Adrenocorticotrophin secreting cells in the hypophysis of the brown spiny mouseMus platythrix (Bennett)

Adrenocorticotrophin secreting cells are identified in the hypophysis of the brown spiny mouseMus platythrix by conventional methods of light microscopy. Quantitative data showed that certain smaller acidophilic cells in thepars distalis, under conditions provoking their hypersecretion such as unilateral adrenalectomy and metopirone treatment, increase in number and size from the pre-existing corticotrophs. There is no evidence for the transmigration of these cells from the chromophobes, basophils or any other cell type. Thepars intermedia revealed two types of cells of which the type II cells are histochemically identical to adrenocorticotrophin secreting cells of thepars distalis     

Effects of adrenalectomy on hormone action on hepatic glucose metabolism. Impaired glucagon activation of glycogen phosphorylase in hepatocytes from adrenalectomized rats.

The effects of adrenalectomy on glucagon activation of liver glycogen phosphorylase and glycogenolysis were studied in isolated hepatocytes. Adrenalectomy resulted in reduced responsiveness of glycogenolysis and phosphorylase to glucagon activation. Stimulation of cAMP accumulation and cAMP-dependent protein kinase activity by glucagon was unaltered in cells from adrenalectomized rats. Adrenalectomy did not alter the proportion of type I and type II protein kinase isozymes in liver, whereas this was changed by fasting. Activation of phosphorylase kinase by glucagon was reduced in hepatocytes from adrenalectomized rats, although the half-maximal effective concentration of glucagon was unchanged. No difference in phosphorylase phosphatase activity between liver cells from control and adrenalectomized rats was detected. Glucagon-activated phosphorylase declined rapidly in hepatocytes from adrenalectomized rats, whereas the time course of cAMP increase in response to glucagon was normal. Addition of glucose (15 mM) rapidly inactivated glucagon-stimulated phosphorylase in both adrenalectomized and control rat hepatocytes. The inactivation by glucose was reversed by increasing glucagon concentration in cells from control rats, but was accelerated in cells from adrenalectomized rats. It is concluded that impaired activation of phosphorylase kinase contributes to the reduced glucagon stimulation of hepatic glycogenolysis in adrenalectomized rats. The possible role of changes in phosphorylase phosphatase is discussed.     

Identification des cellules hypophysaires sécrétant l'ACTH chez le rat

Résumé Dans le but d'identifier la cellule hypophysaire responsable de la sécrétion d'ACTH chez le rat, des études morphologiques, en microscopie optique et électronique, furent entreprises chez des animaux surrénalectomisés, c'est-à-dire dans des conditions où la sécrétion d'ACTH est spécifiquement augmentée. Le prélèvement des hypophyses fut effectué à des intervalles allant de 1 à 21 jours après surrénalectomie. Des hypophyses d'animaux surrénalectomisés et traités par la dexaméthasone, un inhibiteur de la secrétion d'ACTH, furent également étudiées. Il découle de ces expériences qu'un type cellulaire est stimulé en même temps que la sécrétion d'ACTH augmente. Cette cellule, hypertrophiée après surrénalectomie, possède une forme irrégulière et est très souvent en contact avec les cellules somatotropes; son ergastoplasme peu développé contraste avec un appareil de Golgi très important. Les granules secrétoires corticotropes ont un diamètre d'environ 200 m, sont peu abondants et disposés le long de la membrane cellulaire. Ces granules n'ont cependant pas été caractérisés en microscopie optique. L'administration de dexaméthasone provoque une régression spécifique de la cellule corticotrope ainsi qu'une accumulation des granules sécrétoires dans le cytoplasme. Chez l'animal intact, il devient possible d'identifier la cellule corticotrope qui possède les caractéristiques générales de la cellule stimulée, mais dont le cytoplasme et l'appareil de Golgi sont peu importants.

