Restraint stress induces beta-amyloid precursor protein mRNA expression in the rat basolateral amygdala.

Research paper by Maria Luiza Nunes Mamede ML Rosa, Francisco Silveira FS Guimarães, Rubia Maria Welfort RM de Oliveira, Cláudia Maria CM Padovan, Ronald Carl Alan RC Pearson, Elaine Aparecida EA Del Bel

Indexed on: 01 Feb '05Published on: 01 Feb '05Published in: Brain Research Bulletin


Several studies have shown the involvement of beta-amyloid precursor proteins (APP) isoforms in physiological process like development of the central nervous system (CNS), functional roles in mature brain, and in pathological process like Alzheimer's disease, neuronal experimental damage, and stress, among others. However, the APP functions are still not clear. In the brain, APP(695) isoform is predominantly found in neurons while APP(751/770) isoforms are predominantly found in astroglial cells and have been associated to neurodegenerative processes. Acute or chronic stress in rats may trigger specific response mechanisms in several brain areas such as amygdala, hippocampus and cortex with the involvement of multiple neurotransmitters. Chronic stress may also induce neuronal injury in rat hippocampus. In situ hybridization (ISH) was used to investigate the expression of APP(695) and APP(751/770) mRNA in amygdala and hippocampus of male Wistar rats (n=4-6 per group) after acute (2 or 6h) or chronic (2h daily/7 days or 6h daily/21 days) restraint stress. Only the APP(695) mRNA expression was significantly increased in the basolateral amygdaloid nuclei following acute or chronic restraint. No APP isoform changed in hippocampus after any stress condition. These results suggest that restraint stress induces changes in gene expression of APP(695) in basolateral amygdaloid nucleus, an area related to stress response.

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