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N Conforti

Publications and source records attributed to N Conforti.

At least 37 records · Page 2Linked to original sources
PubMed1987

Hypothalamic afferent connections mediating adrenocortical responses that follow hippocampal stimulation.

This study identified some neural pathways which mediate the adrenocortical responses that follow hippocampal stimulation. The increase in plasma corticosterone following dorsal hippocampus stimulation, in rats with electrodes chronically implanted under pentobarbital anesthesia, was blocked by dorsal fornix and lateral septal lesions and by small posterior hypothalamic deafferentation. Fimbria transection, lateral septal lesions, and posterior hypothalamic deafferentation, but not midbrain reticular formation lesions, also blocked the adrenocortical responses to ventral hippocampus stimulation. Our present and previous studies indicate that the dorsal and ventral hippocampal effects on the hypothalamus, which increase plasma corticosterone concentrations, are mediated by the dorsal fornix and fimbria, respectively, as well as by the lateral septum. A posterior hypothalamic input, which does not involve the medial forebrain bundle or the midbrain reticular formation is also essential for the activation of this response.

Adrenal Cortex↗
PubMed1987

Paraventricular nucleus serotonin mediates neurally stimulated adrenocortical secretion.

The purpose of this study was to further elucidate the role of serotonin (5-HT) in adrenocortical regulation. The effects of stimulating the frontal cortex and extrahypothalamic limbic structures, on plasma corticosterone (CS) responses, were studied in rats with vehicle or 5,7-dihydroxytryptamine (5,7-DHT) injection into the midbrain raphe nuclei. In another group of rats the neurotoxin was injected locally into the paraventricular nucleus (PVN) in view of its importance in adrenocortical regulation, and the effects of photic and dorsal hippocampal stimulation on plasma CS were studied. 5,7-DHT caused a significant depletion of hypothalamic 5-HT and blocked the rise in plasma CS following the stimulation of the above neural modalities. These studies suggest that the PVN 5-HT mediates the adrenocortical responses following afferent neural stimuli.

5,7-Dihydroxytryptamine↗
PubMed1986

Effect of serotonergic, corticostriatal and kainic acid lesions on the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) in mice.

In mice, prior destruction of striatal 5-hydroxytryptamine (5-HT) neurons by intrastriatal or intraventricular injections of 5,7-dihydroxytryptamine did not abolish or attenuate DA depletions produced in striatum by 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). This suggests that although they contain monoamine oxidase type B, the oxidative conversion of MPTP to 1-methyl-4-phenyl-pyridinium ion (MPP+) does not take place in 5-HT neurons. Likewise, decortication and kainic acid lesions did not prevent or enhance striatal MPTP-induced DA decrements suggesting that corticostriatal projections and striatal neurons are not involved in the mechanisms of MPTP neurotoxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Norepinephrine depletion in the paraventricular nucleus inhibits the adrenocortical responses to neural stimuli.

In view of the importance of teh paraventricular nuclei of the hypothalamus (PVN) in the regulation of adrenocortical secretion and the possible role of norepinephrine (NE) in this mechanism, we have studied the effects of injecting the catecholamine neurotoxin 6-hydroxydopamine into the PVN on basal corticosterone (CS) secretion and following ether stress and neural stimuli. PVN NE depletion did not affect the basal and the ether stress-induced rise in CS levels. However, it inhibited significantly the adrenal response to photic, acoustic and sciatic nerve stimulation, suggesting that the PVN NE plays a role in the activation of adrenocortical responses following afferent neural stimuli.

Acoustic Stimulation↗
PubMed1985

Involvement of the sensory cortex in adrenocortical responses following photic and acoustic stimulation in the rat.

