Showing papers on "Hypothalamus published in 1985"
TL;DR: The powerful stimulation of feeding elicited by this neuropeptide suggests an important role for hypothalamic NPY, or a structurally related peptide, in the regulation of feeding behavior.
Abstract: Neuropeptide Y (NPY) was injected directly into the paraventricular nucleus of the hypothalamus (PVN) of satiated, brain-cannulated rats, and food and water intake were measured 0.5, 1, 2, 4, and 22 hr postinjection. NPY (24, 78, 235, 783, and 2351 pmol/0.3 mul) produced a large, dose-dependent increase in food intake as well as small increase in water intake. The latency to eat was about 10 min, with substantial feeding occurring in the first 30 min. At dose below 78 pmol, the eating generally occurred only within the first hour. At doses above 235 pmol, however, the subjects' food intake continued to increase such that by 4 hr postinjection they had consumed the equivalent of normal 22-hr intake, and 22 hr postinjection they had also eaten significantly more than control subjects. Previous studies have shown that norepinephrine injected into the PVN stimulates feeding through alpha-adrenergic receptors. To investigate a possible interaction, subjects were given PVN injections of phentolamine (60 nmol) prior to injections of either NPY (78 pmol) or norepinephrine (20 nmol). Phentolamine pretreatment significantly decreased feeding elicited by norepinephrine without affecting feeding elicited by NPY. This suggests that NPY does not stimulate feeding through the release of endogenous norepinephrine. The powerful stimulation of feeding elicited by this neuropeptide suggests an important role for hypothalamic NPY, or a structurally related peptide, in the regulation of feeding behavior.
737 citations
TL;DR: A feminization of the liver develops after continuous, but not intermittent, administration of GH to hypophysectomized rats, suggesting that high, infrequent GH pulses with low plasma GH levels in between promotes growth more effectively than an intermediate, rather constant level of plasma GH.
Abstract: THE CLASSICAL CONCEPT of neuroendocrine control of the pituitary as proposed by Harris stipulates that the endocrine functions of the anterior pituitary are controlled by hypothalamic releasing factors or release-inhibiting factors. It was postulated that these factors are present in hypothalamic neurons which project into the median eminence (ME) of the basal hypothalamus and end in contact with the hypothalamic-hypophyseal portal vessels (1). It has subsequently been shown that growth hormone (GH) secretion is regulated by both stimulatory and inhibitory factors of hypothalamic origin. Like other anterior pituitary hormones, GH is secreted episodically. In all mammalian species so far studied spontaneous episodes of GH secretion occur several times over a 24-h period (2–8). Particularly in the adult male rat there is a striking regularity in the GH pulses which occur at 3- to 4-h intervals and reach levels of several hundred ng/ml.
715 citations
TL;DR: The localization of the GA-like immunoreactivity in the locus coeruleus suggests a partial coexistence with catecholaminergic neurons as well as a possible involvement of theGA-like peptide in a neuroregulatory role.
642 citations
Journal Article•
541 citations
TL;DR: An immunocytochemical analysis with 33 antisera was undertaken to investigate the localization of 25 different neurotransmitter-related antigens in the hypothalamic suprachiasmatic nucleus in the rat, suggesting that dopamine, norepinephrine and epinephrine may occur in a limited number of axons in the nucleus.
537 citations
TL;DR: These data illustrate the physiological independence of MAO A and B and show that neurons may be specialized for their degradative as well as their synthetic functions.
Abstract: Monoclonal antibodies specific for monoamine oxidase (MAO) A and MAO B, respectively, were used to localize these enzymes in primate brain. The reagents recognized different populations of neurons: those that recognized MAO A were located in cell groups containing catecholamines, including the substantia nigra, nucleus locus coeruleus, nucleus subcoeruleus, and the periventricular region of the hypothalamus, whereas those that recognized MAO B were observed in serotonin regions, including the nucleus raphe dorsalis and nucleus centralis superior. These data illustrate the physiological independence of MAO A and B and show that neurons may be specialized for their degradative as well as their synthetic functions.