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Identification of the ACTH secreting cells in the rat pituitary

Summary In order to clarify the identity of the ACTH-secreting cells in the rat pituitary, morphological studies were performed in adrenalectomized rats which have a specific increase in ACTH secretion. Pituitaries were removed and fixed for both light and electron microscopy at different time intervals (1 to 21 days) after adrenalectomy. Pituitaries of adrenalectomized animals which received dexamethasone, a potent inhibitor of ACTH secretion, were also studied. In these experiments, it was found that a specific cell type was stimulated as ACTH secretion was increased. This cell, which became enlarged after adrenalectomy, is characterized by an irregular shape and frequent association with somatotropic cells. The rough endoplasmic reticulum was poorly developed in contrast to a prominent Golgi apparatus. The secretory granules of this corticotropic cell were about 200 m in diameter and located in a single row along the plasma membrane. By light microscopic examination, these secretory granules could not be clearly identified. Dexamethasone administration provoked a specific decrease in size of corticotrophic cells, as well as an accumulation of secretory granules. Identification of corticotrophic cells in control rats was facilitated by comparison with those of adrenalectomized rats. In both cases, the general appearance of this cell type was similar except for size difference. Also in the control animals the Golgi apparatus was less prominent than in adrenalectomized rats.

Boursier du Conseil de la Recherche Médicale du Québec.     

Effects of adrenalectomy on CRH regulation of ACTH release: adenylate cyclase activity, cyclic AMP-dependent protein kinase activity and ACTH release

Corticotropin releasing hormone (CRH) stimulation of ACTH release and cyclic AMP-mediated events involved in the control of ACTH release were compared in sham-operated and adrenalectomized rats. CRH-stimulated adenylate cyclase activity was decreased in pituitary homogenates from adrenalectomized animals. CRH-stimulated cyclic AMP accumulation was essentially abolished and CRH-stimulated cyclic AMP-dependent protein kinase (A-kinase) activity was decreased in freshly prepared anterior pituitary cells from adrenalectomized animals. Basal and CRH-stimulated ACTH release was elevated in these cells. Since ACTH release is increased in adrenalectomized rats despite the down regulation of CRH-linked pituitary mechanisms, we speculate that the site of action of disinhibition by corticosterone of ACTH release (or synthesis) following adrenalectomy is distal to the generation of cyclic AMP and/or that non-CRH mediated mechanisms assume a greater role in ACTH regulation following adrenalectomy.     

Glucose and ketone bodies production in hepatocytes isolated from fetuses at term--II. Effect of maternal adrenalectomy

Glucose and ketone bodies production has been studied in hepatocytes isolated from fetuses at term of fed and fasted adrenalectomized mothers. Maternal adrenalectomy diminishes the fetal liver weight. This effect is increased when the adrenalectomized pregnant rat is fasted for the last 2 days of gestation. Maternal adrenalectomy diminishes glucose production in hepatocytes isolated from fetuses at term. This diminution is markedly greater when the adrenalectomized pregnant rat is fasted for the last 48 hr of gestation. Maternal adrenalectomy diminishes ketone bodies production in hepatocytes isolated from fetuses at term.     

The permissive effects of glucocorticoid on hepatic gluconeogenesis. Glucagon stimulation of glucose-suppressed gluconeogenesis and inhibition of 6-phosphofructo-1-kinase in hepatocytes from fasted rats

