Corticosterone potentiation of conditioned fear in rats.
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Acoustic Stimulation↗
Biomedical subjects
J Schulkin
Publications and source records attributed to J Schulkin.
Effects of corticosterone on CRH mRNA and content in the bed nucleus of the stria terminalis; comparison with the effects in the central nucleus of the amygdala and the paraventricular nucleus of the hypothalamus.
We previously reported that corticosterone (CORT) increased corticotropin-releasing hormone (CRH) mRNA in the central nucleus of the amygdala (CEA), while reducing it in the paraventricular nucleus (PVN) of the hypothalamus by using in situ hybridization histochemistry. The bed nucleus of the stria terminalis (BNST) is closely related to the amygdala, and it is also a source of extrahypothalamic CRH; therefore, we examined CRH mRNA changes in the BNST following systemic treatment with CORT in adrenally-intact rats. Effects of adrenalectomy on CRH mRNA in the BNST, PVN and CEA were also examined. In addition, CRH content in these nuclei and in the median eminence (ME) were determined by micropunch dissection technique combined with CRH radioimmunoassay in CORT pellet implanted rats. Subcutaneous injections of high CORT (5 mg/day, over 14 days) increased CRH mRNA in the dorsal part of the lateral BNST (BSTLD) at 2, 4 and 8 days, although the low dose of CORT (1 mg/kg/day) had no significant effects. By contrast, in the ventral part of the BNST (BSTV) neither the high nor low dose of CORT altered CRH mRNA levels. In a second experiment, a slowly-releasing CORT pellet (200 mg, 60-day release) produced an elevation of CRH mRNA at both 1 and 2 weeks or at 1 week in the BSTLD or in the BSTV, respectively. These results show that glucocorticoids can facilitate CRH mRNA expression in the BSTLD in the same manner as seen in the CEA, and that CRH mRNA in the BSTLD can respond to CORT more than in the BSTV. In a third experiment, bilateral adrenalectomy, however, did not affect CRH mRNA in the BNST although there was a modest decrease in the CEA and a robust increase in the PVN. Finally, in CORT pellet (200 mg, for 2 weeks) implanted rats, CRH content in the ME significantly decreased and modestly increased in the CEA compared with control rats, whereas it did not change in the PVN and BNST. Taken together, these results suggest that (1) CRH in the BNST and the CEA may share some common functions in neuroendocrine and behavioral changes, but that (2) mechanisms of CRH synthesis or its releasing sites may be different in the BNST and CEA.
Amygdala↗
Glucocorticoid treatment increases the ability of CRH to induce seizures.
We examined whether glucocorticoids could enhance the ability of corticotropin-releasing hormone (CRH) to induce seizures. Rats were treated with systemic glucocorticoids (dexamethasone, 100 micrograms) or vehicle for either 3 days (chronic) or 2 h (acute) before intracerebroventricular CRH (3 or 10 micrograms) or saline injections and then monitored for 8 h following each injection. Our results suggest that chronic, but not acute, glucocorticoid pretreatment increases the likelihood of CRH-induced seizures.
Aggression↗
Corticosterone effects on corticotropin-releasing hormone mRNA in the central nucleus of the amygdala and the parvocellular region of the paraventricular nucleus of the hypothalamus.
Using in situ hybridization histochemistry, we report differential expression of corticotropin-releasing hormone (CRH) mRNA in the central nucleus of the amygdala (CEA) and the parvocellular region of the paraventricular nucleus of the hypothalamus (PVN) following systemic treatment with corticosterone (CORT) in adrenally-intact rats. Both injection of low (1 mg/kg/day) and high (5 mg/day) CORT reduced CRH mRNA expression in the PVN in a dose-dependent manner, although it returned to normal at the low dose by 14 days. By contrast, the high dose of CORT increased CRH mRNA transiently in the CEA at 4 days, although the low dose of CORT decreased it at 14 days. In a second experiment, we implanted a slowly-releasing CORT pellet for 2 weeks (200 mg, 60 day release) subcutaneously. This treatment produced an elevation of CRH mRNA in the CEA both at 1 and 2 weeks, whereas CRH mRNA in the PVN was decreased to a large extent as seen in the high CORT group of the first experiment. These results suggest that glucocorticoids can facilitate CRH mRNA expression in the CEA, a site implicated in anxiety and fear, while restraining the hypothalamic-pituitary-adrenal axis as indicated by the reduction in CRH mRNA in the PVN.
Adrenal Glands↗
1,25 (OH)2 vitamin D3 levels in seasonal affective disorder: effects of light.
1,25 (OH)2 vitamin D3 levels were assessed in nine females and six males with winter seasonal affective disorder and in 15 age- and gender-matched controls in winter during periods with and without treatment with light therapy. No difference was found between groups or across conditions, though wide variations within each group make the presence of a type II error possible.
Adult↗
Allostasis, amygdala, and anticipatory angst.
