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PubMed1992

Noradrenergic regulation of type-I and type-II corticosteroid receptors in amygdala and hypothalamus.

The effects of glucocorticoids on various brain functions including the negative feedback control of HPA axis are mediated by two types of receptor (type I or mineralocorticoid and type II or glucocorticoid) in the central nervous system. Furthermore, noradrenergic systems have been showed to stimulate the activity of hypothalamo-pituitary-adrenal (HPA) axis. The neural and receptor controls of HPA axis activity are generally thought to be independent. Although receptor numbers, especially type-II receptors, are thought to be regulated by circulating levels of corticosterone, they may also be under direct neural control. Thus, it may be suggested that these two types of control are functionally related and that noradrenergic systems may affect HPA axis activity either directly or indirectly via change in receptor characteristics. A major problem in the interpretation of studies examining neurotransmitter regulation of corticosteroid receptors is that the effects of drugs or brain lesions on receptors levels may be secondary to their effects on adrenocortical function. In order to demonstrate a neuronal control on corticosteroid receptors, we tested the effect of 6-hydroxydopamine lesion of noradrenergic systems in the pedunculus cerebellaris superior in adrenalectomized animals whose corticosterone levels were maintained within normal limits by corticosterone replacement implants. Both types of receptor were assayed in hypothalamus and amygdala. We show that: (1) corticosteroid receptors are influenced by noradrenergic systems; (2) this effect depends on the brain region and the receptor type. After the noradrenergic lesion type-I receptors were reduced in hypothalamus and amygdala, whereas type-II receptor were only increased in hypothalamus while receptor affinities were unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1994

Stimulation of the hypothalamus initiates the urethrogenital reflex in male rats.

The urethrogenital (UG) reflex is a spinal sexual reflex which is tonically inhibited in the intact male rat by neurons in the nucleus paragigantocellularis (nPGi). The medial preoptic area of the hypothalamus (MPOA) is involved in the activation of male sexual behavior. The present study examines the effect of hypothalamic stimulation on the UG reflex in the intact male rat. Areas of the hypothalamus were stimulated bilaterally with either electrical stimulation or D,L-homocysteic acid (DLH) and the presence of the UG reflex examined. Stimulation of discrete aras of the hypothalamus evoked the UG reflex. The UG reflex could be initiated in the absence of genital stimulation. Microinjections of DLH into the MPOA also initiate the UG reflex. These data suggest that stimulation of neurons in the MPOA overcome the inhibition by the nPGi and facilitate spinal genital reflexes leading to ejaculation.

Animals↗
PubMed1994

Aromatase-immunoreactivity is localised specifically in neurones in the developing mouse hypothalamus and cortex.

Local formation of oestrogens from androgens by aromatase cytochrome P-450 within brain cells is crucial for the sexual differentiation of the mammalian CNS. Aromatase activity has been detected in several brain regions of the developing rodent brain. In the present study, we used a mouse-specific, peptide-generated, polyclonal aromatase antibody to determine whether neurones and/or glial cells in the developing brain are involved in androgen aromatization and if aromatase-immunoreactive (Arom-IR) cells exhibit a sex-specific distribution and regional-specific morphological characteristics. For these experiments, gender-specific cell cultures were prepared from embryonic day 15 mouse hypothalamus and cortex. Specificity of the immunoreaction was confirmed by Western-blot analysis and by inhibition of aromatase activity using tissue homogenates from mouse ovaries and male newborn hypothalamus and from male hypothalamic cultures with known aromatase activity, respectively. Arom-IR cells were found in both hypothalamic and cortical cultures. Double-labeling experiments revealed that Arom-IR cells co-stained only for the neuronal marker MAP II, but never for glial markers. Therefore aromatase immunoreactivity is specifically neuronal. Regional differences in the morphology of Arom-IR neurones were observed between both brain regions. In hypothalamic cultures, IR-neurones represented a heterologous population of phenotypes (magnocellular, small bipolar and multipolar neurones with long processes showing varicose-like structures or without processes). Cortical Arom-IR neurones were always oval in shape with short or no IR-processes. Sexual dimorphisms in numbers of Arom-IR neurones were found in the hypothalamus with significantly higher cell numbers in male cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Modulation of prolactin receptors in the rat hypothalamus in response to changes in serum concentration of endogenous prolactin or to ovine prolactin administration.

