Abstract
The disrupted in schizophrenia 1 (DISC1) gene is found at the breakpoint of an inherited chromosomal translocation, and segregates with major mental illnesses. Its potential role in central nervous system (CNS) malfunction has triggered intensive investigation of the biological roles played by DISC1, with the hope that this may shed new light on the pathobiology of psychiatric disease. Such work has ranged from investigations of animal behavior to detailed molecular-level analysis of the assemblies that DISC1 forms with other proteins. Here, we discuss the evidence for a role of DISC1 in synaptic function in the mammalian CNS.
Highlights
The underpinnings of many mental illnesses are multifactorial, arising from a combination of genetic susceptibilities and environmental factors (Tsuang, 2000; Moffitt et al, 2005; van Os et al, 2010)
The disrupted in schizophrenia 1 (DISC1) gene was originally identified in a unique Scottish pedigree, in which the gene is disrupted by an inherited balanced chromosomal translocation between chromosomes 1 and 11 [t(1;11)(q42.1;q14.3)]
The reported concentration of DISC1 expression in the adult postsynaptic density (PSD) fraction (Kirkpatrick et al, 2006; Clapcote et al, 2007; HayashiTakagi et al, 2010; Carlisle et al, 2011; Wang et al, 2011), along with the known functions of some of the proteins for which it acts as a scaffold (Camargo et al, 2007; Brandon & Sawa, 2011), have led most workers so far to focus their electrophysiological investigations on fast excitatory signaling mediated by postsynaptic ionotropic glutamate receptors
Summary
The underpinnings of many mental illnesses are multifactorial, arising from a combination of genetic susceptibilities and environmental factors (Tsuang, 2000; Moffitt et al, 2005; van Os et al, 2010). A number of studies have indicated that manipulating the levels or nature of expressed DISC1 produces a range of effects on the development of the CNS.
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