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N Conforti

Publications and source records attributed to N Conforti.

At least 55 records · Page 3Linked to original sources
PubMed1983

ACTH and corticosterone secretion following indomethacin, in intact, adrenalectomized and dexamethasone-pretreated male rats.

The present study was designed to determine the role of glucocorticoids in the mediation of the stimulatory effect of indomethacin (IM) on the hypothalamo-hypophyseal-adrenal axis. Intact male rats were treated with a single injection of either dexamethasone (Dex; 20 micrograms/100 g body weight), IM (5 mg/100 g body weight), or IM + Dex or their respective vehicles. In Dex-treated rats, ACTH and corticosterone (CS) were significantly reduced over a period of 20 h as compared to the vehicle-treated group. As we have previously demonstrated, injection of IM markedly elevated serum ACTH and CS for at least 20 h. Administration of Dex 2 h prior to IM treatment delayed the stimulatory effect of IM for 5 h; subsequently, however, Dex was without effect. In adrenalectomized rats, ether stress elicited a marked rise in serum ACTH levels. On the contrary, IM was completely ineffective in these rats. These studies suggest that the mode of action of IM in causing hypersecretion of ACTH and CS is by interfering with the negative feedback effects of the glucocorticoids.

Adrenalectomy↗
PubMed1982

Effects of naloxone on basal and stress-induced ACTH and corticosterone secretion in the male rat--site and mechanism of action.

The acute effects of naloxone upon basal and stress-induced secretion of ACTH and corticosterone (CS) in the adult male rat were investigated. Forty-five minutes subsequent to naloxone injection (5 mg/kg body wt, i.p.), basal serum levels of ACTH (by radioimmunoassay) and of CS (by corticosterone-binding globulin) were more than doubled, as compared to vehicle-treated animals. Upon exposure to either photic or audiogenic stress, the ACTH and CS secretory responses were greater in the naloxone-injected groups. In animals with complete hypothalamic deafferentation basal serum ACTH concentrations were significantly greater than in intact controls (2-fold), and naloxone elicited a further doubling of this parameter. In dexamethasone-pretreated rats (50 micrograms/animal, 4 h prior to naloxone), naloxone had no effect upon ACTH and CS secretion. This study demonstrates: (1) that acute naloxone administration leads to hypersecretion of ACTH, as well as of CS, in the adult male rat; and (2) that its effect is due to an action within the hypothalamo-hypophyseal unit. The data also suggest that these naloxone effects are not mediated by glucocorticoid hormones.

Acoustic Stimulation↗
PubMed1982

Effects of naloxone on basal and stress-induced prolactin secretion, in intact, hypothalamic deafferentated, adrenalectomized, and dexamethasone-pretreated male rats.

The effects of naloxone (Na1) on basal and stress-induced PRL secretion were investigated in intact (N) adult male rats, as were its effects in rats with complete hypothalamic deafferentation (CHD), in adrenalectomized (adrenX) rats, and in rats pretreated with dexamethasone (dex). Forty-five minutes subsequent to Na1 administration (5 mg/kg, BW, IP) basal serum levels of PRL were reduced by approximately 25% (p less than 0.05), in both N and CHD groups. PRL secretory responses to acute exposure to both photic and acoustic stress wee markedly attenuated in Na1-injected, as compared to vehicle-injected animals. Basal serum PRL concentrations were elevated by 40% in adrenX rats (p less than 0.05), as reduced by 25% (p less than 0.05) in dex-treated rats, as compared to controls. In both these experimental groups, Na1 administration caused significant reductions in serum PRL. This study demonstrates that stress-induced, as well as basal PRL secretion, is attenuated by Na1, and points to a hypothalamic site of action in this regard. Furthermore, these Na1 effects are independent of glucocorticoid interactions with the CNS.

Adrenal Glands↗
PubMed1982

ACTH and corticosterone secretion following insulin in intact and in variously hypothalamic deafferented male rats.