Production of [14C]glucose from [14C]lactate in the perfused livers of 24-h fasted adrenalectomized rats was not stimulated by 1 nM glucagon but was significantly increased by 10 nM hormone. Crossover analysis of glycolytic intermediates in these livers revealed a significant reduction in glucagon action at site(s) between fructose 6-phosphate and fructose 1,6-bisphosphate as a result of adrenalectomy. Site(s) between pyruvate and P-enolpyruvate was not affected. In isolated hepatocytes, adrenalectomy reduced glucagon response in gluconeogenesis while not affecting glucagon inactivation of pyruvate kinase. A distinct lack of glucagon action on 6-phosphofructo-1-kinase activity was noted in these cells. When hepatocytes were incubated with 30 mM glucose, lactate gluconeogenesis was greatly stimulated by glucagon. A reduction in both sensitivity and responsiveness to the hormone in gluconeogenesis was seen in the adrenalectomized rat. These changes were well correlated with similar impairment in glucagon action on 6-phosphofructo-1-kinase activity and fructose 2,6-bisphosphate content in hepatocytes from adrenalectomized rats incubated with 30 mM glucose. These results suggest that adrenalectomy impaired the gluconeogenic action of glucagon in livers of fasted rats at the level of regulation of 6-phosphofructo-1-kinase and/or fructose 2,6-bisphosphate content.     

Adrenalectomy-induced alterations in glucagon binding and lipolysis in isolated rat adipocytes.

Adipocytes from adrenalectomized rats nearly lost their lipolytic response to glucagon concomitant with a 90% decrease in the number of glucagon receptors per cell. Quantitative analysis of the relation between amount of cell-bound glucagon and hormone-stimulated lipolysis revealed that the ability of the remaining 10% of glucagon receptors to induce lipolysis was not impaired. Binding of the beta-adrenergic antagonist [3H]dihydroalprenolol and maximal lipolysis induced by (-)-isoproterenol, (Bu)2cAMP, 3-isobutyl-1-methylxanthine, and adenosine deaminase were reduced only 10 to 20% after adrenalectomy. Furthermore, glucagon-stimulated cAMP production was greatly decreased in adrenalectomized animals, but isoproterenol-stimulated cAMP production was not. Hydrocortisone replacement in adrenalectomized rats only partially prevented the loss of glucagon receptors and glucagon effects on both cAMP production and lipolysis. These findings suggest that lipolytic cascade distal to hormone receptors was not greatly impaired in adipocytes after adrenalectomy and that the unresponsiveness of these cells to glucagon was mostly due to a marked reduction in the number of glucagon receptors.     

Evidence for a defect in the number of β-adrenergic receptors and in the adenylate cyclase responsiveness to guanine nucleotides in fat cells after adrenalectomy

Receptor binding studies (?)-[³H]dihydroalprenolol as the ligand revealed, in adrenalectomized rat fat cells, a 50% decrease in the number of β-adrenergic receptors. er cell with no change in the receptor affinity for this ligand. Adrenalectomy caused no change in the binding affinity for isoproterenol of both high affinity and low affinity populations of the β-adrenergic receptors. Guanine nucleotide sensitivity of the agonist binding to β-receptors was also unaltered by adrenalectomy. Adrenalectomy caused a 30–40% decrease in the maximal response of adenylate cyclase to (?)-isoproterenol only when guanine nucleotides were present in the assay, without altering the (?)-isoproterenol concentration giving half-maximal adenylate cyclase stimulation (K_act values). The maximal response of adenylate cyclase to Gpp(NH)p also was lower in adrenalectomized membranes, indicating a defect at the guanine nucleotide regulatory site. Removal of adenosine by addition of adenosine deaminase failed to reverse the decreased adenylate cyclase response to isoproterenol in adrenalectomized rats. However, in intact fat cells, in which cyclic AMP accumulation in response to isoproterenol was decreased by adrenalectomy, removal of adenosine almost completely corrected this defect. These results indicate that the observed changes in the number of β-adrenergic receptors and in the ability of guanine nucleotides to stimulate adenylate cyclase, though explaining the decreased adenylate cyclase responsiveness to catecholamines, do probably not contribute significantly to the mechanism by which adrenalectomy decreases the lipolytic responsiveness of adipocyte to catecholamines. In addition, this study also suggests that the increased sensitivity to adenosine of lipolysis reported in adipocytes from adrenalectomized rats may result from an action of adenosine at a post-adenylate cyclase step, possibly on the cyclic AMP phosphodiesterase.     

