effect of recreational drugs on synaptic transmission in the CNS Flashcards
recreational drugs
includes stimulants, sedatives, hallucinogens and opioids
each kind of drug ‘operates’ in a particular way, increasing or decreasing specific neurotransmitters in at the synapse
cocaine
cocaine has a stimulant effect on the CNS, especially neurons of the brain’s main rewards system - the mesocorticolimbic pathway which connects subcortical emotional brain centres with frontal areas
the drug achieves its affects by altering synaptic transmission which involves several neurotransmitters, such as noradrenaline, acetylcholine and serotonin
cocaine has the largest impact on the activity of dopamine
the role of dopamine
all recreational drugs increase dopamine release (indirectly or directly) in the reward centres of the brain - for example the nucleus accumbens
the ‘rewards centre’ creates a sense of pleasure when activated
cocaine blocks the reuptake of dopamine by binding with dopamine transporter molecules on the terminal buttons of the presynaptic neuron
these are responsible for recycling dopamine back into the neuron which produced it
as cocaine prevents this process, the synapse is flooded with surplus quantities of dopamine, all available for binding with postsynaptic receptors
this is the main cause the for the euphoric ‘high’ associated with cocaine use
research supporting the role of dopamine
one strength of the affect which recreational drugs have on the transmission process in the CNS is that the explanations are supported with research using non-human animals
for example, one commonly-used procedure involves deliberately damaging the mesocorticolimbic path way in mice brains (Weinshenker and Schroeder 2007)
this means neurons are unable to produce levels of dopamine normally associated with reward
when this is done the mice then fail to self-administer cocaine intravenously
this does not occur when the lesions are performed in other parts of the mouses brain
therefore, these findings support the view that cocaine’s effects are due to the activity of dopamine in the brain’s reward system
long term affects of cocaine
after repeated cocaine use, dopamine receptors become down regulated
when these receptors become downregulated, fewer receptors are active - some are damaged and shut down, and the quantity of dopamine produced declines
this explains the withdrawal and craving for the drug and the higher doses which are needed to get the same effects due to individuals tolerance to cocaine which has built up following repeated use
heroin
heroin has depressant effects on the CNS
it slows down CNS activity, including the activity of neurons involved in pain - this is why opiates are valued as painkillers
heroin is usually injected intravenously and once it reaches the brain most of it is processed into a closely-related opioid called morphine
morphine binds with a specific opioid receptor at the synapse and is found in the cerebral cortex, limbic system and hypothalamus
the reason why these receptors exist for heroine / morphine is because the CNS has its own opioid system
endorphins and enkephalins are produced by the body as natural painkillers, a system that heroine readily taps into
it binds with the receptors of the natural opioid system to massively enhance the natural response
treatment for heroin
one strength of having a better knowledge of drug effects on CNS transmission grows, more treatments for addiction become available
for example, once heroin was identified as an agonist that binds to opiate receptors, other drugs were developed with a reverse mode of action
naloxone is an antagonist drug that blocks opiate receptors and prevents heroin from occupying them
naloxone does not produce the rewarding euphoria associated with heroine use, so it can help manage the withdrawal process and reduce symptoms
therefore, this is a treatement that has developed becuase of a better and greater knowledge of the transmission effects of drugs
agonist and antagonist - heroin
heroin is an agonist drug because it mimics the action of another natural biochemical
nalaxone is an antagonist that blocks opiate receptros
long-term affects of heroin
the long-term effects of repeated heroin use on neural transmission include downregulation
regular use of heroin over time means that opioid receptors on postsynaptic neurons are constantly binding with morphine molecules, which desensitises them to the effects of the drug
weakness of research into effect of recreational drugs on synaptic transmission
one weakness of the research into the effect of recreational drugs on transmission in the CNS is that the studies are mainly non-human animal studies
the basic transmission processes in mammals are similar
but some differences arise because the human brain is more complex than the rat brain
for example, isolating the effects of just one neurotransmitter greatly oversimplifies the process
it is very unlikely that the complexity of recreational drugs effect on transmission can be explained by just one mode of action of a drug
the interactions of dopamine with other neurotransmitter systems such as GABA or serotonin are not very well understood
therefore, this means that the extrapolation from non-human animals to humans is risky and should be undertaken very cautiously
COUNTER ARGUMENT TO weakness of research into effect of recreational drugs on synaptic transmission
Evidence of drug effects on CNS transmission comes from studies of humans as well
for example, Nora Volkow used PET scans to track the activity of dopamine transporters during a cocaine-induced ‘high’
they found that the extent to which cocaine occupied dopamine transporters correlated very positively with the course of the subjective experience
in other words, subjective experience intensified as more dopamine transporters were occupied by cocaine and decline as they became less active
therefore, this supports the view that evidence form animal models is valid, as human studies produce similar results
