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PubMedDate not supplied

Brain and pituitary receptors for corticotropin releasing factor: localization and differential regulation after adrenalectomy.

Specific receptors for corticotropin releasing factor (CRF) were identified in two functionally distinct systems within the brain, the cortex and the limbic system. Autoradiographic mapping of the CRF receptors in the brain revealed high binding density throughout the neocortex and cerebellar cortex, subiculum, lateral septum, olfactory tract, bed nucleus of the stria terminalis, interpeduncular nucleus and superior colliculus. Moderate to low binding was found in the hippocampus, nucleus accumbens, claustrum, nucleus periventricularis thalamus, mammillary bodies, subthalamic nucleus, periaqueductal grey, locus coeruleus and nucleus of the spinal trigeminal tract. As in the anterior pituitary gland, CRF receptors in the brain were shown to be coupled to adenylate cyclase. However, in contrast to the marked decrease in CRF receptors observed after adrenalectomy in the anterior pituitary gland, CRF receptor concentration in the brain and pars intermedia of the pituitary was unchanged. The presence of CRF receptors in areas involved in the control of hypothalamic and autonomic nervous system functions is consistent with the major role of CRF in the integrated response to stress.

Adenylyl Cyclases↗
PubMedDate not supplied

Continuous intraventricular infusion of neuropeptide Y evokes episodic food intake in satiated female rats: effects of adrenalectomy and cholecystokinin.

In these studies the pattern of feeding behavior during continuous intraventricular (IVT) infusion of NPY for 4 hr in the satiated female rat was monitored. Whereas saline infusion was ineffective, each of the three doses of NPY (117, 470 or 1175 pmol/hr) increased feeding during the entire 4 hr infusion and 2 hr postinfusion period. The cumulative food intake at the end of 4 hr of NPY infusion was enhanced in a dose-related fashion between 0, 117 and 470 pmol/hr; at 1175 pmol/hr food intake plateaued. In addition, the latency to initiate feeding response decreased in a dose-related fashion and feeding occurred in discrete (35-45) episodes during the 4 hr infusion period. Further, the total time feeding and local eating rate (g/min) increased significantly in response to the higher rates of NPY infusion. Concurrent infusion of cholecystokinin (CCK) at either equimolar or 2.5 x NPY dose, affected neither the NPY-induced cumulative food intake nor any other parameter of feeding behavior. On the other hand, cumulative food intake was significantly decreased in adrenalectomized rats in response to NPY infusion (470 pmol/hr); a response due primarily to a marked suppression in some, and almost complete cessation of food consumption in other rats during the second 2 hr period of NPY infusion. These studies show that continuous central infusion of NPY can produce sustained, intermittent feeding behavior and adrenalectomy significantly curtailed the duration of NPY effectiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1992

Increase in cortical and midbrain tryptophan hydroxylase activity by intracerebroventricular administration of corticotropin releasing factor: block by adrenalectomy, by RU 38486 and by bilateral lesions to the central nucleus of the amygdala.

Corticotropin releasing factor (CRF) infused bilaterally into the lateral ventricles of awake, chronically cannulated, male Sprague-Dawley rats produced a dose-dependent increase in the in vitro activity of cortical and midbrain tryptophan hydroxylase after 60 min. The maximal increase in enzyme activity of 60% over that of vehicle-treated controls was reached 45 min after an infusion of 3 micrograms CRF. The increase in enzyme activity after a single dose of CRF resembled that seen after exposure of rats to an acute sound stress: it was reversed by preincubation of the enzyme preparation with alkaline phosphatase and was nonadditive with the increase in activity obtained in the presence of phosphorylating conditions. The response to intracerebroventricularly administered CRF was abolished by bilateral adrenalectomy, but restored by repeated daily systemic administration of the synthetic glucocorticoid, dexamethasone (500 micrograms/day, i.p. for 3 days), to the adrenalectomized rats. Intracerebroventricular administration of the glucocorticoid antagonist, RU 38486 (200 micrograms/day for 4 days), also blocked the acute increase in tryptophan hydroxylase activity in response to CRF. Finally, bilateral lesions to the central nucleus of the amygdala, a region involved in mediating behavioral, endocrine and autonomic responses to stressful stimuli, abolished the increase in enzyme activity in response to intraventricular CRF. The glucocorticoid sensitivity of the response to CRF, as well as the involvement of the central nucleus of the amygdala support the view that CRF may have a role in mediating the enhancement of tryptophan hydroxylase activity by acute sound stress.

