Marijuana, although still illegal in most countries, is another widely used drug in today’s society both for medical and recreational reasons.
The psychoactive effects of marijuana are largely attributable to a constituent called delta-9-tetrehydrocannabonol as well as over 80 cannabiniods contained in the drug which have roughly the same effect as the delta-9-THC. Like alcohol, cannabiniods have effects common with general anaesthetic and are highly lipid-soluble and alter the fluidity of membranes. Most neuropharmacological findings regarding the effects of cannibis have occurred over the last ten years.In 1990, neural receptors for cannabiniods were identified as being concentrated in the cortex, hippocampus, cerebellum and basal ganglia.
There are also receptors found outside of the nervous system such as the spleen and are associated with the effects of cannabinoids on immune functions. Research has suggested that cannaboid receptors appear to act as neuromodulators than as neurotransmitters and so cannabis’ effects are more likely to be produced by altering the functioning of other neurotransmitters in the body. Cannaboid’s main function is to increase activity in the mesolimbic dopamine reward system.They increase the effects of endogenous opioid peptides, which act as neuromodulators of dopamine transmission. Dopamine release acts similarly to adrenaline and causes the drug user to experience increased emotional response and ability to experience pleasure. A typical behavioural response to using marijuana is characterised by swings of mood from euphoric gaiety to placid dreaminess.
One of the subjective effects of cannabiods is an increased sensory sensitivity although subjective testing of sensory thresholds by Jones (1998) has found only decreases in sensitivity or no change in auditory, visual and tactile thresholds.Cocaine, another widely used drug, is classed as a psychomotor stimulant similar to amphetamines and cathinone. Cocaine is snorted or smoked and travels quickly to the brain where it accumulates in areas which are rich in dopamine synapses. Cocaine binds to the uptake pumps and prevents them from removing dopamine from the synapse. The more dopamine in the synapse, the more dopamine receptors are activated. The effects of cocaine on dopamine synapses are intense but short lived. North (1992) found that the excess dopamine in the synaptic cleft activates autoreceptors on the presynaptic terminal, exerting a negative feedback effect that reduces further release of dopamine.The net result is that within hours after taking the cocaine, the user ‘crashes’ into a depressed state.
During the cocaine ‘rush’, users may experience sleeplessness, tremors, nausea and psychotic behaviour can also occur. The syndrome of psychotic behaviour observed during cocaine sprees is called ‘cocaine psychosis’ and has extreme similarities to schizophrenia. As a result of cocaine’s actions in the nucleus accumbens, there are increased impulses leaving the area, which activates the reward system.
This indicates that with continued use of cocaine, the body relies on the drug to maintain rewardable feelings.The long-term user often looses the ability to feel the positive reinforcement of pleasurable feelings of natural rewards. The effects of stimulants drugs such as cocaine are further limited by the tolerance that a user develops. Carlezon et al (1998) found that after using cocaine repeatedly, the drug releases less dopamine and more of a transmitter called dynorphin, which counteracts the reinforcing properties of the drug. Garrise et al (1999) found similar results, after a rat has learnt to press a lever to self stimulate dopamine releasing axon, further stimulation releases less and less dopamine.Much research has been carried out in recent years into the area of drug effects on behaviour. Laboratory animal models of human abuse of drugs, and interesting new laboratory techniques have been developed to study the reinforcing effects of drugs in humans. From the work carried out by biologists, psychologists and pharmacologists, it is clear that no drug has only one effect.
In most cases, only one effect of a drug is desired and other effects are not wanted. We could call the effect, for which a drug is taken the ‘main effect’ and any other a ‘side effect’. All ‘effects’, via interactions with neural pathways in the brain create physiological, psychological or behavioural changes, which can be short-lived or in some cases, have a permanent damaging effect on the user.
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