Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENALECTOMY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,459 records · Page 81Linked to original sources
PubMed1993

Effects of adrenalectomy or RU-486 on rat muscle fibers during hindlimb suspension.

The purpose of this study was to investigate the effects of a glucocorticoid antagonist, RU-486, and of adrenalectomy (ADX) on rat skeletal muscle structural properties after 3, 7, and 14 days of hindlimb suspension (H). After H, a significant loss in muscle weight was observed as early as 3 days in soleus (SOL; -10%) and adductor longus (AL; -14%) muscles. In SOL, after only 7 days, a reduction (-14%) in type I fiber percent distribution occurred, accompanied by an increase (+129%) in intermediate type I fibers. Fiber type changes increased depending on the duration of H. In AL muscle, no change occurred after H in the fiber type composition despite a similar degree of muscle atrophy. Treatment with RU-486 or ADX significantly reduced the loss of SOL weight observed after 14 days (-42 and -44%, respectively, vs. -50% for H rats), delayed the SOL atrophy (from 3 to 7 days), and normalized the shift in fiber type distribution induced by H. In SOL, administration of RU-486 (but not ADX) partly prevented the reduction in size induced by H of all the fibers. In AL, neither treatment affected the extent of muscle atrophy, even though the reduction in type IIa fiber size was prevented by RU-486 but not by ADX after 14 days of suspension. ADX or RU-486 administration did not prevent the extensor digitorum longus weight loss observed after 14 days of suspension but allowed a recovery of its normal fiber type composition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed2002

Maternal adrenalectomy abrogates the effect of fetal alcohol exposure on the interleukin-1beta-induced febrile response: gender differences.

Fetal alcohol exposure (FAE) has been shown to blunt the febrile component of the primary host-defense response to infection induced experimentally by systemic administration of interleukin (IL)-1beta. Given that maternal adrenalectomy (ADX) can prevent various postnatal effects of FAE, the present experiments were designed to determine whether maternal ADX would prevent the blunted IL-1beta-induced febrile response of fetal alcohol-exposed offspring and whether the effects of maternal ADX would be gender related. Timed-pregnant rats underwent ADX or were sham-operated on gestation day (GD) 7, or remained intact (without any surgery), and were fed ethanol-containing (E) or pair-fed (PF) liquid diets or normal (N) rat chow and water from GD 8 to GD 21. As adults, male and female E, PF and N offspring were injected with saline on day 1 and with IL-1beta (2 microg/kg, i.p.) on day 2 at 09.00 h and the body temperature was recorded biotelemetrically for 8.5 h. IL-1beta produced significantly lower febrile responses in female than in male offspring of intact dams, irrespective of prenatal diet. Furthermore, prenatal surgical stress differentially affected the IL-1beta-induced febrile response of male and female normally fed offspring. Additionally, in both male and female offspring of intact dams, FAE significantly attenuated the IL-1beta-induced febrile response. In males, FAE also attenuated the febrile response in the offspring of maternal sham-operated dams, and this effect was completely reversed by maternal ADX. In females, both maternal sham surgery and ADX reversed the effect of FAE on the febrile response. These findings suggest that maternal adrenal mediators are essential for the long-term effect of FAE on the febrile response in male offspring. In females, early prenatal surgical stress is sufficient to reverse the effects of FAE, possibly via adrenal-independent mechanisms that affect the thermoregulatory system.

Adrenalectomy↗
PubMed2003

Effect of stress and adrenalectomy on urocortin II mRNA expression in the hypothalamic paraventricular nucleus of the rat.

Urocortin II (Ucn II) is a novel corticotropin-releasing hormone (CRH)-related peptide discovered as a selective agonist for type-2 CRH receptor. In the rat or mouse brain, Ucn II mRNA shows weak expression mainly in the hypothalamic paraventricular nucleus (PVN) and the locus coeruleus (LC). Understanding the regulation of Ucn II mRNA expression under varying conditions provides new insights into central stress response. We examined expression of Ucn II mRNA in the PVN and LC following immobilization stress, water deprivation, and adrenalectomy. Rats subjected to immobilization stress exhibited a dramatic induction of Ucn II mRNA expression in the parvocellular part of the PVN at the end of 2 h of immobilization. In contrast, water deprivation for 3 days induced Ucn II mRNA expression mainly in the magnocellular part of the PVN. Although water-deprived rats showed a marked decrease in their food intake, pair-fed rats failed to alter PVN Ucn II mRNA expression, suggesting that osmotic stimuli per se, but not reduced food consumption during water deprivation, caused Ucn II mRNA induction in the magnocellular part of the PVN. Adrenalectomized rats failed to show an increase in Ucn II mRNA in the PVN when compared to sham-operated rats. Double-label in situ hybridization revealed colocalization of Ucn II mRNA in approximately 45% of the CRH mRNA-expressing cells in the parvocellular part of the PVN following immobilization, or colocalization in most of the vasopressin mRNA-expressing cells in the magnocellular part of the PVN following water deprivation. In the LC, no induction of Ucn II mRNA was observed in any of the three experimental conditions, indicating that the regulation of Ucn II mRNA expression was site-specific. The results show a stressor-specific regulation of Ucn II mRNA expression in the PVN and raise the possibility that Ucn II mRNA plays a modulatory role in stress-induced alteration of anterior and posterior pituitary function, depending on the type of stress.