In order to examine the possibility that the sensory cortex participates in the mediation of adrenocortical responses following sensory stimuli, the effects of photic and acoustic stimuli on plasma corticosterone were studied in rats with either visual or auditory cortex ablation. In animals with visual cortex ablation, the adrenocortical response to acoustic stimuli was intact; however, it was significantly reduced following photic stimulation. On the other hand, in animals with auditory cortex ablation, the response to acoustic stimulation was significantly reduced, but the response to photic stimulation remained intact. These data demonstrate the participation of the specific sensory cortex in adrenocortical responses following the stimulation of the corresponding sensory modality. The possible mechanisms involved may be either a tonic facilitatory effect of the specific cortex on subcortical mechanisms or the transmission of the specific stimuli in the primary sensory pathways, to achieve a full adrenocortical discharge.

Adrenal Cortex↗
PubMed1985

Effects of extrahypothalamic structures on the hypothalamic cell nuclear binding of corticosterone.

Hypothalamic or hippocampal slices were taken from adrenolectomized male rats either sham operated or with anterior (AHD) of posterior (PHD) hypothalamic deafferentations and from rats with dorsal hippocampectomy (DHIPP). The slices were incubated in Krebs-Ringer bicarbonate buffer in the presence of 10-60 nM 3H-corticosterone (CS) with or without 500 fold excess of unlabeled CS for 30 min. The cell nuclear binding in the hypothalami from either PHD of DHIPP rats were markedly reduced (by 50-70%) as compared to control or AHD rats. The binding of 3H-CS in hippocampi from AHD or PHD rats was not affected. These results suggest that extrahypothalamic structures can modulate the binding of CS in the hypothalamus by neural inputs entering the medio-basal hypothalamus from the caudal direction; such modulation may explain previously observed influences upon hypothalamic sensitivity to the feedback action of glucocorticoids by extrahypothalamic structures.

Animals↗
PubMed1985

Modifications of adrenocortical responses following frontal cortex simulation in rats with hypothalamic deafferentations and medial forebrain bundle lesions.

With the purpose of delineating the neural pathways in the rat which mediate adrenocortical responses following frontal cortex stimulation, the effects of partial hypothalamic deafferentations and medial forebrain bundle lesion were studied. In intact and sham-operated animals, cortical stimulation through permanently implanted electrodes caused a significant increase in plasma corticosterone levels. In rats with anterior hypothalamic deafferentation and bilateral medial forebrain bundle lesions the adrenal response to cortical stimulation was blocked completely, while in animals with posterior hypothalamic deafferentation there occurred a normal rise in plasma corticosterone. These studies demonstrate that the frontal cortex effects on adrenocortical secretion are neurally mediated and involve an anterior hypothalamic input, more specifically the medial forebrain bundle.

Adrenal Cortex↗
PubMed1984

A temporal study of post-adrenalectomy increase in ACTH secretion in the rat: effect of various hypothalamic deafferentations.

Adult male rats, intact (N) or with complete (CHD), anterior (AHD), or posterior (PHD) hypothalamic deafferentations were bilaterally adrenalectomized. At 3, 6, 12 and 20 days post-adrenalectomy they were decapitated and trunk blood was collected for ACTH determinations. In N rats, ACTH markedly elevated up to 850 pg/ml. A similar ACTH response was found in PHD rats but the values were lower by approximately 20%. In contrast, in either AHD or CHD rats, ACTH responses were markedly attenuated and reached a plateau of about 350 pg/ml. These data suggest that: (1) neural inputs entering the medio-basal hypothalamus (MBH) from both the caudal and rostral directions are important for obtaining maximal ACTH responses following adrenalectomy; (2) at least part of this ACTH response is mediated by sites inside the MBH or in the pituitary.

Adrenal Glands↗
PubMed1984

ACTH and corticosterone secretion following 2-deoxyglucose administration in intact and in hypothalamic deafferentated male rats.

