activity at a specific type of synapse
define tolerance
a process in which the brain becomes used to a drug, so more is needed to produce the same effect.
define dependance
a state where a user is unable to function fully in their normal capacity unless they take a specific drug.