Adrenalectomy↗
PubMedDate not supplied

Cellular nuclear binding and retention of glucocorticoids in rat lymphoid cells: effect of long-term adrenalectomy.

In the present study we have shown for the first time that lymphocytes from the spleen, thymus and mesenteric lymph nodes can specifically bind and retain 3H-dexamethasone in the nuclear fraction. The use of the specific corticosteroid receptor antagonists, RU28362 and RU38486, for the displacement of labeled dexamethasone revealed that binding was mainly of type-II glucocorticoids receptors. In lymphocytes obtained from mesenteric lymph nodes, binding was significantly higher than in cells obtained from spleen and thymus. Long-term adrenalectomy (up to 30 days), which markedly elevated serum ACTH, caused a time-dependent increase in binding in all lymphoid cells. No increase in binding was found in lymphocytes obtained from rats hypophysectomized for 15 days, in which neither serum ACTH nor corticosterone could be measured. These results suggest that the cellular nuclear binding in lymphocytes may be regulated by a pituitary factor.

Adrenalectomy↗
PubMed1976

Effects of continuous light and darkness, and of pinealectomy, adrenalectomy and gonadectomy on uptake of 3H-serotonin by the suprachiasmatic nuclear region of male rats.

Rats exposed to continuous light show no significant differences in serotonin (5-HT) uptake by the suprachiasmatic nuclear region (SNR) at 10.00 and 22.00 L, while in continuous darkness, the uptake at 10.00 D is significantly higher than uptake at 22.00 D. In consideration of the role of the suprachiasmatic nucleus in light-mediated control of neuroendocrine activity, this suggests endogenous generation or control of this uptake rhythm. An effect of sham-pinealectomy in decreasing 5-HT uptake was found, but cannot be fully interpreted at this time. The lack of effect of castration or adrenalectomy suggests that these endocrines have little if any direct effect on 5-HT mechanisms in the SNR.

Adrenalectomy↗
PubMed1977

Pars intermedia ACTH and MSH content: effect of adrenalectomy, gonadectomy and a neurotropic (noise) stress.

Pars intermedia (PI) ACTH and melanocyte-stimulating hormone (MSH) content and pars distalis (PD) ACTH concentration were measured following 3 experimentally induced 'perturbations'. The feedback-induced increase in ACTH release following adrenalectomy is not accompanied by a change in PI ACTH and MSH contents, while the feedback-induced increase in gonadotropin secretion following gonadectomy is associated with significant changes in PI ACTH and MSH contents. A well-defined neurotropic (noise) stressor resulted in significant increases in PI ACTH and MSH. A striking finding in all of the studies was a positive correlation between PI ACTH and MSH contents. We conclude that PI ACTH and MSH secretion are altered with feedback-induced alterations in gonadotropin secretion and with neurotropic stressors.

Adrenal Glands↗
PubMed1978

Effect of adrenalectomy on temporal patterns of serum gonadotropin levels.

To determine whether adrenocortical function influences rhythmic gonadotropin patterns in male rats, blood samples were obtained by rapid decapitation from control and adrenalectomized male rats at 3-h intervals over a 24-h period (14 h light/day, 4 a.m.--6 p.m.). Control animals showed periodicity in serum LH, prolactin (Prl) and corticosterone similar to that reported previously. Peak and trough serum levels of corticosterone and Prl occurred at 5 p.m. and 8 a.m. respectively whereas those for LH occurred at 11 p.m. and 11 a.m. Serum FSH levels did not vary with circadian periodicity. 15 days after adrenalectomy, serum LH levels continued to fluctuate with a circadian periodicity but showed a marked phase shift; peak LH levels were observed at 8 a.m. The absence of adrenal hormones did not result in altered FSH levels nor was the phase of the Prl rhythm significantly altered.

