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Query: UNIPROT:P50502 (Hip)
 7,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise appears to improve hippocampal plasticity and cognitive function, leading us to postulate that exercise may activate hippocampal neurons, which in turn increase hippocampal cerebral blood flow (Hip-CBF). Recent studies using laser-Doppler flowmetry (LDF) have shown that Hip-CBF increases with behavior and locomotion, but it has not been examined whether these changes are due to neuronal activation. We aimed to examine whether functional hyperemia, an increase in cerebral blood flow in response to neuronal activation, can occur in the exercising rat hippocampus. We applied a treadmill running model of rats and LDF combined with microdialysis. Prolonged mild treadmill running (10 m/min) resulted in an increase in Hip-CBF of 26+/-9% versus basal level. When tetrodotoxin was infused via microdialysis into the loci where Hip-CBF was monitored, the increased Hip-CBF with running was completely suppressed. These results provide evidence that functional hyperemia occurs in the rat hippocampus during mild treadmill running and suggest that our running animal model may be useful for examining the underlying mechanisms of exercise-induced hippocampal functional hyperemia.
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PMID:Evidence of functional hyperemia in the rat hippocampus during mild treadmill running. 1636 80

Current studies have demonstrated that exercise increases regional cerebral blood flow (rCBF), an index of neuronal activity. However, neuronal regulation of the increased rCBF in the brain parenchyma is poorly understood. We developed a running model with rats for monitoring hippocampal cerebral blood flow (Hip-CBF) and found that mild treadmill running increases Hip-CBF in a tetrodotoxin-dependent manner, suggesting that functional hyperemia, an increase in rCBF in response to neuronal activation, occurs in the running rat's hippocampus (Nishijima T and Soya H. Neurosci Res 54: 186-191, 2006). To further support our hypothesis, it was important to discover the neurogenic pathways behind the increase in Hip-CBF that occurred during running. Here, we examine the possible role of N-methyl-d-aspartate (NMDA) receptor/nitric oxide (NO) signaling and group I metabotropic glutamate receptors in mediating the Hip-CBF increase. Hip-CBF during running was measured by laser-Doppler flowmetry. Intrahippocampal drug administration was performed by microdialysis. Mild treadmill running (10 m/min) increased Hip-CBF, which was remarkably attenuated by either NMDA receptor antagonists (1 mM MK-801) or NO synthase inhibitors (2 mM N(G)-nitro-l-arginine methyl ester). However, group I metabotropic glutamate receptor antagonists {1 mM 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester + 1 mM 2-methyl-6-(phenylethynyl)pyridine hydrochloride} augmented the running-induced Hip-CBF increase. We also found that rCBF in the olfactory bulb was unchanged with running. These results strongly suggest that Hip-CBF during mild exercise is regulated locally under hippocampal neuronal activity, mediated mainly through NMDA receptor/NO signaling. Collectively, these results, together with our previous findings, support our hypothesis that mild exercise elicits neuronal activation, which then triggers functional hyperemia in the rat hippocampus.
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PMID:Hippocampal functional hyperemia mediated by NMDA receptor/NO signaling in rats during mild exercise. 2194 Aug 46