Adrenalectomy↗
PubMed1988

Changes in serum potassium concentration with exercise in Hereford calves: effects of adrenalectomy.

1. Serum potassium concentration [K+] was measured pre- and postadrenalectomy in three Hereford steer calves before, during and following 3.5 min exercise at their maximal speed capability. 2. Both before and after adrenalectomy, serum [K+] increased an average of 2.4 mEq.1(-1) during exercise and was at control levels 10 min postexercise. 3. Hormones from neither the adrenal cortex nor the adrenal medulla influence serum [K+] dynamics during acute exercise.

Adrenal Glands↗
PubMed1991

Lowering of pancreatic amylase activity induced by cold exposure, fasting and adrenalectomy in rats.

1. Alteration of amylase activity in the pancreas was studied in rats under different stressful situations. 2. Cold-exposed rats had reduced amylase activity, hypertrophy of adrenal glands, and lowered plasma insulin and glucose. 3. In fasted rats, amylase activity decreased and plasma insulin and glucose lowered. 4. Immobilized animals failed to produce the reduced amylase activity, despite existence of higher plasma corticosterone. 5. Adrenalectomy caused reduction of amylase activity accompanied by decreases in plasma insulin and glucose. 6. Glucocorticoid hormone is not correlated with suppression of amylase synthesis. The lowered amylase activity might involve changes in glycolytic flux and/or suppression of amylase synthesis by insulin deficiency.

Adrenal Glands↗
PubMed1989

Changes in rat pituitary nuclear and cytoplasmic pro-opiomelanocortin RNAs associated with adrenalectomy and glucocorticoid replacement.

While the transcriptional effects of glucocorticoid hormone manipulation on the pituitary pro-opiomelanocortin (POMC) gene have been documented, it is not yet clear whether glucocorticoids activate additional post-transcriptional mechanisms to regulate POMC gene expression. We have used RNA probes that span exon/intron junctions in sensitive nuclease protection assays in order to examine changes in POMC precursor RNA as well as mature mRNA in nucleus and cytoplasm following both adrenalectomy (ADX) and administration of exogenous glucocorticoids. ADX led to a rapid and sustained 8- to 10-fold increase in the level of POMC primary transcript in the anterior lobe (AL), from 1 to 14 days after ADX. Stimulation of mature POMC mRNA in the nucleus was also rapid, with 7- to 8-fold increases evident by 1 day after ADX. In sharp contrast, the time-dependent accumulation of POMC mRNA in the cytoplasm was slow in comparison, reaching levels approximately 2-fold higher than sham-operated animals by 1 day post-ADX and 12-fold higher by 14 days after ADX. Despite the constant elevated level of nuclear POMC precursor RNA, the rate of accumulation of POMC mRNA in the corticotroph cytoplasm after ADX was not linear, with the greatest increase occurring within the first 1-4 days post-ADX. This led to alterations in the molar ratio of POMC primary transcript: nuclear mRNA: cytoplasmic mRNA in the AL at 1 and 4 days after ADX and showed a relative increase in the proportion of POMC RNA transcripts within the nucleus. Acute administration of dexamethasone to ADX rats resulted in rapid 80-90% inhibition of POMC primary transcript levels in the AL that was maximal by 30 min but with no associated change in mature mRNA. No significant changes in POMC RNA were seen in neurointermediate lobe in any of these studies. These studies suggest that following ADX, time-dependent alterations in nuclear transport of mature POMC mRNA and/or changes in POMC mRNA stability, in addition to changes in gene transcription may account for the overall level of POMC mRNA expressed in the AL. Furthermore, we have illustrated the use of exon/intron probes for accurately quantitating rapid alterations in steady-state levels of nuclear precursor RNA that may reflect transcriptional responses and/or changes in post-transcriptional processing of the primary transcript.