Metabolic and immunological responses associated with in vivo glucocorticoid depletion by adrenalectomy in mature Swiss albino rats

The study is undertaken to determine the effect of adrenal corticosteroid depletion after adrenalectomy on carbohydrate, protein and fat metabolism as well as maturation and functional efficacy of the immunocompetent cells. Beside biochemical and hematological parameters, whether in vivo glucocorticoid depletion has any modulatory effects on splenic macrophage responses to bacterial challenge with regards to intracellular killing, nitric oxide release and cellular integrity, were determined. Major findings of our study indicate that blood glucose, urea and total inorganic phosphate levels showed a time dependent increase in adrenalectomized rats compared to control. Total glycogen content in liver was decreased gradually due to adrenal corticosteroid insufficiency. Hematological parameters like hemoglobin concentration, hematocrit value, total leukocyte count and differential count were also found to increase in the adrenalectomized group with respect to intact group. From the functional study of immunocompetent cells, intracellular killing capacity of splenic macrophages recovered from control and adrenalectomized rats after 10 and 20 days of adrenalectomy showed no significant alteration; however, the function of splenic macrophages recovered from rats after 30 days of adrenalectomy showed altered response. Nitric oxide released from splenic macrophages of adrenalectomized rats was less than that of control animal even after stimulation with lipopolysaccharide. DNA fragmentation assay showed a lesser degree of fragmentation of splenic macrophages obtained from adrenalectomized rats indicating, apoptotic death of cells in this group decreases. Adrenal corticosteroid insufficiency due to adrenalectomy interferes with metabolic and hematopoietic functions and modulates the development and maintenance of normal immunitary status, which in turn influences the inflammatory response.     

Alterations in response of rat white adipocytes to insulin, noradrenaline, corticotropin and glucagon after adrenalectomy. Correction of these changes by adenosine deaminase.

1. Adipocytes isolated from rats 6--9 days after adrenalectomy had significantly increased sensitivity to insulin action against noradrenaline-stimulated lipolysis. In the presence of adenosine deaminase there was no significant difference in insulin sensitivity between cells from adrenalectomized and sham-operated rats. 2. Adipocytes from adrenalectomized rats had decreased lipolytic responses to all concentrations of noradrenaline and glucagon tested and a decreased lipolytic response to low but not high concentrations of corticotropin. There was no difference in lipolytic response to theophylline after adrenalectomy. Adenosine deaminase corrected the differences in response to noradrenaline and glucagon resulting from adrenalectomy. 3. In the presence of adenosine deaminase rates of lipolysis, after stimulation by high concentrations of noradrenaline, glucagon, corticotropin or theophylline, were the same in cells from adrenalectomized or sham-operated rats. 4. These findings and previously reported effects of adenosine and adrenalectomy on adipocyte function are discussed. It is proposed that changes in adipocyte hormone responsiveness after adrenalectomy may result from changes in adenosine metabolism or release.     

Role of the pituitary-adrenal system in mechanism regulating vascular permeability during stress

Disturbances of the microvascular permeability were studied by the "vascular labelling" technique during the immobilization stress of hypophysectomized and adrenalectomized rats. Animals with sham operations served as controls. As revealed, hypophysectomy and adrenalectomy caused disturbances of vascular permeability in the mesentery. Vascular permeability disturbances in the hypophysectomized and adrenalectomized rats under conditions of immobilization were more expressed than in the sham-operated animals. Removal of the pituitary and adrenal glands produced mast cell degranulation at the earlier immobilization period.     

