ABSTRACT
Acute and chronic hypoxia influence blood glucose levels and decrease body weight. Ghrelin increases appetite and body weight and regulates energy metabolism and also glucose homeostasis. Therefore, in the present study the effects of ghrelin administration on blood glucose, body weight, food intake and hematocrit were investigated in a model of systemic normobaric acute and chronic hypoxia in adult male rats. Forty-eight adult male Wistar rats were divided into six groups [acute control + saline, chronic control + saline, acute or chronic hypoxia + saline, acute or chronic hypoxia + ghrelin [80 microg/kg/day, ip]]. Control groups remained in room air [21% O[2]] and hypoxia [11% O[2]] induced by a normobaric hypoxic chamber for two days [acute] or ten days [chronic]. Blood glucose levels, body weight, food intake and hematocrit were assessed. Chronic hypoxia caused a significant [P<0.001] decrease in blood glucose levels. Administration of ghrelin increased blood glucose levels significantly in acute [P<0.05] and chronic [P<0.01] hypoxia. Body weight decreased [P<0.001] in both acute and chronic hypoxic groups. Administration of ghrelin could [P<0.001] prevent decrease in body weight in chronic hypoxia group. Acute and chronic [P<0.001] hypoxia significantly decreased food intake. Ghrelin however increased food intake in both the acute [P<0.001] and chronic [P<0.05] hypoxia groups. Acute [P<0.01] and chronic [P<0.001] hypoxia also increased hematocrit. Ghrelin administration is useful in modulating blood glucose, body weight and food intake in hypoxic situations
ABSTRACT
Epilepsy is one of the most common neuronal disorders in man. The amygdala is one of the important locations for seizures originated from piriform cortex. Neverthless, its role in development of such seizures has not been reported so far. Therefore in this study, the effects of amygdala inhibition on kindling rate of piriform cortex was investigated. Under two study protocols, thirty male Wistar rats[300-350 g] in 5 groups [n=6] were studied. In the first protocol animals were divided into three groups; first group only were canulated without any treatment, second group received artificial CSF and third group received 0.5 micro l of 2% lidocaine intra amygdaloid. The second protocol, included two groups; in the first group the amygdala was lesioned by electrical DC current and animals were stimulated 24 h later and in the second group animals canulated but amygdala was not lesioned In this study, intra amygdala injection of 2% lidocaine and electrical lesion of it increased number of stimulation to receive S4 and S5 stages of seizure, but had no effects on number of stimulations to receive S1, S2, S3 stages cumulative after discharge duration [ADD], after discharge threshold and ADD after the first duration. We concluded that the amygdala has a critical role in the development of epileptic seizures from piriform cortex to other regions and this role is significantly affected by transient and permanent inhibition of neuronal activity of amygdala