Adrenalectomy↗
PubMed1990

Effect of adrenalectomy and glucocorticoid treatment on the levels of an insulin-sensitive glycosyl-phosphatidylinositol in isolated rat hepatocytes.

Insulin resistance caused by dexamethasone administration to rats was accompanied by a marked decrease in the hepatocyte content of an insulin-sensitive glycosyl-phosphatidylinositol, as well as by a blockade of its hydrolysis in response to this hormone. In contrast, bilateral adrenalectomy provoked a significant increase of the cellular glycosyl-phosphatidylinositol levels. Under all the assayed metabolic conditions, a close direct correlation was established between the basal content of this compound and the number of insulin receptors present in the isolated hepatocytes.

Adrenal Glands↗
PubMed1984

Vasopressin release from rat medial basal hypothalamus in vitro after adrenalectomy or lesions of the paraventricular nuclei.

Rat medial basal hypothalami (MBH) or neurointermediate lobes of the hypophysis (NIL) were superfused in vitro and stimulated electrically. The evoked release of vasopressin from the MBH was enhanced to 700% of controls when the tissue was taken from adrenalectomized rats. By contrast, the evoked release of vasopressin from the NIL was not changed after adrenalectomy. After bilateral lesions of the paraventricular nuclei, the evoked release of vasopressin from the MBH was reduced in subsequent in vitro experiments. The marked changes in vasopressin release occurred in spite of no or only small changes in the total tissue content of vasopressin. These data support the view that vasopressin may be released from the external layer of the median eminence into the hypophysial portal blood after activation of the hypothalamo-pituitary-adrenal axis.

Adrenalectomy↗
PubMed1986

Quantitative in situ hybridization histochemistry reveals increased levels of corticotropin-releasing factor mRNA after adrenalectomy in rats.

A 35S-labeled 48-base synthetic oligonucleotide complementary to a portion of the rat corticotropin-releasing factor (CRF) mRNA was used for in situ hybridization histochemistry. CRF-synthesizing cells were located in the paraventricular nucleus of the hypothalamus. These cells were observed in the medial parvocellular subdivision where there was a 90% increase in the amount of CRF mRNA per unit volume after adrenalectomy.

Adrenalectomy↗
PubMed1988

Adrenalectomy but not gonadectomy affects rat pineal beta-adrenergic receptor density.

Bilateral adrenalectomy, like chronic pineal denervation by means of superior cervical ganglionectomy, induced an increase in the morning levels of [125I]iodopindolol (IPIN) binding to rat pineal membranes; this change may be related to the reduced input of catecholamines to the pinealocytes as suggested by the decrease in nocturnal pineal melatonin synthesis previously reported in adrenalectomized rats. Castrated rats did not show changes in IPIN binding to pineal membranes when measured either at middark or in chronically superior cervical ganglionectomized rats, suggesting that the regulation of pineal beta-adrenergic receptors is independent from gonadal control.

Adrenal Glands↗
PubMed1990

Restraint stress and adrenalectomy do not affect the level of rat cerebral enolase.

Gamma gamma (gamma gamma) enolase amount and enolase isozyme activities were measured in brain structures involved in stress response (hypothalamic paraventricular and supraoptic nuclei, locus coeruleus, hippocampus, A1 and A2 regions, hypophysis). Analyses were made in rats after immobilization or adrenalectomy, two experimental conditions that have been reported to increase brain glucose consumption and protein synthesis. In control rats enolase content was highest in the A1 region and hippocampus and lowest in hypophysis. A positive correlation was found between the enzyme level and its activity in the brain regions studied. However, in stressed or adrenalectomized rats, the level of glycolytic enzyme enolase was not significantly modified.

