A comparison of two immediate-early genes, c-fos and c-jun in rat brain after occlusion of superior mesenteric artery (SMAO)
© Biomed central limited 2002
Published: 1 March 2002
Changes in level of consciousness and/or emotion are frequently experienced in the lethal gut necrosis. However, little is yet known about what a mechanism is underlying beneath the alteration of neuronal function. The aim of the present study was to investigate how the brain was influenced by massive gut necrosis. In an attempt to examine functionally activated neuron, we applied immunohistochemistry (IHC) for c-Fos and c-Jun, cellular transcriptional factors encoded by immediate early genes c-fos and c-jun, respectively, and widely used as metabolic markers for neuronal activity.
Materials and methods
Adult male Wistar rats (n = 30) were used. Under general anesthesia, 25 rats underwent celiotomies. Twenty of them received SMA clipping and the others were used as control. Control and treated rats at 2, 4, 8 hours were perfused and fixed. The brain were sectioned in 20 μm thick every 200 μm and stained by avidine–biotin-complex method using anti-c-Fos and c-Jun antibodies.
Results and discussion
Very low or absent c-Fos immunoreactivity (IR) in control rat brain. In treated rat, c-Fos IR was increased in time course. The predominant c-Fos IR were demonstrated in the specific nuclei including the hypothalamus (PVN; paraventricular nuc.), amygdala (CeA; central amygdaloid nuc.), locus ceruleus and nucleus tractus solitarii. These areas were congruent with c-Jun IR.
Basal c-Jun IR was evident in most brain site and higher than c-Fos IR. There were several notable differences from c-Fos IR: (1) in the treated rat, intense c-Fos IR was observed in the habenula, circumventricular organ (area postrema, subfornical organ) but c-Jun IR was very low; (2) c-Jun IR was very high in the hippocampus, cerebellum and cingulum, but c-Fos IR was very subtle. The congruent sites of both IR could be interpreted that the hypothalamus, brain stem and limbic system are activated in response to extensive gut necrosis, and participating in neuroendocrine, autonomic or behavioral responses.