The Dysfunction Of Hypothalamic-pituitary-adrenocortical System In Epilepsy Rats Induced By PTZ And The Expression Of C-fos In Amygdala

IntroductionEpilepsy is regarded as a clinical syndrome with sudden, repeated occur-rance and unknown reasons until now. The relationship have been elevating by man between the cause of epilepsy and the dysfunction of hypothalamic pituitary adrenocortical system during the past few years . Especially, which role did the hyperendocrinism of the hypothalamic pituitary adrenocortical system play in the pathophysiology of the epilepsy. C - fos is a member of the immediate - early genes family that regulate a large number of pathophysiologieally relevant genes, so it is associated with neuron proliferation. The expression of c - fos in the a-mygdale can explain the secret of the brain under the stress or toxin.MethodsThe rats including half male and that of female were injected by PTZ in the abdominal cavity with controlled by that of dexamethasone and saline solution. After 12 hours later, repeated the progression and explored the level of cortisone and adrenocorticaltropin. Then inspect the level of the plasma corticoid and ad-renocorticotropin with dioxetane, observing the expression of c - fos with immu-nohistology in the amygdale. Using SPSS 10. 0 software deal the data and the level of significance is 0. 05 , the interaction is q - test.ResultThe hyperendocrinism of hypothalamic pituitary adrenocortical system is not the cause but the result of the epileptic animals induced by PTZ. The expression of c - fos in the seizure animals displayed the tendency that rose at the first, topped at about 2 hours, and then decrease, after 12 hours there is no expression can be detected by mean of immunohistology. The level of the plasma cortisone and adrenocorticotropin of seizure animals jump at a high level and last some hours. The hormone of this two can curb the flash or degree of epilepsy for rats induced by PTZ in short time.DiscussionIn this study we demonstrated that the dysfunction of hypothalamic pituitary adrenocortical system in the seizure animals and the level of hormone in plasma can delay some hours after stress. There was a tendency for the increase of expression of c -fos in amygdale. However, that chronically reduced c -fos mR-NA expression is not consistently observed across all animal models of epilepsy, suggesting that frequent seizures may not be sufficient . Dexamethasone markedly reduced the expression, but not curbed the secretion of cortisone and ACTH. Nowadays, the more and more studies demonstrate that all sorts of stresses effecting the body, first localized with CRH neurons in the PVN and activated the CRH receptor. The antagonism observed was substantial but not complete as the ir - ACTH concentration of antalarmin - infused fetuses increased slightly in response to 1 fig CRH. As the endogenous cortisol concentration is the best available bioassay of the endogenous ACTH action. It seems likely that much of im-munoreactive ACTH present in both experimental models is not bioactive. The long term influence of cortisone and ACTH is not fully understood, that should be noted.ConclusionThe hyperendocrinism of hypothalamic pituitary adrenocortical system is just the result but the cause for the epileptic animals induced by FIZ. The hormone of adrenal cortex can inhibit the seizure.