Adult male rats were given a single i.p. injection of 2-deoxyglucose (2-DG, 100-400 mg/kg b. wt). The animals were decapitated 1-4 h later and trunk blood was collected for ACTH, corticosterone (CS) and glucose determinations. Serum ACTH and CS were markedly elevated when compared with saline-treated animals; these elevations were correlated with given doses of 2-DG so that with the higher dose, an approximately 6-fold increase in serum levels of both hormones was observed. Injection of 2-DG up to 200 mg/kg did not change serum glucose levels; injection of 400 mg/kg of 2-DG increased serum glucose by approximately 2-fold. A time course study showed that levels of serum ACTH, CS and glucose were maximal 1 h after 2-DG administration and returned to basal values 3 h later. Injection of 2-DG to animals with complete hypothalamic deafferentation failed to induce any change in serum ACTH, CS or glucose. This study demonstrates that: (1) 2-DG can stimulate the hypothalamo-hypophyseal-adrenal (HHA) axis as measured by ACTH and CS; this effect is not related to blood glucose levels; (2) the HHA response to 2-DG is mediated by sites outside the mediobasal hypothalamus.

Adrenal Cortex↗
PubMed1984

Deafferentation reduces the hypothalamic cell nuclear binding of corticosterone.

Hypothalamic or hippocampal slices and adenohypophyseal lobes taken from adrenalectomized male rats either intact or with complete hypothalamic deafferentation (CHD) were incubated in Krebs-Ringer bicarbonate buffer in the presence of either 10-50 nM [3H]corticosterone or [3H]dexamethasone with or without 500-fold excess of unlabeled steroid for 15-60 min. The cell nuclear binding in the hypothalamic slices from the CHD rats, was markedly reduced by approximately 50% but remained unchanged in the hippocampi and in the pituitaries. These results suggest that brain sites outside the mediobasal hypothalamus are important for the regulation of corticosterone binding in the hypothalamus.

Adrenalectomy↗
PubMed1984

Inhibition in corticotrophin and corticosterone secretion following photic stimulation in rats with 6-hydroxydopamine injection into the medial forebrain bundle.

Changes in corticotrophin (ACTH) and corticosterone (CS) serum levels, were examined in rats in which either 6-hydroxydopamine or vehicle were injected into the medial forebrain bundle (MFB) and which were sacrificed by decapitation 14 days later. The injection of the neurotoxin, which depleted very significantly the norepinephrine (NE) content of the mediobasal hypothalamus, elevated significantly the basal levels of serum ACTH and CS, but inhibited the rise in the levels of these hormones following photic stimulation. These results would suggest that the hypothalamic NE system has normally an inhibitory effect on basal ACTH and CS secretion and that the hormonal response to photic stimulation is mediated by that system and possibly by NE MFB fibers.

Adrenocorticotropic Hormone↗
PubMed1984

Effect of central serotonin depletion on adrenocortical responses to neural stimuli.

In view of the possible role of serotonin in adrenocortical regulation, basal plasma corticosterone concentrations and the response to ether stress, photic, acoustic, or sciatic nerve stimulation, were studied in rats with 5,7-dihydroxytryptamine or vehicle injected into the raphe nuclei. The neurotoxin inhibited the response to photic stimulation without affecting the other modalities. This may suggest that the depletion of brain serotonin has a differential effect on the transmission of neural impulses which activate the adrenal cortex.

Acoustic Stimulation↗
PubMed1984

Adrenocortical responses to ether stress and neural stimuli in rats following the injection of 6-hydroxydopamine into the medial forebrain bundle.

Adrenocortical responses, as expressed by changes in plasma corticosterone concentrations, after ether stress, or photic, acoustic, or sciatic nerve stimulation were studied in rats, with 6-hydroxydopamine or vehicle injected into the medial forebrain bundle (MFB). The neurotoxin partially inhibited the response to photic stimulation only, indicating the involvement of MFB catecholaminergic fibers in the transmission of this response which stimulates adrenocortical secretion.

Acoustic Stimulation↗
PubMed1983

Effect of intracerebroventricular injection of nicotinic acetylcholine receptor antibodies on ACTH, corticosterone and prolactin secretion in the male rat.