Adrenalectomy↗
PubMed1992

Alteration of pituitary-adrenal responses to adrenalectomy by the immunological targeting of CRF neurons.

We previously demonstrated that cellular toxins added to a cytotoxic IgG2a monoclonal antibody to corticotropin releasing factor (CRF-MAb) may specifically penetrate some hypothalamic CRF neurons, after central injection near the paraventricular nuclei. We attempt here to evaluate the consequential effects on the CRF neurons functioning. Such a toxic mix, 4 weeks after its central injection, caused a marked reduction (66%) of the chronic adrenocorticotropic hormone (ACTH) release in response to a bilateral adrenalectomy (7th day). This change was accompanied by a reduction in the CRF concentration (43%) measured in the median eminence. We concluded that specific internalization of toxins, by the way of CRF-MAb, leads to a long-term dysregulation of the CRF synthesis and/or neuronal transport.

Adrenalectomy↗
PubMed1992

CRH gene expression in the fetal rat is not increased after pharmacological adrenalectomy.

A regimen of twice daily metyrapone injections (100 mg/kg), resulted in pharmacological adrenalectomy of pregnant rats and fetuses in utero, i.e. depression of plasma corticosterone and elevation of plasma adrenocorticotropic hormone (ACTH). Toxicity was minimal on days 14-17 of pregnancy, and increased with higher maternal weight and pregnancy progression. Corticotropin releasing hormone (CRH) messenger RNA abundance in the pregnant adults increased significantly within 48 h of metyrapone initiation. No change in CRH gene expression in the paraventricular nucleus of fetuses (days 17-18) was seen, even after 72 h of the regimen. This is compatible with the independence of CRH gene expression of glucocorticoid feedback in the fetal rat.

Adrenalectomy↗
PubMed1996

Effects of adrenodemedullation and adrenalectomy on the 5-HT2 receptor agonists DOI-and mCPP-induced hypophagia in rats.

Effects of adrenodemedullation and adrenalectomy on the serotonin2 (5-HT2) receptor agonists-induced hypophagia were investigated. Hypophagia induced by both the 5-HT2A/2C, receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and the 5-HT2C-receptor agonist 1-(3-chlorophenyl)piperazine (mCPP) were not affected by adrenodemedullation. In adrenalectomized rats. DOI did not induce hypophagia, while mCPP elicited apparent effects. These results suggest that neither DOI- nor mCPP-induced hypophagia was not associated with adrenaline release from the adrenal medulla. Moreover, our results suggest that DOI-induced hypophagia is involved in corticosterone-sensitive feeding, although other mechanisms which are not related to corticosterone are involved in mCPP-induced anorexia.

Adrenal Medulla↗
PubMed1993

Effects of neonatal adrenalectomy on 5-HT and TRH-like immunoreactivity in the rat spinal cord.

This study investigated the effects of neonatal unilateral adrenalectomy on the serotonin- (5-HT) and thyrotropin-releasing hormone-like immunoreactivities (TRH-LI) in the intermediolateral cell column (IML) of the rat spinal cord where the sympathetic preganglionic neurons innervating the adrenal medulla are located. The density of the innervation was measured by a computer-assisted image analysis. Two weeks after the lesion, only one rat (1/3) showed a 30% decrease of 5-HT-LI in the ipsilateral IML, although no modifications were observed for TRH-LI. At 1 month, we observed a variable decrease of 19% to 30% for either 5-HT- or TRH-LI in the ipsilateral IML. However, one animal (1/3) showed nonsignificant modifications. At 3 months, we showed a 17% mean loss of 5-HT-LI and TRH-LI in the ipsilateral IML. However, the decreases of 5-HT-LI and TRH-LI did not always appear similar. These results appear different from those obtained after neonatal removal of the superior cervical ganglion.

