Recovery From Schizophrenia: Psychiatry And Political Economy

20 BACKGROUNDbiochemical and functional disturbance that may express itself in somewhatdifferent ways under the influence of environmental stresses.Recent genetic linkage studies have led to the identification of severalsuspected gene locations each associated with a proportion of the risk ofdeveloping schizophrenia; a single major gene locus has not emerged. Geneticsusceptibility regions have been detected on chromosomes 5, 6, 8, 15 and 22, andeach region could harbor one or more relevant genes. Genetic researchers suspectthat susceptibility genes are present in a large proportion, perhaps seven to ten percent, of the general population, and that the interaction of multiple genes andadditional environmental factors are necessary to produce the illness. 38Just what is the deficit that might be inherited?Brain chemistryEmotions and thought processes are regulated by the complex interaction ofsystems of nerve cells throughout the brain. Each nerve cell (or neuron) exerts itseffect by the release of a chemical mediator at the synapse—the point of contactwith another neuron. Biochemical theories attempting to explain the appearanceof symptoms of schizophrenia have focused on abnormalities in the action ofsome of these chemical neurotransmitters.A prominent biochemical theory of schizophrenia—the dopamine hypothesis—suggests that the underlying abnormality may be a relative overactivity of tracts ofneurons in which dopamine is the chemical mediator. Acute stress, leading tosudden increases in dopamine turnover, could thus precipitate an episode ofpsychosis in a vulnerable individual. 39 It is likely, however, that the disturbance ofdopamine function is a consequence other abnormalities elsewhere in the brainwhich have not yet been clearly identified. Attention has been focused, forexample, on whether an abnormality in the functioning of the inhibitoryinterneurons, which release gamma-amino butyric acid (GABA), is responsible forproducing changes in the dopamine-releasing neurons. 40 Inhibitory interneuronsdamp down the action of primary neurons and prevent the brain beingoverwhelmed by sensory input. GABA release is decreased in the brains of peoplewith schizophrenia, suggesting that they may be at greater risk of brain overloadfrom environmental stimuli.The dopamine hypothesis (which will be dealt with in detail in Chapter 10) issupported in large part by the observation that the standard antipsychotic drugsachieve their effect by blocking the dopamine-2 receptor. With the introductionof the modern “atypical” or “novel” antipsychotic drugs in the past decade,however, researchers have begun to realize that many more receptors areimplicated in the illness. Besides the dopamine-2 receptor, the atypicalantipsychotic drugs (like clozapine and olanzapine) block the action of a numberof other neurotransmitters, such as serotonin, 5-HT 2 , NMDA and otherdopamine receptors, suggesting that these neurochemicals also play a role inschizophrenia. 41