Specific binding of 125I-labeled rat prolactin (125I-rat PRL) to hypothalamic membranes was studied in Sprague-Dawley rats after ovine PRL administration and in relation to rat PRL serum variations induced by ectopic pituitary implants or by drugs which stimulate (domperidone) or inhibit (bromocriptine) PRL release. Repeated treatments with ovine PRL markedly increased specific binding values of 125I-rat PRL to hypothalamic membranes of female rats. Repeated treatments with domperidone also increased specific PRL binding in the hypothalamus. This effect was associated with an increase in PRL serum levels. Similar results were obtained in male rats after renal pituitary implants which resulted in a state of chronic hyperprolactinaemia. In contrast, a subchronic treatment with bromocriptine decreased specific PRL binding in the hypothalamus and concomitantly caused a sharp reduction in PRL serum levels. Scatchard analysis of data obtained from competition curves showed that the variations in the level of PRL binding to hypothalamic membranes were related to the number of PRL binding sites but not to the dissociation constant (Kd), which was unaffected by different treatments or by pituitary implantation. These results demonstrate a correlation between circulating concentrations of PRL and number of its receptors in the rat hypothalamus and give further support to the hypothesis that these binding sites may have a specific functional role in regulating the homeostasis of pituitary PRL secretion.

Animals↗
PubMed1995

Photoperiod affects the expression of neural cell adhesion molecule and polysialic acid in the hypothalamus of the Siberian hamster.

Immunohistochemical and immunoblot procedures were used to examine the effects of inhibitory short day (SD) photoperiod on the expression of neural cell adhesion molecule (NCAM) and its polysialylated form (PSA-NCAM) in the hypothalamus and preoptic area (POA) of the adult male Siberian hamster. In animals that had undergone SD-induced gonadal regression, immunoblot analyses revealed significant reductions in the content of immunoreactive PSA in anterior hypothalamic (AH) and mediobasal hypothalamic (MBH) regions. These changes were accompanied by increased contents of the 180 kDa NCAM isoform in the POA and AH, and decreased content in the MBH. The 140 kDa NCAM isoform also was elevated in the AH. Light microscopic analysis revealed a marked reduction in the density of NCAM-immunoreactive tanycyte-like processes in the MBH of animals exposed to SD. This effect was not blocked by castration, indicating that this may be a primay (sex steroid-independent) effect of altered photoperiod in the hypothalamus. Also, photoperiod-induced alterations in NCAM expression were not evident in non-responsive hamsters that maintained active testes under SD exposure. Collectively, these results are evidence that seasonal changes in photoperiod affect the expression of NCAM and PSA in the hypothalamus. Such changes could help promote plastic morphological rearrangements related to the regulation of seasonal reproductive and/or metabolic cycles.

Analysis of Variance↗
PubMed1996

Survival and regeneration of neurons of the supraoptic nucleus following surgical transection of neurohypophysial axons depend on the existence of collateral projections of these neurons to the dorsolateral hypothalamus.

The aim of the present study was to compare the postlesional responses of vasopressin-producing (VP) and oxytocin-producing (OT) neurons of the supraoptic nucleus (SON) to transection of neurohypophysial axons. At different times after sectioning the median eminence of adult rats, immunocytochemical staining of both types of neuronal cell bodies and axons indicated that: (1) the number of OT neurons detected within the SON was only slightly decreased as compared with controls (-20%), whereas the number of VP neurons was severely decreased (-60%); and (2) the large majority of axonal sprouts that regenerated into the external layer of the median eminence were OT neurohypophysial axons. The injection of a retrograde tracer into various areas surrounding the SON further showed that numerous SON neurons could be retrogradely labeled when the injection was centered in the lateral hypothalamus dorsal to the SON. The immunocytochemical identification of these retrogradely labeled neurons demonstrated that most of them were OT neurons. When animals were subjected to median eminence transection and to a unilateral surgical cut placed in the lateral hypothalamus above the SON, the survival of both OT and VP neurons was dramatically reduced in the SON ipsilateral to the hypothalamic lesion, as compared to the contralateral SON. Taken together, these data indicate that OT (and to a lesser extent VP) neurons of the SON display collateral projections towards the lateral hypothalamus that protect them from retrograde degeneration following the lesion of their neurohypophysial projections.

Animals↗
PubMed1996

Pyroglutamyl peptidase I levels and their left-right distribution in the rat retina and hypothalamus are influenced by light-dark conditions.