Adrenal Cortex↗
PubMed1983

Quantitation of changes in the content of neurohypophyseal peptides in hypothalamic nuclei after adrenalectomy.

In adrenal insufficiency there is an increase in the content of vasopressin in the external zone of the median eminence as determined by immunohistology. We studied rats after bilateral adrenalectomy and obtained punched samples of the supraoptic, the paraventricular, and the suprachiasmatic nuclei, and from the median eminence and the posterior pituitary. Vasopressin, neurophysin and oxytocin were all decreased in content in the posterior pituitary but in the suprachiasmatic nucleus and in the median eminence there was a significant increase in the content of vasopressin. The increased levels of vasopressin in the median eminence are interpreted as representative of the content in axons and demonstrate a large increase of transport of vasopressin. In the SON and PVN there was no increase in the content of vasopressin during this state of augmented synthesis and transport, indicating that vasopressin moves rapidly from the site of synthesis into the transport system. The increased content of vasopressin in the suprachiasmatic nucleus shows that vasopressin at this level also varies with changes in adrenal function. Levels of oxytocin throughout the neurohypophysis did not change in parallel with vasopressin demonstrating relatively selective responses of the neurohypophyseal hormones.

Adrenalectomy↗
PubMed1986

Predominant release of vasopressin vs. corticotropin-releasing factor from the isolated median eminence after adrenalectomy.

In an in vitro system, we have demonstrated concomitant release of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) from the median eminence (ME) of normal and adrenalectomized rats. The ME were incubated in a Krebs-Ringer bicarbonate medium, CRF and AVP released into the medium were measured by radioimmunoassay. The release of both neuropeptides was stimulated by increasing concentrations of potassium (28-56 mM) in the incubation medium, or by addition of veratridine (5-20 microM). In both cases the release process was dependent on the presence of calcium in the incubation medium. Interestingly, potassium-induced release was found to be relatively insensitive to calcium channel antagonists that are potent inhibitors in smooth and cardiac muscle. The sodium channel antagonist, tetrodotoxin (1 microM), completely blocked the effect of veratridine, while no change was seen in the response to potassium. Adrenalectomy increased the ratio of AVP:CRF release from 2:1 in ME removed from sham-operated rats to 8:1 in ME from the adrenalectomized group. We suggest that this ratio of AVP:CRF release may also pertain in vivo, and that AVP could be the predominant corticotropic stimulus in adrenalectomized rats.

Adrenalectomy↗
PubMed1989

Study of the influence of stress and adrenalectomy on central and peripheral neuropeptide Y levels. Comparison with catecholamines.

Neuropeptide Y (NPY) is colocalized with catecholamines in brainstem-hypothalamus neuronal pathways implicated in the regulation of the hypothalamo-hypophyso-adrenocortical system (HHAS) and may interact with catecholamines in the regulation of neuroendocrine stress responses. On the other hand, the presence of corticosteroid receptors in these neurons suggests that adrenocortical hormones may regulate central NPY levels. NPY and biogenic amine levels were therefore measured in punched brain regions (ventrolateral and dorsomedial medulla, paraventricular and arcuate nucleus of the hypothalamus, frontal cortex) in basal conditions and up to 4 h after a 30-min period of restraint stress. Despite a massive activation of the HHAS (measured by plasma levels of ACTH and glucocorticoids), and a large increase of prolactin levels, no change of NPY levels could be found in any of the above-mentioned structures. The same parameters, as well as plasma levels of NPY and catecholamines and NPY levels in cardiac tissue were also measured 2, 20 and 96 h after adrenalectomy. Again, despite the large changes of brain and peripheral catecholamine levels, and the intense activation of the HHAS, no change of NPY levels was observed in any of the structures studied. These data question the nature of the relationships between NPY and neuroendocrine stress responses.

Adrenal Glands↗
PubMed1991

Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action.

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗
PubMed1991

Adrenalectomy and experimental hypercorticalism modulate the basal, corticotropin-releasing-hormone- and arginine-vasopressin-stimulated release of hypothalamic beta-endorphin.

