Increased corticotropin-releasing factor immunoreactivity in select brain sites following kainate-elicited seizures

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• 作者：Piekut ; D.T. ; Phipps ; B.
• 关键词：Corticotropin-releasing factor ; Seizure ; Hypothalamus ; Extrahypothalamus ; Neuronal injury ; Neuronal degeneration
• 刊名：Brain Research
• 出版年：1998
• 出版时间：January 19, 1998
• 年：1998
• 卷：781
• 期：1-2
• 页码：100-113
• 全文大小：2.93 M

文摘

The literature has focused on the localization, regulation and function of corticotropin-releasing factor (CRF)-expressing neurons localized in the paraventricular nucleus (PVN) of hypothalamus. However, less information is available on the expression, regulation, and function of CRF at extrahypothalamic sites. The current study examined the induction of CRF in extrahypothalamic brain sites following generalized clonic seizures induced by kainic acid. At 24 h post seizure onset, there was a marked increase of CRF immunolabeled perikarya in select brain areas, which contained little, if any, CRF in control brains. This CRF-like labeling was observed in olfactory structures such as the main olfactory bulb (internal granular layer), anterior olfactory nucleus, and deep layers of piriform cortex. Other sites of increased CRF-like immunoreactivity included the tenia tecta, inner layers of cingulate cortex, lateral septum, dorsal endopiriform nucleus, fundus striatum, and nucleus of the lateral olfactory tract. Additionally, CRF-like labeling was atypically increased in the amygdala (lateral and basolateral amygdaloid nuclei) and hippocampal formation (pyramidal cells of regions CA1/CA3 and polymorph cells within the dentate hilus). An association between the increased CRF immunoreactivity and neuropathological processes, characteristic of this seizure model, is hypothesized and discussed.