To evaluate the effects of light and darkness on pyroglutamyl peptidase I activity (pGluPI) and its left-right distribution, pGluPI was measured bilaterally in the retina and hypothalamus under selected light-dark schedules. Rats under a 12 h light-dark cycle were divided into four experimental groups. After the end of the 12 h dark period, the animals were kept two additional hours in darkness (group 1), or light (group 2). After the end of the 12 h light period, the animals were kept two additional hours in darkness (group 3), or light (group 4). Experiments were done in light or darkness depending on the 2 h period. In the retina, a previous 12 h light period led to higher values of enzyme activity than dark periods. Left-right predominance, however, depended on the previous 2 h period: the light period led to left predominance, whereas right predominance was found after the 2 h dark period. In the hypothalamus, a left predominance was found only in group 3. These results demonstrate that environmental light conditions influence pGluPI activity in the rat retina and hypothalamus.

Adaptation, Ocular↗
PubMed1985

The effect of acute ethanol administration on GABA receptor binding in cerebellum and hypothalamus.

The effect of the intraperitoneal administration of ethanol on [3H]GABA binding and glutamic acid decarboxylase (GAD) in cerebellum and hypothalamus was investigated. Acute ethanol administration produced an increase in the binding capacity of the high affinity GABA binding sites and a decrease in the binding capacity of low affinity sites. A decrease in the binding capacity of the high affinity GABA binding sites and an increase in the binding capacity of the low affinity sites were observed in the hypothalamus. No apparent changes were detected in the binding affinities for the two types of GABA receptor sites in both brain areas following ethanol treatment. Ethanol enhanced GAD activity in the cerebellum and reduced GAD activity in the hypothalamus. Changes in GABA binding may be involved in some of the neuropharmacological effects of ethanol.

Animals↗
PubMed1987

Neural mechanisms mediating the hyperthermia elicited by prostaglandin E2 injected into the preoptic-anterior hypothalamus.

The neuromechanism mediating the hyperthermia induced by injection of PGE2 into the preoptic/anterior hypothalamus (PO/AH) was investigated in the rat. Pretreatment of rats with intraperitoneal injection of atropine sulfate blocked, whereas pretreatment with atropine methyl bromide had no significant effect on the hyperthermia. In a second series of experiments, atropine sulfate was microinjected into different regions of the hypothalamus and the thalamus in an attempt to locate the central cholinergic synapses involved in the PGE2-induced hyperthermia. The hyperthermia was blocked by atropine injection into the dorsal/dorsomedial hypothalamic area (DH), but was not significantly affected by injection into the PO/AH, ventromedial hypothalamus, or the thalamic area above the DH. Moreover, microinjection of the cholinergic agonist carbachol (0.5 microgram) into the DH could also elicit hyperthermia. Thus, our data suggest that the hyperthermia induced by PGE2 administration into the PO/AH is mediated by a cholinergic mechanism in the DH.

Animals↗
PubMed1993

Taurine release in the hypothalamus is altered by blood pressure changes and neuroactive drugs.

The release of endogenous taurine was determined in the posterior hypothalamus of the conscious, freely moving rat by using the push-pull superfusion technique. At the start of superfusion, the outflow of endogenous taurine declined rapidly with a half-time of 7.9 min and reached a steady state after approximately 1 h. Thereafter, the release rate was constant and amounted to 2.6 +/- 0.3 pmol/min. During depolarization either with K+ (50 or 90 mM) or veratridine (1 or 10 microM), taurine outflow was increased in a concentration-dependent way. Hypothalamic superfusion with tetrodotoxin (1 microM) elicited a sustained decrease in the taurine release to 60% of the control values. Intravenous infusion of noradrenaline led to a rise in blood pressure (45 mm Hg) and enhanced the release of taurine in the hypothalamus. A fall of blood pressure (30 mm Hg) caused by an intravenous infusion of nitroprusside diminished taurine outflow. The results suggest that a considerable amount of the taurine detected is released from hypothalamic neurons. Changes in the release rate of taurine by experimentally induced alterations of blood pressure indicate that, in the posterior hypothalamus, the amino acid might play an important role as a neurotransmitter or neuromodulator possessing a hypotensive function.

Animals↗
PubMed1995

Serotonin outflow in the hypothalamus of conscious rats: origin and possible involvement in cardiovascular control.