Adrenalectomy↗
PubMed1994

Long-term adrenalectomy reduces hippocampal granule cell excitability in vivo.

Ten days after bilateral adrenalectomy (ADX), neural transmission between the perforant path and hippocampal dentate granule cells was severely impaired in the anaesthetized rat, in that the slope of the stimulus-response curve was reduced to less than half the value in sham controls, the stimulation current necessary to elicit a standard population spike (PS) field potential was increased approximately threefold, the amplitude of PS and its ratio to the slope of the field excitatory postsynaptic potential (EPSP) were reduced, and high-frequency tetanization (TET) of the perforant path resulted in potentiated PS with smaller amplitude and higher onset latency in ADX rats than in sham controls. However, the fractional increase of PS amplitude and its decay following TET were similar in 10 day-ADX and sham groups, from which it is inferred that long-term ADX entails a general decrease of dentate granule cell excitability, particularly at somatic membrane level, without specifically affecting the mechanism of long-term potentiation. None of the above changes occurred 24 h after ADX.

Adrenalectomy↗
PubMedDate not supplied

Adrenalectomy prevents the development of alcohol preference in male rats.

By forcing adrenalectomized (ADX) and sham-operated (SHAM) rats to chronically drink ethanol by mean of presentation of only one drinking bottle containing 10% ethanol, no differences occurred between both groups. ADX and SHAM rats were then exposed to chronic alcoholization using an inhalation procedure. After sejourning 3 weeks into the alcoholization chamber, rats were submitted to a free-choice paradigm [water vs. a 10% (v/v) ethanol solution]. The sham-operated rats presented an alcohol-induced behavioral preference towards alcohol whereas adrenalectomized animals never exhibited a preference to ethanol. In the adrenalectomized rats treatment with hydrocortisone (30 micrograms/ml) given orally during the pulmonary alcoholization failed to modify this preference whereas treatment with corticosterone (25 micrograms/ml) given orally abolished the difference with SHAM animals. These data showed that adrenalectomy prevented the development of ethanol preference and the clear involvement of the hypothalamo-pituitary-axis in alcohol preference.

Administration, Inhalation↗
PubMed1993

Effect of thyroidectomy and adrenalectomy on changes in liver glutathione and malonaldehyde levels after acute ethanol injection.

At low concentrations ethanol is metabolized largely by alcohol dehydrogenase to acetaldehyde, while at higher concentrations a microsomal ethanol oxidising system (MEOS) is involved, namely cytochrome P450 IIE1, which also probably generates free radical species. In hyperthyroidism hepatic glutathione stores are depleted and net superoxide anion production occurs. In contrast, in hypothyroidism hepatic glutathione may be increased and thus renders the liver less sensitive to alcohol generated free radical production. Steroid hormones inhibit lipid peroxidation. Sixty male Wistar rats either underwent thyroidectomy, adrenalectomy, or sham procedures. Twenty control animals were pair fed with thyroidectomized animals, whilst another twenty fed ad libitum. An intraperitoneal injection of alcohol (75 mmol/kg) was given 2.5 h prior to sacrifice to half the animals in each group, the remainder receiving saline. The total hepatic glutathione contents of the pair fed and the ad libitum groups were not different, but were significantly increased by thyroidectomy (p = < 0.001). This effect was significantly reduced by alcohol (p < 0.01). The sham procedures and dietary restrictions had no effect. The ethanol alone reduced total hepatic glutathione, but this only reached statistical significance in the thyroidectomized and sham-adrenalectomized groups. Hepatic malonaldehyde (MDA) levels were significantly reduced in the thyroidectomy group but alcohol had no effect on them. We conclude that hypothyroidism increased hepatic glutathione status, presumably by reducing radical production by enzyme systems, which would otherwise consume this important scavenger. Long term exposure to ethanol with induction of MEOS is probably required for it to generate toxic levels of free radical species.

Adrenal Glands↗