496 citations
TL;DR: A sexually dimorphic cell group is described in the preoptic area of the human hypothalamus, located within an area that is essential for gonadotropin release and sexual behavior in other mammals.
Abstract: A sexually dimorphic cell group is described in the preoptic area of the human hypothalamus. Morphometric analysis revealed that the volume of this nucleus is 2.5 +/- 0.6 times (mean +/- standard error of the mean) as large in men as in women, and contains 2.2 +/- 0.5 times as many cells. Between the ages of 10 and 93 years, the nucleus decreases greatly in volume and in cell number. Although no function has yet been established for this nucleus, it is located within an area that is essential for gonadotropin release and sexual behavior in other mammals.
495 citations
TL;DR: High affinity and pharmacologically specific receptor- binding sites for CRF were found in discrete areas within the rat CNS, and data strongly support a physiological role for endogenous CRF in regulating and integrating functions in the CNS.
Abstract: Corticotropin-releasing factor (CRF) receptor-binding sites have been localized and quantified in the rat central nervous system (CNS) by autoradiography with an iodine-125-labeled analogue of ovine CRF substituted with norleucine and tyrosine at amino acid residues 21 and 32, respectively. High affinity and pharmacologically specific receptor- binding sites for CRF were found in discrete areas within the rat CNS. CRF receptors were highly concentrated in laminae 1 and 4 throughout the neocortex, the external plexiform layer of the olfactory bulb, the external layer of the median eminence, several cranial nerve nuclei in the brainstem including the facial, oculomotor, trochlear, vestibulocochlear, and trigeminal nuclei, the deep cerebellar nuclei, and the cerebellar cortex. Moderate concentrations of CRF receptors were present in the olfactory tubercle, caudate-putamen, claustrum, nucleus accumbens, nucleus of the diagonal band, basolateral nucleus of the amygdala, paraventricular nucleus of the hypothalamus, mammillary peduncle, inferior and superior olives, medullary reticular formation, inferior colliculus, and brainstem nuclei including tegmental, parabrachial, hypoglossal, pontine, cuneate, and gracilis nuclei, and in spinal cord. Lower densities of CRF binding were found in the bed nucleus of the stria terminalis, central and medial amygdaloid nuclei, and regions of the thalamus, hypothalamus, hippocampus, and brainstem. The distribution of CRF-binding sites generally correlates with the immunocytochemical distribution of CRF pathways and with the pharmacological sites of action of CRF. These data strongly support a physiological role for endogenous CRF in regulating and integrating functions in the CNS.
483 citations
TL;DR: The results provide a quantitative profile of AA in specific hypothalamic and limbic nuclei of the rat brain as well as information on the control of AA within these discrete regions.
