The Activities of D2 Receptor Genes and Heritability of Schizophrenia: A biopsychoneurogenetic Investigation.

Abstract

The devastating effects of schizophrenia on human persons have raised puzzling and overwhelming concern among mental health professionals and researchers. Due to the revenging and hallmark of this ailment, neuropsychologists, as well as psychiatrists are in continuous controversial debate as what may constitute the actual etiology of schizophrenia. Many of the researchers have unequivocally maintained that schizophrenia is a genetically transmitted mental disorder. They sustain the argument with the studies of the monozygotic twins and the experiment with amphetamine, chlorpromazine, and phenothiazines. They maintain that the dopamine receptor genes are the agents that perpetuate the genetic transmission of heritability of schizophrenia. The sequence of argument has been referred to as the dopamine hypothesis. The strong genetic component of this hypothesis has spilt neurobiologists into two camps, “lumpers” and “splitters.” The lumpers believe that the symptoms manifested by schizophrenic patients may be the result of underlying abnormality, defect, or deficit in integrative functioning in the central nervous system. Wexler (1991) remarked that the basic problem in the schizophrenics is their inability to handle complex tasks. The reason he presented was that, when a schizophrenic patient is presented with almost any task that activates a group of cortical neurons, there is a failure of those neurons to recruit, activate, connect, or link to additional cortical brain regions for effective coordination. Such linkage helps the individual to get ready for the next response. The lumpers did not emphasize the heritability of these defect, rather they maintained that the low frontal cortex dopamine secretion is hamper at the base of abnormal neural linkage. On the other side of the camp, the splitters think of schizophrenia as having unfortunate inheritance of three semi-independent genes