Regions of the amygdala are involved in anticipation of negative events. Chronic anticipation of negative events leads to what we call allostatic load, or arousal pathology. Two hormones appear to be involved in arousal pathology; corticotropin-releasing hormone in the brain and glucocorticoids. We suggest that increases in corticotropin-releasing hormone, by stress or glucocorticoids, in the amygdala may have functional consequences for allostatic load. Whereas, corticotropin-releasing hormone in the parvocellular region of the paraventricular nucleus of the hypothalamus is decreased by glucocorticoids thereby under negative feedback and homeostatic control, the central nucleus of the amygdala is to some extent under positive feedback and is increased by glucocorticoids, and perhaps under allostatic control. The human and animal literature suggest that a variety of psychopathologies (e.g., melancholia) may be tied to neurohormonal signals activating regions of the amygdala.
Amygdala↗
Dietary calcium deficiency causes a reduction in calretinin mRNA in the substantia nigra compacta-ventral tegmental area of rat brain.
Dietary calcium deprivation (3 weeks) affected neuronal gene expression of calretinin. Calcium deprived rats exhibited calcium appetite, weight loss, and a 28% decrease in calretinin mRNA in the substantia nigra compacta-ventral tegmental area, compared to controls. No changes were detected in 2 other mRNAs (tyrosine hydroxylase, beta-actin) and 5 other brain regions examined. This region-specific reduction of calretinin mRNA may relate to the altered physiology or behavior.
Actins↗
Curt P. Richter - February 20, 1894-December 21, 1988.
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History, 20th Century↗
The effects of lesions of the bed nucleus of the stria terminalis on sodium appetite.
Lesions of the bed nucleus of the stria terminalis result in decrements in sodium ingestion. Specifically, sodium ingestion that is aroused by mineralocorticoids, in addition to sodium depletion, was reduced in rats with large lesions of the bed nucleus of the stria terminalis. Need-free salt ingestion was also reduced. These results suggest that the bed nucleus of the stria terminalis may be involved in the regulation of sodium appetite.
Animals↗
Lesions of the central nucleus of the amygdala. I: Effects on taste reactivity, taste aversion learning and sodium appetite.
Bilateral damage to the central nucleus of the amygdala (CeAX) in the rat blunts need-induced NaCl intake and abolishes daily need-free NaCl intake when measured with a two-bottle test. Such a deficit could be the result of impaired taste function. To assess the taste function of the CeAX rat various taste stimuli were introduced directly into the oral cavity and taste-elicited oral motor responses were measured. Oral motor responses elicited by 0.62 M and 0.13 M sodium chloride, 0.3 M sucrose and 0.01 M citric acid, were similar in control and CeAX rats. Additionally CeAX and control rats acquired a taste aversion for fructose or maltose when either was paired with LiCl. Finally, in CeAX rats, like in control rats, the pattern of oral motor responses to 0.5 M NaCl was dependent on internal state; sodium depletion dramatically altered taste-elicited oral motor behavior. These results suggest that, in the rat, the deficits in NaCl intake behavior that follow CeAX do not appear to be a result of dramatic changes in gustatory function.
Amygdala↗
Lesions of the central nucleus of the amygdala. II: Effects on intraoral NaCl intake.
Bilateral lesions of the central nucleus of the amygdala (CeAX) disrupt both need-free and need-induced NaCl intake. Quite surprisingly, in response to sodium depletion, the same rats who fail to augment their NaCl consumption dramatically increase the numbers of oral motor behaviors associated with ingestion that they display when NaCl is presented intraorally. The present study attempts to resolve these apparently contradictory results by measuring the intake of a NaCl solution delivered directly into the mouth. Controls enhanced their intraoral intake of 0.5 M NaCl in response to sodium depletion while CeAX rats did not. CeAX rats, however, showed discriminative intake responses to tastes. Like controls, CeAX rats promptly rejected 0.3 mM quinine infusions and ingested 1.0 M sucrose for prolonged periods. In addition, food deprivation enhanced the intraoral intake of a dilute sucrose solution in both CeAX and control rats. Thus, in the CeAX rat some tastes and some internal states modulate intake as they do in intact rats. These results are consistent with the hypothesis that central nucleus of the amygdala damage interferes with the consummatory phase of NaCl intake behaviors.
Administration, Oral↗
Facilitation of cocaine kindling by glucocorticoids in rats.
We report that glucocorticoids significantly facilitated the development of cocaine-induced kindled seizures. These results suggest that glucocorticoids may have effects on the development of kindled seizures which are similar to those of the neuropeptide, corticotropin-releasing hormone (CRH), with which they show a close functional relationship. These results may be of interest in the light of data showing that glucocorticoids increase CRH expression in the central nucleus of the amygdala, which is an important site for the development of kindling.
Animals↗
Medial region of the amygdala: involvement in adrenal-steroid-induced salt appetite.
We report the following observations: first that cell body damage induced by ibotenic acid within the medial region of the amygdala resulted in the abolition of corticosterone-potentiated, aldosterone-induced salt appetite. Sodium depletion-induced salt appetite was not impaired by the lesion, nor was angiotensin-dependent salt appetite via captopril treatment. These results provide evidence that the medial region of the amygdala has a major role in the natriorexigenic effects of the adrenal steroids.
Aldosterone↗
Glucocorticoids facilitate mineralocorticoid-induced sodium intake in the rat.