Recent in vitro studies have shown that the release of hypothalamic beta-endorphin (beta-END), like that of adenohypophysial origin, is enhanced by both corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). However, whereas AVP merely synergizes with CRH in the pituitary, it seems to be essential for the release of hypothalamic beta-END by CRH. The present paper reports on the effects of long-term adrenalectomy (ADX) and subsequent replacement with supraphysiological doses of corticosterone (compound B, CB) upon the in vitro basal and CRH- and AVP-stimulated release of beta-END from the rat hypothalamus. Basal release of beta-END was significantly elevated by ADX, and returned to control levels following CB overdosage. Both ADX and CB replacement significantly reduced the stimulatory effect of CRH (10(-8) M) upon beta-END release. ADX caused no significant change in the AVP (10(-6) M)-induced release of beta-END. However, the AVP-stimulated release of beta-END was completely abolished in ADX rats treated with a high dose of CB. The hypothalamic content of beta-END was also measured following ADX and subsequent CB treatment. Compared with control tissues, those from ADX animals had significantly greater contents of beta-END; the hypothalami from rats with experimentally induced hypercorticalism had markedly reduced concentrations of the opioid peptide. Measurements of basal release and content of AVP in the hypothalamus following long-term ADX and CB treatment revealed that AVP neuronal activity is also subject to manipulations of the glucocorticoid hormone environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1992

Effects of adrenalectomy and glucocorticoids on rat brain dopamine receptors.

The effects of adrenalectomy (ADX) and dexamethasone (DEX) treatment on brain dopamine (DA) receptors of ovariectomized (OVX) rats were investigated by autoradiography using binding of the D1 and D2 antagonists ligands [3H]SCH 23390 and [3H]spiperone, respectively. Fourteen days after ADX, D1 receptors decreased in the middle striatum (M.CPu) and in the dorsal area of the posterior striatum (P.CPu). A more pronounced decrease was observed in the substantia nigra (SN) and no significant changes occurred in the anterior striatum (A.CPu), globus pallidus (GP) and accumbens (Acb). D2 receptors decreased in the M.CPu and dorsal area of the P.CPu and remained unchanged in the A.CPu as compared to OVX rats. Twenty-eight days after ADX, D1 and D2 receptors decreased in the A.CPu (D2), in the M.CPu (D2) and substantially in the SN (D1). DEX treatment (14 days, 0.5 mg/kg, b.i.d., IM, starting 14 days after ADX) reversed these effects in the A.CPu (D2), M.CPu (D2) and SN (D1) when compared to ADX+OVX rats. DEX also increased the density of D1 receptors in Acb, A.CPu and M.CPu when compared to OVX rats. Striatal homogenates of rats treated chronically with ACTH and corticosterone had an increased density of D1 receptors while these treatments alone left these receptors unchanged, thus suggesting either a minor role or no role of the changes in ACTH levels following glucocorticoids manipulations. Our results suggest that the adrenals play a role in the modulation of DA receptors activity in the rat brain.

Adrenalectomy↗
PubMed1992

Autoradiographic analyses of the effects of adrenalectomy and corticosterone on 5-HT1A and 5-HT1B receptors in the dorsal hippocampus and cortex of the rat.

Quantitative autoradiography was used to evaluate the effects of adrenalectomy (ADX) and corticosterone (CORT) on binding at 5-HT1A and 5-HT1B receptors in the dorsal hippocampus and cortex of the rat. ADX increased binding of [3H]8-hydroxy-2-(di-n-propylamino)tetralin at 5-HT1A receptors in the oriens and lacunosum moleculare layers of CA2 and CA3, in the lacunosum moleculare layer of CA4 region, and in the dentate gyrus. In restraint-stressed ADX rats, binding was increased only in the oriens and lacunosum moleculare layers of CA2. Restoration of baseline levels of CORT reversed the effects of ADX on 5-HT1A receptors in the hippocampus, while high levels of CORT decreased binding at 5-HT1A receptors in the dentate gyrus. No treatment affected binding at 5-HT1A receptors in the CA1 region of the hippocampus or in the cortex. ADX increased binding of [125I]iodocyanopindolol at 5-HT1B receptors in the infrapyramidal dentate, but this effect was not observed in ADX rats that were restrained. CORT treatment in both ADX and SHAM (adrenally intact) rats resulted in binding at 5-HT1B receptors that was lower than that in untreated ADX and SHAM rats in the infrapyramidal dentate, and lower than that in ADX rats in the suprapyramidal dentate and CA4. In ADX and SHAM rats, CORT also reduced binding at 5-HT1B receptors in area 2 of the cortex. It is suggested that decreases in binding at 5-HT1A and 5-HT1B/1D receptors resulting from chronic exposure to high levels of CORT may also occur in animals that fail to adapt to chronic severe stress. Such changes in binding may play important roles in the etiology of depression.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1993

Effects of adrenalectomy and hypertonic saline on neuropeptide Y content in the posterior pituitary of the rat.

