With reference to recent research, discuss the ways in which drugs affect human behaviour.

University Degree Subjects allied to Medicine

Behaviour is a hard word to define as it has no clear beginning or end. The analysis of behaviour is specifically to describe the interaction of the organism’s brain with the environment. This environment consists of the outside world and the organism’s internal environment. The brain plays a major part of that internal environment and the behaviour produced becomes a part of the external environment. Behaviourism was first introduced in the early twentieth century by an American Psychologist, John Watson. He claimed that behaviour was the real subject matter for psychology as it was public, measurable, reproducible and open to scientific method. Psychologists and pharmacologists who study particular effects of drugs on behaviour often refer to their field as psychopharmacology. There have been several principles put forward to explain behavioural pharmacology, the main principle states that ‘changes in our brain chemistry produce changes in our behaviour’.

Virtually all our behaviour is under the control of the nervous system, and the effect of most behaviourally active drugs can ultimately be traced to a direct or an indirect action on some aspect of the functioning of the nervous system. The source of power for the electrical activity of the nervous system comes from an uneven distribution of charged particles across the membranes of neurones. When an effective stimulus is applied to a neurone, local changes take place inside the membrane, which allows sodium ions to rush through the membrane. This influx of positive charge counteracts the negative resting potential and the cell becomes positively charged. As a result of the movement of charged particles, a wave of electrical activity travels down the axon. This controlled wave of change in the electrical charge that appears across the cell membrane is called the ‘action potential’. As neurones are not in direct contact with each other nerve impulses pass from one neurone to another via specialised junctions called synapses. There are two types of synapses, electrical and chemical. Most of our human neurone activity is powered by chemical synapses, particularly when drugs are involved in the process. Chemical synaptic transmission begins as the action potential reaches the synaptic knob of the pre-synaptic neurone and calcium channels in the membrane open, allowing the diffusion of calcium ions in. This increased concentration of calcium stimulates vescicles to move towards the pre-synaptic membrane and release transmitter substance into the synaptic cleft. Transmitter molecules diffuse across the synaptic cleft and bind to receptors on the post-synaptic membrane causing ion channels in the membrane to open. Further movement of sodium, calcium and potassium ions result in the generation of a post-synaptic action potential. It is primarily at synapses where drugs have the opportunity to interfere with the chemical process. Some drugs act by mimicking neurotransmitters by occupying some or all of the receptor sites that cause the drug’s affect and facilitating activity, these are called ‘agonists’. Alternatively, ‘antagonists’ are drugs, which occupy receptor sites and have no effect. Instead, this action blocks the transmitter from having its normal effect and inhibits neural activity. Effectiveness of drugs very from person to person, because each drug affects several kinds of synapse, causing different behavioural functions.

The two main neurotransmitters involved in behaviour change are serotonin and dopamine. Serotonin (5HT) plays a main role in human mood changes and treatment for mood disorders. Depression is effectively treated with drugs, which specifically block the reuptake of serotonin and result in reduced sensitivity of presynaptic autoreceptors for serotonin. This drug treatment is also used to treat obsessive compulsive disorders, aggressive behaviours and perception problems. Drugs that elevate serotonin levels are used to reduce appetite and treat insomnia. Dopamine plays a major role in mental and physical health. Dopamine antagonists are used to treat schizophrenia by ‘turning down’ ...

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The most commonly abused drugs in today’ society are tobacco, alcohol, marijuana, and cocaine. This essay will focus on these types of drugs, their effects on the nervous system and the resulting behavioural changes.

Next to caffeine, tobacco is the most widely used psychoactive drug in our society. When a cigarette is smoked, nicotine, the major psychoactive ingredient of tobacco, and numerous other chemicals, including carbon monoxide, are absorbed through the lungs. In 1980, Romano and Goldstein identified two basic types of cholinergic receptor sites inside the body; muscarinic and nicotinic. Nicotine from cigarettes stimulates the nicotinic receptors but occupying nicotinic cholinergic receptor sites. In low doses nicotine only stimulates these receptors, in higher doses the receptor sites can become blocked. These receptors are part of cholinergic synapses in the brain and are similar to nicotinic cholinergic receptors in the peripheral nervous system. Pomerleau and Pomerleau (1992) also found that nicotine causes the release of serotonin, beta-endorphin and growth hormone, all known to have effects on behaviour. In the peripheral nervous system, nicotine receptor sites are located primarily in the neuromuscular junctions of voluntary muscles. As nicotine stimulates these receptors, a user is likely to experience muscular tremors. Peripheral nervous system changes include increased heart rate and blood pressure and vasoconstriction of the blood vessels. This constriction causes a drop in skin temperature and explains the cold touch that smokers have and why they tend to age faster. The release of epinephrine arouses the sympathetic system yet most smokers report that they smoke because it relaxes them. This unexpected observation was named ‘Nesbitt’s paradox’ by Schacter (1973). Smoking also has positive effects on mood as the smoker uses nicotine to control their response to stress. Despite this, a survey carried out in the UK by West (1993) found that smokers have lower levels of psychological well-being than non smokers and ex-smokers.

Ethyl alcohol is another psychoactive drug, which is classified as a depressant as it inhibits neural firings. However, at low doses it can also act as a mild stimulant. Research has shown that alcohol’s effects share many similarities with general anaesthetics. Anaesthetic has an effect by dissolving the lipid layer of membranes and perturbing some property of the membrane. Miller (1993) suggested that when alcohol, like anaesthetic, dissolves in the membranes, the membranes exert pressure on the ion channels embedded in the membranes and interfere with their ability to open and allow ions to pass through. In turn, the ability of the membrane to form resting and acting potentials is altered. Alcohol stimulates serotonin receptors causing a rapid depolarisation of the membrane which, in turn, helps to stimulate the release of dopamine in the nucleus’ of brain cells. These serotonin antagonists cause the decrease of the stimulant properties of alcohol in large doses. High doses of alcohol have many behavioural influences on humans. It has a detrimental effect on visual acuity as well as decreasing sensitivity to taste and smell, a decrease in pain sensitivity occurs also. Performance level decreases extremely as a result of alcohol consumption. Reaction times slow by about 10% and complex tasks require the subject to scan stimuli several times before making a response. Deficits are also seen in hand-eye co-ordination as the subject’s performance is effected by alcohol induced drowsiness, loss of balance and a lack of concentration caused by alcohol’s depressant qualities within the brain. Recent research carried out by Palleres et al (2001) by studying the effects of ethanol on rat behaviour, found that after the animals were given access to alcohol for one hour a day for nineteen days, alcohol consumption deteriorated psychomotor performance and improved the animal’s ability to learn simple associations. Results suggested that prolonged ethanol intake could induce permanent psychomotor impairment as well as an impairment of inhibition related to the intoxicated state. This disinhibitation effect of alcohol is caused as the user becomes more relaxed, talkative, friendly and more likely to do things they normally wouldn’t do for fear of adverse consequences.

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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