We confirm and extend the finding that glucocorticoids facilitate mineralocorticoid-induced sodium intake in the rat. First, we report that subcutaneous injections of dexamethasone (DEX) increase deoxycorticosterone-induced sodium intake. Second, we demonstrate that continuous intravenous infusions of either DEX or corticosterone or the TYPE II glucocorticoid receptor agonist RU28362 increases the sodium intake of aldosterone-treated rats. And third, we measured urine sodium loss and found that rats were in positive sodium balance while receiving aldosterone and the glucocorticoid agonist, suggesting that the increased intake of sodium was primary to renal sodium loss. When taken together with the fact that glucocorticoids can increase the TYPE I aldosterone-preferring receptor population in the brain, the results suggests a role for the glucocorticoid hormones in the arousal of sodium appetite in the rat.
Aldosterone↗
Sex differences in salt preference and taste reactivity in rats.
Previous studies have shown that female rats consume significantly more sodium chloride (NaCl) than do age-matched males. The gustatory contribution to this sex difference was examined in the following experiments. In Experiment 1, female rats demonstrated a higher two-bottle preference for NaCl ranging from 0.03 M to 1.0 M than did age-matched males. Next, to determine if the animal's sex modified gustatory sensitivity for NaCl, taste reactivity responses elicited by intraoral infusions (0.8 ml) of NaCl (0.03 M, 0.15 M, 0.3 M, and 1.0 M) were measured in age-matched male and female Sprague-Dawley rats. Intraoral infusions of NaCl were administered in ascending concentration order on successive days. During the intraoral infusion, the animal's oral motor taste reactivity responses were videotaped and subsequently analyzed to determine the number of ingestive and aversive responses. Intraoral infusions of 0.15 M and 0.3 M NaCl elicited reliably more ingestive responses and 1.0 M NaCl more aversive responses in females than in males. Because differences in taste reactivity were not found for all those concentrations for which female rats showed a higher preference than did males, changes in gustatory sensitivity contributes to, but does not appear to fully account for the female rats' preference for NaCl.
Animals↗
The anteroventral wall of the third ventricle and the angiotensinergic component of need-induced sodium intake in the rat.
Because the anteroventral wall of the third ventricle (AV3V) has been implicated in the control of sodium intake it was studied in rats with damage of the AV3V region in the sodium-replete and sodium-deplete states, and when they were treated with either pulse intracerebroventricular (pICV) injection of renin to activate brain angiotensin or daily subcutaneous injections of deoxycorticosterone (DOCA). The response of rats with AV3V damage to sodium depletion was retarded and the excess sodium intake that is induced by pICV renin was absent, but their daily need-free sodium intake and the sodium intake that is induced by DOCA were essentially normal. The results suggest that the AV3V is responsible for the angiotensinergic, but not the aldosteronergic, component of the ANG II/ALDO synergy that controls need-induced sodium appetite in the rat. The integrity of the AV3V is not necessary for daily need-free sodium intake or for its enhancement by sodium depletions, suggesting that ANG II is probably not important for these phenomena. But ANG II action within the AV3V might be important for the rapid burst of sodium intake that immediately follows a period of depletion.
Aldosterone↗
Deficits in NaCl ingestion after damage to the central nucleus of the amygdala in the rat.
These studies examined the NaCl intake behaviors of rats with bilateral electrolytic lesions of the central nucleus of the amygdala (CeAX). Daily need-free intake of 3% NaCl was abolished by CeAX even in rats in which it had been enhanced preoperatively by a history of repeated sodium depletions but was slightly restored by three successive postoperative sodium depletions. CeAX rats drank water but not 3% NaCl to high doses of DOCA and to the activation of cerebral angiotensin II, and expressed small but reliable salt intake (need-induced salt intake or salt appetite) after postoperative sodium depletions. Other ingestive behaviors (water drinking, intake of food and 5% sucrose) were normal. When given decreasing concentrations of NaCl solution the CeAX rats rejected them until the concentration reached 0.2%. These findings suggest that lesions to the central nucleus of the amygdala produce a global impairment in salt intake behaviors that is possibly due to an alteration in the central processing of the salt taste signal.
Amygdala↗
Transection of the stria terminalis without damage to the medial amygdala does not alter behavioural sodium regulation in rats.
Damage to the medial region of the amygdala has been shown to impair mineralocorticoid-induced sodium appetite, while leaving intact sodium appetite induced through sodium depletion. This effect may result from the interruption of the flow of information through the stria terminalis (ST), a neural pathway linking the medial amygdala with the ventral forebrain. We determined the effect of transecting the ST of the rat, at a point remote from the medial amygdala, on sodium appetite induced with the administration of mineralocorticoids and with the natriuretic furosemide. Similar to control and amygdala lesioned rats, rats with ST knife-cuts displayed a normal sodium appetite following treatment with furosemide. However, unlike medial amygdala lesions, transection of the ST alone did not block mineralocorticoid-induced sodium appetite. Therefore, the inability of mineralocorticoids to induce a salt appetite in medial amygdala lesioned rats does not result from damage to the stria terminalis.
Amygdala↗