The push-pull technique was used to investigate the effects of neuroactive compounds and experimentally induced blood pressure changes on the release of endogenous serotonin in the posterior hypothalamic area of the rat. Hypothalamic superfusion with artificial cerebrospinal fluid which contained 80 mM K+ or 1 microM veratridine enhanced the rate of serotonin release. Superfusion with tetrodotoxin (5 microM) led to a pronounced decrease in the serotonin release rate. Increases in blood pressure elicited by intravenous infusions of noradrenaline (3-4 micro g/kg/min) or phenylephrine (10 microg/kg/min) enhanced the release of serotonin in the hypothalamus. Similarly, the serotonin release rate was enhanced by hypervolaemia. Decreases in blood pressure elicited by intravenous administration of nitroprusside (30-40 microg/kg/min) or chlorisondamine (3 mg/kg) reduced the release of serotonin. Likewise, the serotonin release rate was decreased by hypovolaemia. With one exception (hypothalamic superfusion with tetrodotoxin) neither neuroactive drugs, nor experimentally elicited blood pressure changes modified the release rate of the metabolite 5-hydroxyindoleacetic acid (5-HIAA). These findings show that changes in blood pressure lead to counteractive alterations in the release of serotonin. Thus, serotoninergic neurons of the posterior hypothalamus seem to be involved in the homeostasis of blood pressure by exerting a hypotensive function. At least in the hypothalamus, the concentration of 5-HIAA in the superfusate does not seem to be a reliable marker for the activity of serotoninergic neurons.

Animals↗
PubMed1984

Immunological detection of pro-corticotropin releasing factor (CRF) in rat hypothalamus and pancreatic extracts. Evidence for in vitro conversion into CRF.

Extracts of both rat hypothalamus and pancreas were analyzed for their corticotropin releasing factor (CRF)-like immunoreactivity by radioimmunoassay (RIA). In the case of the hypothalamus, besides the rat CRF, further identified by high-pressure liquid chromatography (HPLC), two peptide components, a 20-kDa and a 10-kDa species were detected. The 20-kDa component was stable under acidic pH conditions and was further purified by reverse-phase HPLC. When exposed to proteolytic activities coeluting with 'high-molecular-mass CRF' at pH 6, processing was observed and the CRF generated was identified both by RIA, molecular sieve filtration and HPLC under different experimental conditions. It is concluded that this 20-kDa CRF may represent the CRF precursor and that hypothalamic extracts may contain processing enzymes involved in its selective post-translational cleavage. In the pancreatic extract two immunoreactive forms of CRF were detected, the smaller coeluting with the rat CRF and the other corresponding to the intermediate 10-kDa component detected in the hypothalamus. Pancreatic rat CRF, analyzed using RIA both by molecular sieve filtration and HPLC, was indistinguishable from the hypothalamic rat CRF.

Animals↗
PubMed1987

Regional distribution of leukotriene and mono-hydroxyeicosatetraenoic acid production in the rat brain. Highest leukotriene C4 formation in the hypothalamus.

The regional distribution of ionophore A23187-induced synthesis of leukotrienes and mono-hydroxyeicosatetraenoic acids in the rat brain in vitro was investigated. Pronounced differences in leukotriene C4 formation were observed, with the highest synthetic capacity in the hypothalamus. The formation of leukotriene C4 was about 12-times higher in the hypothalamus as compared to the cerebellum. This finding is in agreement with a possible neuroendocrine role for leukotriene C4. In contrast, the activity of leukotriene B4 synthesis was widely distributed without pronounced regional differences in the rat brain. Formation of 5-, 9-, 11-, 12- and 15-monohydroxyeicosatetraeonoic acid was detected in all regions. The major lipoxygenase product in the hypothalamus and thalamus was 5-hydroxyeicosatetraenoic acid, while other monohydroxyeicosatetraenoic acids predominated in the remaining regions tested.

Animals↗
PubMed1983

Immunological characterization of endorphins, adrenocorticotropin, and melanotropins in frog hypothalamus.