Adult male rats, intact (N) or with posterior (PHD), anterior (AHD) or complete (CHD) hypothalamic deafferentations, were injected with either 0.04 or 0.2 mu/100 g b.wt. of insulin. Forty-five minutes later they were decapitated and trunk blood was collected for serum glucose, adrenocorticotropic hormone (ACTH) and corticosterone (CS) determinations. The high insulin dose reduced serum glucose by approximately 50% and elicited a marked increase in serum ACTH and CS levels in all groups of animals as compared to the vehicle-treated group. In contrast, the low insulin dose which reduced serum glucose approximately 30% elicited a significant adrenocortical response only in the intact or PHD groups but failed to stimulate this response in animals with CHD or AHD. These results demonstrate that (1) CNS sites, outside the medial basal hypothalamus (MBH), mediate the adrenocortical response during the initial stages of hypoglycemia by a neural pathway impinging upon the CRF neurons from the rostral direction, and (2) the adrenocortical response during the more enhanced hypoglycemia stages is mediated by a systemic mechanism which acts directly on the MBH.

Adrenocorticotropic Hormone↗
PubMed1982

Corticotrophin and corticosterone secretion following delta 1-Tetrahydrocannabinol, in intact and in hypothalamic deafferentated male rats.

Adult male rats, either intact (N) or bearing complete hypothalamic deafferentations (CHD), were injected with delta 1-tetrahydrocannabinol (THC: 5 mg/kg BW, IP). Forty-five minutes later, they were decapitated and trunk blood was collected for serum ACTH and corticosterone (CS) determinations. In the N animals, serum levels of both ACTH and CS were markedly elevated in the drug-treated, as compared to the vehicle-treated group (approximately 8-fold and 10-fold, respectively). In CHD rats, on the contrary, THC administration did not significantly alter serum concentrations of either ACTH or CS. These results demonstrate (1) that acute treatment with THC stimulates the secretion of ACTH as well as of CS; and (2) that extrahypothalamic sites and/or neural pathways mediate this effect.

Adrenocorticotropic Hormone↗
PubMed1982

The effect of methionine enkephalin on prolactin and luteinizing hormone levels in intact and castrated rats.

The methionine enkephalin (ME) induced responses of prolactin (PRL) and luteinizing hormone (LH) were studied in control and castrated rats bearing chronically-implanted cannulae in the right lateral ventricle. In control rats, 500 microgram ME caused a rise in PRL from a mean +/- SD basal value of 22.8 +/- 12.2 ng/ml to a peak of 195.2 +/- 93.8 ng/ml (p less than 0.001). The peak control occurred 10 min after ME administration and was short-lived. In the same rats, 14 days after castration, there was a significant reduction in both basal (p less than 0.001) and peak PRL response to ME (p less than 0.01), similar to that previously observed with other PRL-inducing stimuli. LH levels, on the other hand, were unaffected by ME treatment in both control and castrated rats.

Animals↗
PubMed1982

Adrenocortical responses following limbic stimulation in rats with hypothalamic deafferentations.

In view of the involvement of limbic structures in adrenocortical regulation, their afferent projections to the mediobasal hypothalamus were investigated. Electrical stimulation via chronically implanted electrodes in the dorsal hippocampus, the medial septal nuclei, the basolateral amygdala or the mesencephalic reticular formation all elicited a significant increment in plasma corticosterone levels in adult male rats under pentobarbital anesthesia. Complete or anterior hypothalamic deafferentation blocked these adrenocortical responses completely, and posterior hypothalamic deafferentation attenuated them to a marked extent. In animals with bilateral medial forebrain bundle lesions, hippocampal stimulation had no effect upon plasma corticosterone levels. These studies demonstrate that extrahypothalamic effects upon adrenocortical secretion are neurally mediated, and that the integrity of neural pathways impinging upon the mediobasal hypothalamus from both the rostral and the caudal directions is essential to these effects.

Adrenal Cortex↗
PubMed1981

Effects of hypothalamic deafferentations on adrenocortical responses in the rat following hippocampal stimulation.

Adrenocortical responses, as expressed by changes in plasma corticosterone levels, following ether stress and dorsal hippocampal stimulation, were studied in intact rats and in rats with complete, anterior of posterior hypothalamic deafferentations. Ether stress produced normal responses in all experimental groups. In the three groups with hypothalamic deafferentations, the adrenocortical response following hippocampal stimulation was completely blocked, when compared to intact animals. The results suggest that the hippocampal signal enters the hypothalamus anteriorly, but that caudal propagation and posterior re-entry into the hypothalamus are also essential for the adrenocortical activation by the hippocampus.