Demonstration that corticotropin-releasing factor binding to rat peripheral tissues is modulated by glucocorticoid treatment in vivo and in vitro

In a recent study we reported the presence of specific binding sites for corticotropin-releasing factor (CRF) in peripheral tissues of the rat (Endocrinology, 116, 2151, 1985). The objective of this study was to determine if CRF binding to peripheral tissues was modified following adrenalectomy and glucocorticoid replacement therapy. Adult male rats were adrenalectomized and CRF binding to liver, spleen and testicular membranes was determined at 5, 7 or 14 days following adrenalectomy. An additional group of adrenalectomized rats received subcutaneous injections of dexamethasone (75 micrograms/day) for 14 days. Adrenalectomy of rats for 14 days increased CRF binding to liver, kidney, testis, spleen and ventral prostate by approximately 65%-125% above sham-control values. CRF binding to membrane preparations obtained from the pancreas of sham-operated rats was undetectable; however, adrenalectomy produced detectable CRF binding in this tissue. Adrenalectomy produced a time-related increase in CRF binding to ventral prostate, spleen and liver tissue. Administration of dexamethasone to adrenalectomized animals prevented increased CRF binding to peripheral tissues observed following adrenalectomy alone. In vitro dexamethasone treatment of prostatic or hepatic homogenates from adrenalectomized rats resulted in a dose-related decrease in CRF binding activity. However, similar in vitro treatment of prostatic or hepatic homogenate with progesterone exhibited no significant effects on CRF binding. Our results suggest that glucocorticoids may be a regulator of peripheral CRF receptors.     

Adrenalectomy affects pain behavior of rats after formalin injection

Stressful stimuli can activate the hypothalamo-pituitary-adrenal-axis and the endogenous opioid system. In addition, corticosterone and opioid release might cause analgesia. This rat study used adrenalectomy for corticosterone withdrawal and naloxone administration for opioid antagonism in order to study pain behavior and hypophyseal hormone release in the plasma after a formalin test. Twelve days before the formalin testing, male Sprague Dawley rats underwent adrenalectomy or sham-adrenalectomy, and non-operated rats were used as reference. The number of flinches and the duration of licking or biting behavior were measured during the early and late phase. In reference and sham-operated rats, injection of formalin 5% resulted in a marked pain behavior in the early and late phase with significant increases in ACTH and corticosterone plasma levels. In adrenalectomized rats, pain behavior was decreased during both phases. Naloxone, administered before the late phase, did not alter pain behavior in sham or reference rats, whereas in adrenalectomized rats pain reactivity returned to those levels observed in reference rats. Beta-endorphin plasma levels above the detection limit were more frequently found in adrenalectomized rats. Thyrotropin and prolactin levels were not different between studied groups. We speculate that the observed reduced pain behavior in adrenalectomized rats after formalin, is the result of an increased production of pro-opiomelanocortin, the pro-drug of both adrenocorticotrophic hormone and beta-endorphin.     

Effects of diabetes on glucose oxidation in rat aorta after hypophysectomy and adrenalectomy

The influence of diabetes, hypophysectomy and adrenalectomy on glucose oxidation in rat aorta was studied. Diabetes was induced in normal, adrenalectomized and hypophysectomized-cortisone substituted rats by streptozotocin (65 mg/kg body weight). The oxidation of glucose to CO2 was determined during incubation of rat aorta in vitro for 2-3 hours. The aortic glucose oxidation was reduced after hypophysectomy but was unaffected by adrenalectomy. After streptozotocin treatment the rise in blood glucose concentration was similar in normal, adrenalectomized and hypophysectomized-cortisone substituted rats. In shamoperated diabetic rats the aortic glucose oxidation was reduced after a diabetes duration of 4 days. In adrenalectomized diabetic rats the aortic glucose oxidation was not significantly affected after 4 days but was reduced after a diabetes duration of 14 days. When adrenalectomized diabetic rats were treated with hydrocortisone the aortic glucose oxidation was reduced after diabetes for 4 days. After incubation of normal rat aorta in vitro for 6 hours with cortisol (1 microgram/ml) in the incubation medium a decrease in the aortic glucose oxidation was found. Incubation of aorta with only growth hormone had no effect. These results suggest that cortisol is of importance for the lowered glucose oxidation in diabetic rat aorta.     