The aim of the present study was to investigate the involvement of CNS nicotinic receptors for acetylcholine in the secretory activity of the hypothalamo-hypophyseal-adrenal axis and prolactin (PRL). Adult male rats received a daily intraventricular injection of partially purified nicotinic acetylcholine receptor antibodies (anti-AChR) obtained from a female patient with myasthenia gravis, for 5 consecutive days. Control animals were treated similarly with immunoglobulins obtained from a healthy woman. Blood samples were withdrawn either under basal conditions or following ether stress. Treatment with anti-AChR increased basal ACTH and corticosterone (CS) levels (by approximately two-fold) but completely inhibited the responses of these hormones and PRL to ether stress. In control animals, normal basal and stress-induced responses of ACTH, CS and PRL were observed. This study demonstrated the importance for nicotinic acetylcholine receptors in the mediation of basal and stress-induced adrenocortical activity as well as for the mediation of PRL secretion in response to stress.

Adrenocorticotropic Hormone↗
PubMed1983

Role of medial forebrain bundle catecholaminergic fibers in the modulation of glucocorticoid negative feedback effects.

The possible role of medial forebrain bundle (MFB) catecholaminergic fibers in the previously observed MFB-mediated modulation of hypothalamic sensitivity to glucocorticoid negative feedback effects has been investigated. MFB catecholaminergic fibers were destroyed by bilateral MFB injections of 6-hydroxydopamine (6-OHDA) to adult male rats. The inhibitory effect of dexamethasone (10 micrograms, i.p., 4 h) upon the adrenocortical secretory response to ether stress, as estimated by serum corticosterone levels, was enhanced in the 6-OHDA-treated animals, as compared to vehicle-injected controls. This study suggests that MFB noradrenergic neurons are at least partially responsible for the MFB-mediated modulation of hypothalamic sensitivity to glucocorticoid hormones.

Animals↗
PubMed1983

Differential effects of medial forebrain bundle lesions on adrenocortical responses following limbic stimulation.

Adult male rats had electrolytic lesions placed bilaterally in the medial forebrain bundle and were subsequently implanted with stimulating electrodes in one of the following limbic regions: (1) dorsal hippocampus; (2) ventral hippocampus; (3) medial septal nucleus; (4) basolateral amygdala; (5) mesencephalic reticular formation. Following electrical stimulation, blood was drawn by acute venesection, under either, for plasma corticosterone determinations. In non-lesioned animals, electrical stimulation in all of the limbic regions led to elevated plasma corticosterone levels. In rats with lesions in the medial forebrain bundles, the adrenocortical response to stimulation in the dorsal hippocampus, the basolateral amygdala or the reticular formation was markedly attenuated. On the contrary, the same lesions were without effect upon the corticosterone secretory response to medial septal stimulation, and had only a slight inhibitory effect upon the response to electrical stimulation in the ventral hippocampus. The results demonstrate that the medial forebrain bundle plays a major role in the transmission of impulses to the mediobasal hypothalamus, originating in the dorsal hippocampus, basolateral amygdala or mesencephalic reticular formation, which activate adrenocortical secretion; its role in the transmission of cues arising in the ventral hippocampus or medial septum is, however, minor.

Adrenal Cortex↗
PubMed1983

Effect of decortication on striatal dopamine turnover.

In rat striatum, frontal decortication did not affect the basal and the haloperidol-induced increases in dopamine (DA) turnover and the elevation in DA and dihydroxyphenylacetic acid concentrations produced by systemic administration of L-Dopa. These findings fail to support a role for the corticostriatal afferents in modulation of dopamine synthesis and release by nigrostriatal neurons. They suggest that DA receptors presumably localized on presynaptic corticostriatal terminals do not mediate the acceleration of DA turnover induced by neuroleptics. Data also indicate that corticostriatal terminals do not represent a locus for decarboxylation of exogenous L-Dopa to DA in the striatum.

3,4-Dihydroxyphenylacetic Acid↗