Adrenal Cortex↗
PubMed1981

Effects of sciatic nerve stimulation on ACTH secretion, in intact and in variously hypothalamic deafferentated male rats.

Serum ACTH levels were determined by RIA following sciatic nerve stimulation, in intact rats and in rats bearing anterior (AHD), posterior (PHD) or complete (CHD) hypothalamic deafferentations. In both N and PHD groups, serum ACTH concentrations were markedly elevated following stimulation. In CHD animals this response was completely eliminated, and in the AHD group only a very slight and marginally significant increase in serum ACTH occurred, upon stimulation. These results demonstrate that the increased corticosterone secretion which occurs following sciatic nerve stimulation is due to elevated blood levels of ACTH, and confirm that this somatosensory stimulation impinges upon the hypothalamus from the rostral directions.

Adrenocorticotropic Hormone↗
PubMed1981

The role of the medial forebrain bundle in the mediation of the hypothalamic-hypophyseal-adrenal responses to acute neurogenic stress.

Adult male rats, intact (N) or bearing bilateral lesions in the medial forebrain bundle (MFB), were acutely exposed to visual, audiogenic, or thermal stress, during the following which serum ACTH and corticosterone (CS) levels were determined. The marked elevations in serum concentrations of both ACTH and CS which occurred in intact animals following photic stimulation were absent in MFB rats. The normal ACTH and CS responses to audiogenic stress were slightly delayed and attenuated, respectively, in the operated group, whereas the responses of both hormones to exposure to elevated environmental temperature were partially blocked in lesioned, as compared to intact, animals. These results demonstrate that the MFB is involved in mediating the ACTH, as well as the CS secretory responses to acute stress exposure. More specifically, the role of the MFB, vís-à-vis the hypothalamo-hypophyseal-adrenal axis, appears to be in the transmission of sensory input from rostral brain areas posteriorly.

Adrenocorticotropic Hormone↗
PubMed1981

Amygdalectomy Inhibits adrenocortical responses to somatosensory and olfactory stimulation.

Adrenocortical responses, as measured by plasma corticosterone, to ether stress, photic, acoustic, sciatic and olfactory stimulation, were studied in amygdalectomized and in intact rats. While amygdalectomy had no effect on the adrenocortical responses following ether stress or photic and acoustic stimulation, the responses following sciatic and olfactory stimulation were markedly reduced. These results, taken together with our previous studies, suggest that the amygdala participates in the transmission of adrenocortical responses to olfactory stimulation and has also a modulatory facilitatory effect on the adrenocortical response to somatosensory stimulation. Amygdalectomy also reduced the effect of dexamethasone on basal plasma corticosterone secretion, indicating that the amygdala may participate in the feedback regulation of pituitary-adrenal function.

Acoustic Stimulation↗
PubMed1981

Neural pathways mediating basal and stress-induced secretion of luteinizing hormone, follicle-stimulating hormone, and testosterone in the rat.

Adult male rats, intact or bearing complete, anterior, or posterior hypothalamic deafferentations (CHD, AHD, or PHD, respectively) or bilateral medial forebrain bundle (MFB) lesions, were acutely exposed to visual, audiogenic, or thermal stress. Two to 30 min after stress onset, the rats were decapitated, and trunk blood was collected from serum LH, FSH, and testosterone (T) determinations. While basal serum LH levels were found to be normal in all experimental groups, FSH levels were reduced in CHD and AHD rats, and serum T concentrations were found to be 3-fold greater than control values in the AHD group. In intact animals, exposure to all modalities caused significant elevations in serum levels of both LH and T, with no effect on FSH secretion. In the CHD and AHD groups, the LH and T responses were eliminated, with the exception of the T response to heat exposure, which persisted in CHD animals. In the PHD group, the LH and T responses persisted and were, in fact, potentiated. Bilateral medial forebrain bundle lesions inhibited the LH and T responses to audiogenic and thermal, but not to visual, stimulation. These data demonstrate that 1) basal FHS, but not LH, secretion is dependent upon extrahypothalamic afferents to the medial basal hypothalamus; 2) acute neurogenic stress stimulates LH and T, but not FSH, secretion; and 3) central nervous system sites, rostral to the medial basal hypothalamus, mediate the stress-induced elevations in LH release.