We have examined the effects of adrenalectomy (ADX) on neuropeptide Y (NPY) content in the posterior pituitary of the rat. In rats given 2% saline to drink for 12 days, plasma osmolality increased to 343 +/- 18 compared to 291 +/- 5 mosm/kg in control animals on water (mean +/- SEM). Hypertonic saline treatment resulted in increased posterior pituitary NPY content measured by radioimmunoassay (2.42 +/- 0.36 ng) compared to the control group (1.18 +/- 0.16 ng). Total NPY immunoreactivity in tissue extracts coeluted with synthetic NPY(1-36) on reversed-phase high-performance liquid chromatography. In ADX rats given 2% saline to drink, plasma osmolality increased to 355 +/- 35 mosm/kg, but posterior pituitary NPY content was not different from the control group (1.41 +/- 0.11 ng). Immunohistochemical staining for NPY in the posterior pituitary also revealed a saline-induced increase in the number of NPY-immunoreactive nerve fibers, an increase which was not evident in the ADX group. No NPY immunoreactivity was observed in the intermediate zone. These results are the first evidence that the saline-induced increase in NPY in the posterior pituitary is under corticosteroid control.

Adrenalectomy↗
PubMed1994

Response of calcitonin-gene-related peptide-like immunoreactive nerve fibers of the anterior pituitary to adrenalectomy in the rat.

The mammalian anterior pituitary is known to be regulated by humoral factors only, no direct neural influence having ever been discovered. Our recent studies have shown in several species that there are substantial amounts of substance P and calcitonin-gene-related peptide-like immunoreactive (CGRP-LI) nerve fibers in the anterior pituitary and that they can make synaptic contacts with secretory cells, among which corticotropes. In the present study, we investigated changes in CGRP-LI nerve fibers of the anterior pituitary after bilateral adrenalectomy in the rat. The results show that the number of CGRP-LI nerve fibers increases significantly. In parallel, they cover a wider area of the gland after the operation, suggesting a direct neural influence.

Adrenalectomy↗
PubMed1996

Hippocampal long- and short-term potentiation is modulated by adrenalectomy and corticosterone.

The effect of acute corticosterone (CORT) treatment on elaboration of long-term potentiation (LTP) and short-term potentiation (STP) in intact and adrenalectomized rats was investigated. Both forms of synaptic plasticity were evaluated as fractional increases in population spike amplitude in dentate gyrus granule cells following brief, high-frequency stimulation of the medial perforant pathway in vivo. LTP was distinguished from STP by the magnitude and time course of population spike facilitation. Adrenalectomy resulted in profound reduction of LTP extent, without any significant effect upon STP. Replacement of glucocorticoid by a single injection of CORT to previously adrenalectomized rats restored LTP to control levels. When CORT was applied to intact subjects, it slightly, but significantly, impaired LTP development. No effect of CORT on STP induction and time course was found. Taken together, these results show that the modulation of synaptic efficiency in hippocampal dentate gyrus by circulating glucocorticoid depends on the form of plasticity examined. LTP was found to be more susceptible to the impairment induced by both high and low levels of glucocorticoid than STP.

Adrenalectomy↗
PubMed1997

Effect of adrenalectomy in kindled rats.

It has previously been observed that adrenalectomy (ADX) increases the amplitude of transient Ca currents in CA1 hippocampal neurons. In the present study, the effect of ADX on cellular properties of CA1 neurons was investigated under conditions that challenge the CA1 network, i.e. in fully kindled rats, 5-6 weeks after the last kindling session. At this time, adrenally intact kindled rats showed, in comparison to non-kindled controls, a reduced population spike amplitude evoked in the CA1 area by Schaffer/commissural fiber stimulation, an increased amplitude of low-threshold, transient Ca currents and a decrease of the high-threshold, sustained Ca currents. As observed before, ADX in non-kindled rats increased the amplitude of transient Ca currents while sustained Ca currents were not affected. In kindled rats, ADX did not increase the transient Ca current amplitude beyond the level reached by kindling alone. The kindling-induced reduction of the sustained Ca current was partly normalized after ADX. Field responses of kindled rats were not affected by ADX. These data support the view that lack of adrenal hormones does not exacerbate but, to some extent, normalizes the kindling-induced changes in cellular properties and network function of the CA1 area. The hormonal effects on kindling may be reciprocal in nature, since kindling, in turn, was found to affect the stress response and the corticosteroid receptor mRNA expression in the hippocampus.

Adrenal Glands↗