PubMed Health⌕ Search

Biomedical subjects

N Conforti

Publications and source records attributed to N Conforti.

At least 91 records · Page 5Linked to original sources
PubMed1976

Inhibition and facilitation of feedback influences of dexamethasone on adrenocortical responses to ether stress in rats with hypothalamic deafferentations and brain lesions.

In order to elucidate the mechanisms and the sites of action of the negative feedback of corticoids in the regulation of ACTH secretion, the effects of systemically administered dexamethasone on adrenocortical responses to ether stress were studied in intact rats and in 11 experimental groups. These included animals with partial anterior, anterolateral, posterolateral, posterior and small posterior deafferentations as well as bilateral lesions in the medial forebrain bundle (MFB), fasciculus longitudinalis dorsalis (FLD), medial and lateral midbrain reticular formation (MRF) and in the ventrolateral pons. In rats with posterior hypothalamic deafferentation the degree of the inhibitory effect of dexamethasone was much smaller than that in intact animals. In animals with lesions in the FLD and MRF, dexamethasone also produced a reduction in the suppression of the response, though the difference was not significant. Bilateral lesions in the MFB and MP have on the other hand very significantly enhanced the effect of the negative feedback of dexamethasone when compared to intact rats. These data would indicate that hypothalamic deafferentations and brain lesions may change the sensitivity of the hypothalamus for the feedback control of corticoids and that there exist two antagonistic systems, an inhibitory and a facilitatory, in the brain which mediate this effect.

Adrenal Glands↗
PubMed1975

Effect of cortisol on the excitability of limbic structures of the brain in freely moving rats.

The effects of cortisol on the excitability of the dorsal hippocampus, septum, hypothalamus and the pontine reticular formation in unrestrained, unanesthetized rats with permanently-implanted electrodes were investigated. The hormone produced a slowing in the spontaneous activity in these regions. The stimulation of the septum, hypothalamus and reticular formation had no appreciable influence on the local or propagated electrical activity of the brain after cortisol injection; however in 14 out of 29 experiments hippocampal stimulation with the same voltages as before cortisol administration, induced generalized convulsive activity. The attacks consisted of high-voltage spikes and slow-wave activity and were followed by a post-seizure exhaustion in the hippocampus. In half of the rats behavioral convulsions also appeared. The convulsive effects of cortisol on the brain are briefly reviewed and the specificity of hippocampal involvement in the present experiments is emphasized. The possible significance of the present findings in relation to the feedback of glucocorticoids on the brain, in the regulation of ACTH secretion, is discussed. The experiments described may also contribute to our understanding of the mechanisms of the convulsive effects of cortisol on the brain.

Animals↗
PubMed1975

Subcortical pathways involved in the mediation of andrenocortical responses following sciatic nerve stimulation.

Previous experiments from this laboratory using the hypothalamic island have demonstrated that the adrenocortical discharge following sciatic nerve stimulation is mediated by neural pathways only. With the purpose of identifying the neural structures involved, this response was studied in rats with bilateral lesions in the medial forebrain bundle (MFB), mammillary peduncle (MP), fasciculus longitudinalis dorsalis (FLD), midbrain reticular formation MRF) and the medial geniculate body (GM). Lesions in the MFB, MP and MRF have inhibited the adrenocortical response following sciatic nerve stimulation. These and other data indicate that the above structures are involved in the mediation of this response and that the afferent pathway enters the mediobasal hypothalamus anteriorly.

Adrenal Cortex↗
PubMed1975

Complete inhibition of adrenocortical responses following sciatic nerve stimulation in rats with hypothalamic islands.

Previous studies from this laboratory have demonstrated that in rats with hypothalamic islands the adrenocortical response to photic and acoustic stimulation was partially inhibited indicating that they were at least to a certain degree neurally mediated, though ether stress produced normal adrenocortical responses. With the purpose of determining to what extent afferent somatosensory connections to the hypothalamus participate in the activation of adrenocortical responses following sciatic nerve stimulation, the effects of this stimulus applied through chronically implanted electrodes were studied on the plasma corticosterone levels in pentobarbital anaesthetized intact animals and in rats with hypothalamic islands. Ether stress or sciatic nerve stimulation for 2 min in intact rats produced a rise of plasma corticosterone to 32.1 plus or minus 1.2 and 32.1 plus or minus 1.8 mug/100 ml, respectively. However, in animals with hypothalamic islands the corresponding values were 29.2 plus or minus 1.8 and 12.4 plus or minus 0.8 mug/100 ml, respectively. The latter value was not significantly different from the basal corticosterone levels (13.0 plus or minus 1.2 mug/100 ml) found in rats 15 min after pentobarbital anaesthesia, the time when the sciatic stimulus was applied. The present data indicate that the adrenocortical discharge following sciatic nerve stimulation is completely inhibited by hypothalamic deafferentation and therefore depends entirely on the activation of the afferent neural pathways to the hypothalamus.

Adrenal Cortex↗
PubMed1975

Adrenocortical responses following sciatic nerve stimulation in rats with partial hypothalamic deafferentations.

Studies from this laboratory have demonstrated that the adrenocortical response following sciatic nerve stimulation is completely inhibited in rats with hypothalamic islands, indicating that this response depends entirely on the activation of afferent neural pathways to the hypothalamus. With the purpose of identifying the site of entry of these neural pathways into the mediobasal hypothalamus the effects of partial hypothalamic deafferentations were studied. It was found that in rats with posterior or posterolateral deafferentation the adrenocortical responses were similar to those obtained in intact rats, while anterior and anterolateral deafferentation resulted in a reduction of 62.3 and 53.3%, respectively. These results would indicate that the sciatic impulses which activate the adrenocortical response involve neural afferents which enter the mediobasal hypothalamus by an anterior pathway.

Adrenal Cortex↗
PubMed1975

Effects of changing levels of glucocorticosteroids on heat exposure in rabbit.

Rabbits exposed for one hour to a temperature of 40degrees Cand 35-37% humidity showed elevated plasma osmolality and pH. Most of the animals were not able to withstand the heat. Dexamethasone-treated rabbits under the same conditions withstood the heat better and their plasma pH and osmolality remained constant. Metopirone-treated rabbits withstood the heat and showed a rise in plasma osmolality and a slight change in plasma pH. The highest rise in rectal temperature was observed in the metopirone-treated rabbits. Only the untreated animals were unable to regain pre-exposure rectal temperature. The results suggest that high levels of glucocorticosteroids enhance neurogenic and metabolic mechanisms which have protective functions during acute exposure to heat.

Animals↗