Acoustic Stimulation↗
PubMed1981

Site and mode of action of indomethacin on the hypothalamo-hypophyseal-adrenal axis: a temporal study in intact, hypothalamic-deafferentated, and hypothalamic-lesioned male rats.

Adult male rats were given single sc injections of indomethacin (IM; 5 mg/100 g BW) and sacrificed 2-24 h later. IM effects upon serum ACTH and corticosterone (CS) levels, rectal temperature, and hypothalamic and adenohypophyseal prostaglandin E2 (PGE2) and cAMP contents were observed. Rectal temperature was normal for 5-10 h post injection and later decreased by approximately 2.5 C. Both hypothalamic and adenohypophyseal PGE2 concentrations were reduced from 2-24 h after IM administration; no changes in cAMP content were observed. Serum ACTH and CS levels were elevated 4- and 6-fold, respectively, over the entire period observed. In animals with complete hypothalamic deafferentations, the ACTH and CS responses to IM were as marked as they were in intact rats. In rats with hypothalamic lesions in which the ACTH and CS responses to ether stress were attenuated, marked ACTH and CS secretory responses to IM were seen. It is concluded: 1) that the main site of action of systemically administered IM on the hypothalamohypophyseal-adrenal axis, is within the adenohypophysis; 2) that this effect is mediated by PGE2, and cAMP is not involved; and 3) that central nervous system PGs may be involved in the maintenance of basal body temperature in the rat.

Adrenal Glands↗
PubMed1980

Neural pathways mediating the prolactin secretory response to acute neurogenic stress in the male rat.

Adult male rats, intact (N) or bearing complete, anterior or posterior hypothalamic deafferentations (CHD, AHD or PHD, respectively), or bilateral medial forebrain bundle (MFB) lesions, were acutely exposed to visual or audiogenic stimulation. At 2, 4, 10 or 30 min following stress onset the animals were decapitated and trunk blood was collected for prolactin (PRL) determinations. Basal serum PRL levels were found to be similar in all groups. In N animals, exposure to both modalities resulted in rapid and marked PRL secretory responses. These responses were totally abolished in the CDH group. In AHD rats, no significant elevation in serum PRL concentration was found upon stress exposure. In PHD animals, the PRL secretory responses were only slightly attenuated when compared with the N group. In MFB-lesioned rats, a marked elevation in serum PRL concentrations was recorded following visual stimulation; contrary thereto, the PRL secretory response following audiogenic stress was markedly attenuated. These data (1) describe the temporal aspects of the PRL secretory response to acute exposure to neurogenic stresses in the male rat, and (2) demonstrate that these PRL responses are elicited via a neural pathway impinging upon the medial basal hypothalamus from the rostral direction.

Acoustic Stimulation↗
PubMed1980

Corticotrophin and corticosterone secretory patterns following acute neurogenic stress, in intact and in variously hypothalamic deafferented male rats.

Adult male rats, intact (N) or bearing complete (CHD), anterior (AHD), or posterior (PHD) hypothalamic deafferentations, were acutely exposed to either visual or audiogenic stimulation. At 2, 4, 10 or 30 min following the onset of stress exposure the animals were decapitated and trunk blood was collected for ACTH (RIA) and corticosterone (CS, CBG) determinations. Basal serum concentrations of both hormones were elevated in CHD and AHD, but not in PHD animals as compared to N animals. In N rats, exposure to both stresses resulted in elevated serum ACTH and CS concentrations, with the ACTH response to audiogenic but not visual stimulation being biphasic. In CHD animals, serum ACTH concentrations decreased, and those of CS were unchanged following stress exposure. While audiogenic stimulation caused elevation in serum levels of both hormones in AHD rats, the normal ACTH and CS response to visual stimulation were completely abolished by anterior hypothalamic deafferentation. In PHD animals, no ACTH response to either of the stress exposures was apparent; in spite of this, partial CS responses were elicited. These data thus describe the temporal aspects of the ACTH and CS secretory responses to different neurogenic stresses, and provide insight into the neural pathways mediating these responses.

Adrenocorticotropic Hormone↗