Adrenocorticotropic (ACTH) cells of rats after head irradiation.

The heads of intact rats and of rats 15 days after adrenalectomy were irradiated with 1200 R. Some of the adrenalectomized animals with irradiated heads were treated with 5 mg of deoxycorticosterone acetate. In adrenocorticotropic cells of adrenalectomized rats 15 and 30 days after irradiation, the decreased amount of the granular endoplasmic reticulum and the Golgi regression imply a considerably decreased protein synthesis. The finding of an increased number of granules and of granules larger than normal suggests that they are the result of slowed down transport and secretion of the products of these cells' activities. After head irradiation an increased number of degenerative cells was evident in the pituitary of both intact and adrenalectomized rats. The degree of the degenerative changes and the number of degenerative cells was higher 30 than 15 days after irradiation and both were decreased if the adrenalectomized rats were treated with deoxycorticosterone acetate.     

Structural alterations of the hippocampal formation of adrenalectomized rats: an unbiased stereological study

Previous studies have demonstrated that adrenalectomy rapidly induces cell death in hippocampal formation. However, these previous studies have involved only qualitative observations or biased estimates. Therefore, the selectivity of the effects of adrenalectomy and the magnitude of changes occurring, remain controversial. The present work employed unbiased stereological tools to examine the effects of adrenalectomy on the number of neurons in, and the volume of, the hippocampal formation. Male rats were adrenalectomized 15,30 or 120 days before sacrifice at 180 days of age. The total number of neurons in the somal layers and hilus of the hippocampal formation was estimated using the optical fractionator. The volume of the different layers of each subdivision in the hippocampal formation was determined according to the Cavalieri principle. A progressive reduction, reaching 43%, was found in the total number of granule cells. Adrenalectomized animals exhibited a reduction in the volume of all layers of the dentate gyrus. No other region of the hippocampal formation displayed significant cell loss or a reduction in volume. In addition, the main neuronal subpopulations of the dentate gyrus were also evaluated, and a reduction in the total number of GABA- and neuropeptide Y-immunoreactive neurons in the molecular and granule cell layers of adrenalectomized rats was found. No quantitative changes were observed in the hilus. To characterize the glial response to the neuronal degeneration, we estimated the total number of cells immunoreactive for glial fibrillary acidic protein in the dentate gyrus. Although no variation in the total number of glial cells was found, signs of astroglial activation were observed in the adrenalectomized group. The present data strengthen the evidence pointing to the critical role of corticosteroids in maintaining the structural integrity of the dentate gyrus.     

Behavioral effects of L-tryptophan and p-chlorophenylalanine after adrenalectomy or dexamethasone administration in rats

Effects of acute administration of L-tryptophan (L-TRP. 250.0 mg/kg, i.p.) on active avoidance conditioning and "open-field" behavior were studied in male rats after adrenalectomy of dexamethasone administration. L-TRP inhibited the acquisition and reproduction of active avoidance reaction in adrenalectomized and dexamethasone-treated rats. Moreover, L-TRP decreased horizontal locomotor activity and grooming behavior in the "open field" on adrenalectomized rats. On the contrary, p-CPA restored the active avoidance conditioning in adrenalectomized rats and rats with excess of glucocorticoids. Also, p-CPA increased the total locomotor activity and grooming behavior in the "open field" in adrenalectomized rats, but decreased horizontal locomotor activity and enhanced emotional reaction in dexamethasone-treated rats in the "open field".     

