Hippocampus neuronal gene expression

Here, we review the abnormalities of hippocampal structure and function in schizophrenia and consider how they can give rise to memory deficits and psychotic symptoms. While it is unlikely that the hippocampus is the sole locus of pathology in schizophrenia, there is now compelling evidence that (1) hippocampal volume and shape are abnormal early on in the disease process, (2) specific regions of the hippocampus show alterations of neuronal gene expression, protein expression, and cell number, and (3) cognitive deficits and the experience of psychotic symptoms are linked to abnormalities of hippocampal function. 

Harrison PJ. 2004. The hippocampus in schizophrenia A review of the neuropathological evidence and its pathophysiological implications. Psychopharmacology 174 151-162. Hemby SE, Ginsberg SD, Brunk B, Arnold SE, Trojanowski JQ, et al. 2002. Gene expression profile for schizophrenia Discrete neuron transcription patterns in the entorhinal cortex. Arch Gen Psychol 59 631-640. 

Other putative laminin-binding proteins have been described from a number of sources (for example, Smalheiser and Schwartz, 1987). Kleinman et al. (1991) used a synthetic peptide derived from the a chain of laminin to elute a 110 kDa protein from brain tissue however, the resulting molecule had sequence similarity to nucleolin. This putative receptor appears to be expressed in postnatal brain, particularly the hippocampus (Luckinbilledds et al., 1995). Albini et al. (1992) have described the isolation of a similar 100 kDa molecule from Y-79 retinoblastoma cells that is eluted from laminin affinity columns by 20 mM EDTA this binding protein has only intermediate affinity for laminin, however, but may act to influence gene expression independent of attachment. Laminin has been reported to bind to Ng-CAM on the basis of antibody inhibition studies, an interaction important for the formation of neuron-glia adhesion (Grumet etal., 1993). 

Li, W., F. Trovero, J. Coidier, et al. 2003. Prenatal exposure of rats to Ginkgo biloba extract (EGb 761) increases neuronal survival/ growth and alters gene expression in the developing fetal hippocampus. Brain Res. Dev. Brain Res. 144(2) 169-180. 

COXs thus catalyze the same first committed step of the AA cascade (Fig. 33-2). COX-2, however, is expressed in response to mitogenic and inflammatory stimuli and encoded by an early-response gene. To date we do not understand how COX-3 expression is regulated. In contrast, COX-1 expression is not subject to short-term regulation. Neurons in the hippocampus, as well as in a few other brain regions, are unlike other cells in that they display basal COX-2 expression [36]. This expression is modulated by synaptic activity, such as long-term potentiation, and involves the NMDA glutamate receptors [36,40]. 

Mice completely lacking BDNF have reduced sensory neuron survival, other neuronal deflcits, and are viable only a few weeks (Ernfors et al. 1995). Heterozygote BDNF mice exhibit gene dose-dependent reductions in BDNF expression in forebrain, hippocampus, and some hypothalamic nuclei (Kernie et al. 2000 MacQueen et al. 2001) as well as decreased striatal dopamine content, decreased potassium-elicited dopamine release (Dluzen et al. 2002), and... 

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