To gain more information about the nature and regulation of opiomelanocorticotropic peptides in the frog diencephalon, radioimmunological determinations of alpha- and beta-MSH. ACTH, beta- and gamma-endorphins have been performed in hypothalamic extracts. Sephadex G-50 gel filtration revealed a single peak of alpha-MSH-like immunoreactivity (alpha-MSH-LI) comigrating with synthetic alpha-MSH. Two peaks of ACTH-LI were observed; the major one eluting slightly before human ACTH. Using a porcine beta-endorphin antiserum which exhibited 45% cross-reaction (on a molar basis) with ovine beta-LPH, one major peak of beta-endorphin-LI and two additional components were observed in the elution profile; none of these peaks coeluted with synthetic porcine beta-endorphin. No significant beta-MSH or gamma-endorphin-LI was detected. To investigate a possible role of glucocorticoids on the level of opiomelanocorticotropic peptides in frog hypothalamus, 60 male frogs were treated with dexamethasone (300 micrograms/day) during 8 days. Dexamethasone treatment did not modify the chromatographic distribution and the total amount of alpha-MSH-LI and ACTH-LI in hypothalamic extracts. A slight (15%) increase in beta-endorphin-LI was even observed after 8 days of dexamethasone treatment. From these results it is concluded that three classes of opiomelanocorticotropic peptides are present in the frog hypothalamus in the following order of concentration: beta-endorphin-LI greater than alpha-MSH greater than ACTH. In addition, circulating glucocorticoids which significantly reduce the concentration of opiomelanocorticotropic hormones in the distal lobe of the frog pituitary (S. Jégou, M. C. Tonon, F. Leboulenger, C. Delarue, J. Côté, G. Pelletier, and H. Vaudry (1981a). In "Adv. Physiol. Sci.' E. Stark, G. B. Makara, Zs. Acs, and E. Endröczi, eds., Vol. 13, pp. 129-133. Pergamon, Budapest.) do not modify the amount of these peptides in the hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1988

Hypothalamus-hypophysis and testicular GnRH control of gonadal activity in the frog, Rana esculenta: seasonal GnRH profiles and annual variations of in vitro androgen output by pituitary-stimulated testes.

The binding of a gonadotrophin-releasing hormone (GnRH) long acting analog (GnRHA), D-Ser (But)6,Pro9-NEt GnRH (HOE 766), to pituitary and testicular extracts and the presence of GnRH-like material in testes and hypothalamuses were measured in the frog, Rana esculenta. Also, the cellular localization of immunoreactive GnRH was investigated in testes by immunohistochemical staining. Furthermore, lyophilized preparations of pituitary crude homogenates from animals caught monthly were tested in vitro for their ability to stimulate androgen production by December testes. Satisfactory results on specific 125I-GnRH binding were difficult to obtain in view of its low binding capacity. Moreover, binding in testicular homogenates was of the same order of magnitude (about 2%) as that found in pituitaries. In a cospecific radioimmunoassay for GnRH nonapeptide, both hypothalamic and testicular extracts gave displacement parallel to the standard curve. Immunoreactive GnRH did not significantly fluctuate in hypothalamuses, while it peaked in testes during December and July. Immunoreactive GnRH was evidenced in June and September testes employing immunohistochemical staining. In particular, the interstitial cells and the Sertoli cells were faintly stained. Testes of December animals stimulated by February pituitaries produced larger quantities of androgens as compared with testes stimulated with hypophyseal preparations from the remaining periods of the year. In conclusion, the present results are consistent with the idea that seasonal changes of the hypothalamus-hypophyseal activity play an important role in regulating the hormonal response in vertebrate testes. Moreover, we report that, in addition to rats, GnRH-like material is present in frog testes and for the first time it has been shown that such putative intratesticular material undergoes seasonal fluctuations in a vertebrate.

Androgens↗
PubMed1984

Growth hormone releasing effect of hpGRF-40 in rats at different time intervals following ablation of the mediobasal hypothalamus.