Corticosterone replacement restores normal morphological features to the hippocampal dendrites, axons and synapses of adrenalectomized rats

A thorough evaluation of hippocampal dendrites, axons and synaptic contacts has not been undertaken following prolonged periods of absence of corticosteroids despite the marked granule cell loss which occurs in the dentate gyrus of adrenalectomized rats. Thus, we have applied morphometric techniques to analyse the dendrites of granule and pyramidal cells, the mossy fiber system, and the number and morphology of synapses between the mossy fibers and the excrescences of CA3 pyramidal cells in rats submitted to different periods of adrenalectomy. In addition, to search for the presence of neuritic reorganisation in the hippocampal formation once normal corticosteroid levels were re-established, we incorporated in this study a group of rats replaced with corticosterone one month after adrenalectomy. The results obtained in adrenalectomized rats showed a striking impoverishment of the dendrites of surviving granule cells, subtle alterations in the apical dendritic arborization of CA3 pyramidal cells and no changes in the apical dendrites of CA1 pyramidal cells. In addition, in adrenalectomized rats there was a progressive reduction in the total number of synapses established between mossy fibers and CA3 pyramids, as a consequence of a reduction in the volume of the suprapyramidal part of the mossy fiber system, and profound changes in the morphology of mossy fiber terminals and CA3 dendritic excrescences. A remarkable reorganisation of neurites was found to occur following the administration of low doses of corticosterone, completely reversing the adrenalectomy-induced synaptic loss and partially restoring the morphology of hippocampal axons and dendrites. These plastic mechanisms provide a sound structural basis for the reversibility of cognitive deficits observed after corticosterone administration to adrenalectomized rats.     

Corticosterone regulates calbindin-D28k mRNA and protein levels in rat hippocampus

Corticosterone was administered to normal and bilaterally adrenalectomized rats (250-300 g), and hormonal regulation of brain calbindin-D28k (CaBP28k) levels was investigated by radioimmunoassay for CaBP28k protein and by slot and Northern blot analyses for CaBP28k mRNA. The specificity of the changes observed in CaBP28k mRNA levels was tested by reprobing blots with calmodulin and B-actin cDNAs. Rats were either adrenalectomized, adrenalectomized treated with corticosterone, intact, or intact treated with corticosterone. Chronic corticosterone administration (subcutaneous injection for 7 days, 10 mg/day) to normal intact rats significantly increased levels of CaBP28k immunoreactivity (43%) and mRNA (125%) in the hippocampus. Adrenalectomy (animals were killed 7 days after adrenalectomy) produced a significant decrease in hippocampal CaBP28k immunoreactivity (85%) and mRNA (80%) compared with intact controls. Immunocytochemical analysis of tissue sections inducated a marked depletion of CaBP28k immunoreactivity in the dentate gyrus of the hippocampus 2 weeks after adrenalectomy. When adrenalectomized rats were treated with corticosterone (10 mg/day for 7 days), CaBP28k protein and mRNA levels in hippocampus were restored to levels observed in intact controls. No changes in CaBP28k protein and mRNA in kidney, cerebellum, striatum, or cerebral cortex were noted in adrenalectomized rats or in intact rats treated with corticosterone when compared with controls, indicating the specificity of the effect on CaBP28k for the hippocampus. These studies present the first evidence of a regulator of CaBP28k gene expression in the brain.     

Influence of gonadotropins on adrenalectomy induced changes in the testis of albino mouse

Effects of adrenalectomy and administration of gonadotropins on cell counts of different cell types of spermatogenesis and morphology of the Leydig cells were studied in 30 day old mice. Adrenalectomy (duration, 12 days; age at autopsy 42 days) caused a significant decrease in the diameters of seminiferous tubules and Leydig cell nucleus and, cell counts of intermediate spermatogonia, round and elongated spermatids. Administration of FSH (75 micrograms/0.1 ml saline) + LH (25 micrograms/0.1 ml saline) everyday for 12 days to adrenalectomized mice restored testicular activity as revealed by significant increases in mean diameter of the Leydig cell nuclei and cell counts of intermediate spermatogonia and elongated spermatids over those of adrenalectomized mice. The results indicate that (i) testis of adrenalectomized mouse responds to gonadotropin treatment and (ii) impairment in gonadotropin secretion is possibly a major factor in inducing testicular regression following adrenalectomy.