Addiction
centre'. This circuitry, called the mesolimbic reward system, involves the neurotransmitters dopamine and serotonin. 163 Serotonin reaching a part of the brain called the nucleus accumbens is what is thought to create the feeling of satisfaction, and so causes our body to want no more of that stimulus. Dopamine, on the other hand, increases the desire for it. Dopamine is created in an area of the brain called the ventral tegmental area (VTA), which is sent to the nucleus accumbens via the axons of the neurons. Many animal studies seem to show that all drugs increase the production of dopamine in the nucleus accumbens, but reduce that of serotonin, 164 possibly explaining how these drugs biologically cause the continued desire for them in a person, eventually leading to addiction. The reactions in this pleasure centre have been shown to be a main reason for addiction: in tests where animals were used to investigate drug addiction, animals with lesions in the brain regions related to this system, no longer showed any interest in the various substances of abuse, whereas previously they had. 165 Almost all drugs have been shown to increase the effect of dopamine in some way, either by increasing the amount of dopamine released in the brain, or boosting its activity. 166 For example, nicotine will stimulate the release of more dopamine in the brain, causing the mood-altering effects of the drug. 167 Amphetamines, meanwhile, work by blocking the dopamine transporters, leading to abnormally high levels of dopamine loose in the brain. Caffeine can again stimulate the release of dopamine, while THC, the main psychoactive component of cannabis, also binds to some of the receptors in the brain which are thought to be involved in the pleasure circuit. Cocaine works in a similar way to amphetamines, preventing the uptake of dopamine and serotonin into the postsynaptic neurons. 168 It will also prevent the neurotransmitters being degraded in the synapse, so the dopamine will stay in the gap between the neurons, the synaptic cleft,
longer. 169 The postsynaptic receptors will be therefore be overly saturated, resulting in an over active impulse being transmitted and causing a increased state of arousal. 170 Studies seem to show, however, that the long- term addiction to drugs is not simply the high levels of dopamine causing an increased desire for them, but the result of permanent physiological changes to the nervous system as a result of chronic exposure to them. 171 The brain of a person suffering from addiction has been shown to be significantly different to one of a normal person at all levels: molecular, cellular, structural and functional. 172 A person who has become addicted to a drug tends have a lifelong addiction, as, even if they abstain for the habit for a long time, they are more likely to relapse late in life. This would suggest that the changes that occur in the brain are extremely stable. 173 One theory suggests that regular use of the drugs which mimic endorphins (neurotransmitters released during exercise, excitement and pain) 174 reduces the natural endorphin production of the body, eventually meaning that the body becomes reliant on the drug. 175 Researchers who mapped the relevant regions of the brain also discovered that drugs stimulated the pleasure circuit of the brain far more aggressively than most natural rewards did. 176 Some drugs were found to release up to 10 times more dopamine in the brain than any natural reward could. 177 The brain responds to this overwhelming rush by either producing less dopamine or reducing the number of receptor sites for the neurotransmitter. This decrease in the number of available receptors is caused by the long-term presence of excessive neurotransmitter molecules, and is called down-regulation. 178 In the absence of the drug, therefore, dopamine will have a much lower than normal effect on the brain's 169 (Addiction Science Network, 1998) 170 (Spark Notes, 2012) 171 (Wikipedia, Physical Dependence, 2012); (Nestler & Malenka , op. cit. ). 172 (Leshner, 1997) 173 (Nestler, Molecular Basis of Long-Term Plasticity Underlying Addiction, 2001) 174 (Randall, 2012) 175 (Spark Notes, 2012) 176 (Nestler & Malenka, op. cit. ); (Nestler, op. cit. ).
163 (Phillips, 2006) 164 (Dubuc, 2002)
165 (Nestler & Malenka, op. cit. ) 166 (Providence Projects, 2011) 167 (Encyclopaedia Britannica , 2010) 168 (New Scientist, 2006)
177 (NIDA, 2010) 178 (ARTS, 2000)
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