We have investigated the effect of hypothalamo-pituitary disconnection in the rat on the growth hormone (GH) responsiveness to human pancreatic GH-releasing factor (hpGRF). Adult female rats, sham-operated (sham-op) or bearing a complete mechanical ablation of the mediobasal hypothalamus (MBH-A) were challenged, while under urethane anesthesia, with hpGRF-40 (20,100,500 ng/rat i.v.) at different time intervals after surgery. In sham-op rats only 500 ng/rat of hpGRF-40 stimulated GH release, while in 1-and 7-day MBH-A rats the stimulation also occurred with the lower hpGRF doses and the rise in plasma GH was greater than in sham-op controls. Twenty-one and 42 days after the placing of the lesions the GH response to hpGRF-40 was still present at the 500 ng/rat dose, though it was smaller than in sham-op controls. Evaluation of pituitary GH content demonstrated a progressive and rapid decline starting the first day after the placing of the lesions. These data indicate that GH responsiveness to hpGRF is: enhanced in the anterior pituitary shortly after hypothalamo-pituitary disconnection and, despite a striking reduction of the pituitary GH stores, it is maintained after these lesions. The physiologic growth hormone (GH) releaser in the rat is GH-releasing factor and, recently, a group of peptides has been characterized from human pancreatic tumors (hpGRFs) (1,2) which are potent and specific GH-releasers in both animals and man. The availability of these peptides, which show a high degree of homology with the physiologic rat hypothalamic GRF, offers the unique opportunity to assess somatotrope responsiveness to GRF molecules in rats with hypothalamo-pituitary disconnection. In this study we have first evaluated the GH pituitary responsiveness to increasing doses of hpGRF-40 in rats following mechanical ablation of the medio-basal hypothalamus. These rats, by definition, lack the effect of both central nervous system (CNS) inhibitory (e.g. somatostatin) and stimulatory (e.g. GRF) influences to GH release. With the aim to ascertain how the lack of these two opposing inputs reflects on the secretory capacity of the somatotropes, we also investigated the GH response to hpGRF-40 at different time intervals after the lesioning. In a study in rats with electrolytic lesions of the ventromedial-arcuate region of the hypothalamus Tannenbaum et al had shown persistence of the GH response to huge doses of a hpGRF analog.

Animals↗
PubMed1986

Effects of opioid peptides on immunoreactive corticotropin-releasing factor release from the rat hypothalamus in vitro.

Effects of opioid peptides on immunoreactive corticotropin-releasing factor (I-CRF) release from the rat hypothalamus were examined using a rat hypothalamic perifusion system and a rat CRF RIA in vitro. beta-Endorphin (0.3 - 30 nM), dynorphin (0.3 - 30 nM) and FK 33-824 (1 - 10 microM) suppressed basal I-CRF release in a dose-dependent fashion. At 2.2 nM concentrations of these peptides, mean percent inhibition was 56% for beta-endorphin; less than 5% for alpha-endorphin; 44% for dynorphin; 23% for leucine-enkephalin; 6% for methionine-enkephalin; less than 5% for FK 33-824; and less than 5% for D-ala2, D-leu5-enkephalin. The inhibitory effects of beta-endorphin and enkephalins were completely blocked by naloxone, but those of dynorphin were only partially blocked. These results suggest that opioid peptides act through opioid receptors and inhibit I-CRF release from the hypothalamus under our conditions. Therefore, endogenious opioid peptides may have a physiological role in the CRF-releasing mechanism of the hypothalamus.

Animals↗
PubMed1989

Effect of ethanol on androgen receptors in the anterior pituitary, hypothalamus and brain cortex in rats.

The purpose of this study was to investigate ethanol-induced changes in androgen receptor sites in the anterior pituitary, hypothalamus, and brain cortex. Young adult male King-Holtzman rats were fed for 5 months a nutritionally complete liquid diet, with ethanol or isocaloric sucrose constituting 36% of the total calories. Androgen receptor sites were measured by sucrose density gradient and charcoal assay using tritiated dihydrotestosterone (DHT). Scatchard plot analysis of the data revealed that apparent dissociation constants of DHT-receptor complex for the anterior pituitary, hypothalamus, and brain cortex from alcohol-fed animals were estimated to be 0.7 +/- 0.13, 0.6 +/- 0.16 and 0.9 +/- 0.15 nM, respectively. These values are identical to those of their isocaloric controls. The concentrations of cytosol androgen receptors of the pituitary, hypothalamus, and brain cortex from alcohol-fed rats were 8.0 +/- 1.2, 6.2 +/- 1.0 and 4.9 +/- 0.7 fmol/mg protein, respectively. This represents about a 34, 24, and 22% reduction when compared to the values of the isocaloric control animals. In contrast to control rats, neither castration nor androgen or LHRH replacement to castrated alcohol-fed rats altered an alcohol-induced reduction of androgen receptor contents. Serum LH and testosterone levels were significantly decreased in alcohol-fed rats but these hormone levels were increased by administration of LHRH or norepinephrine. Such reduction of androgen receptors, serum LH and testosterone, but enhancement of these hormone levels by treatment with neurohormone and neurotransmitter in these animals suggests that ethanol exerts an adverse effect on the hypothalamic-pituitary unit and the neurotransmitter-hypothalamic hormone relationship, resulting in impairment of the androgen-induced sexual events and a suppression of the pituitary gonadotropin secretion.

Androgens↗