Abstract: Conversion of androgen to estrogen in the rat brain is catalyzed by aromatase enzymes. The maximum concentrations of these enzymes are found within the hypothalamus and amygdala, where they appear to play an important role in the process by which androgens affect both behavior and neuroendocrine function. In the present study, we measured the levels of aromatase activity (AA) in 20 nuclei and brain regions of the adult rat brain. Individual nuclei were microdissected from 600-micron frozen sections. Tissues from 3 animals were pooled, and AA was measured by an in vitro radiometric assay that quantifies the stereospecific production of 3H2O from [1 beta-3H]androstenedione as an index of estrogen formation. We report that AA is heterogeneously distributed within the rat brain. The greatest amounts of activity were found in the bed nucleus (n.) of the stria terminalis (700 protein fmol/h . mg) and in the medial (MA) and cortical amygdala (400-600 fmol/h . mg protein) of the male. There was an evident rostral-caudal and medial-lateral gradient in AA throughout the diencephalon. Activity was high in the periventricular preoptic n. and medial preoptic n.; intermediate in the suprachiasmatic preoptic n., anterior hypothalamus, periventricular anterior hypothalamus, and ventromedial n.; and low in the arcuate n.-median eminence, lateral preoptic n., supraoptic n., dorsomedial n., and lateral hypothalamus. Regions devoid of measurable AA included the medial and lateral septum, caudate-putamen, hippocampus, and parietal cortex. In the female, AA was greatest in the MA and cortical amygdala. We found that AA in the MA, stria terminalis n., suprachiasmatic preoptic n., periventricular preoptic in., medial preoptic n., anterior hypothalamus, and ventromedial n. was significantly greater (P less than 0.05) in males than in females. Orchidectomy reduced AA to levels seen in females, and administration of testosterone to castrated males restored AA in these areas. No significant sex differences were observed in any other hypothalamic or amygdaloid nuclei, although AA was increased by testosterone treatment in the periventricular anterior hypothalamus, arcuate n.-median eminence, and lateral hypothalamus. Our results provide a quantitative profile of AA in specific hypothalamic and limbic nuclei of the rat brain as well as information on the control of AA within these discrete regions.
424 citations
TL;DR: Early postnatal handling appears to influence the development of the glucocorticoid receptor system in the hippocampus and frontal cortex in Norway rat pups, providing a possible mechanism for some of the previously reported effects of early handling on theDevelopment of the pituitary-adrenal response to stress.
Abstract: Norway rat pups were either handled (H) or undisturbed (nonhandled, NH) in the period between birth and weaning on Day 21. Following weaning, half of the animals in each group were housed socially (Soc), and half were housed in isolation (Isol). At 120-150 days of age, all animals were sacrificed, and the following regions were dissected and frozen at -70 °C until the time of assay: frontal cortex, hippocampus, hypothalamus, amygdala, septum, and pituitary. [3H]Dexamethasone (3H Dex) binding in each region was examined by an in vitro, cytosol, receptor assay. 3H Dex binding was significantly higher in the hippocampus of both H-Soc and H-Isol than in NH groups. In the frontal cortex, 3H Dex binding was higher in the H-Soc animals than in the H-Isol and NH-Isol animals. There were no significant handling or housing effects found in the amygdala, hypothalamus, septum, or pituitary. Thus, early postnatal handling appears to influence the development of the glucocorticoid receptor system in the hippocampus and frontal cortex. These results are discussed as providing a possible mechanism for some of the previously reported effects of early handling on the development of the pituitary-adrenal response to stress.
314 citations
TL;DR: The arcuate nucleus surrounds the ventral part of the third ventricle and contains densely packed small neurons with 1-3 dendrites that communicate primarily with the pituitary gland, hypothalamus, limbic system, midbrain periaqueductal gray and autonomic nuclei of the brain stem.
TL;DR: The findings that NPY was effective in the hypothalamus, as opposed to sites anterior, posterior, lateral or dorsal to this structure, suggest a hypothalamic site(s) of action for this neuropeptide.
TL;DR: The results suggest that glucocorticoids exert their feedback effect at the level of gene expression on both hypothalamic CRF neurons and pituitary corticotropes.
Abstract: RNA blot hybridization analysis with cloned rat CRF precursor (prepro-CRF) cDNA as a probe showed that prepro-CRF mRNA existed in rat hypothalamic and extrahypothalamic brain tissue, whereas it was undetectable in the pituitary and adrenal. To study the effect of glucocorticoid on the level of prepro-CRF mRNA in the hypothalmus and that of ACTH/beta-lipotropin (beta LPH) precursor mRNA in the pituitary, effects of adrenalectomy and dexamethasone administration were studied in rats. Adrenalectomy markedly raised mRNA coding for ACTH/beta LPH precursor in the anterior pituitary, but not in the neurointermediate pituitary lobe. Hypothalamic pre-pro-CRF mRNA increased only to 152% of the control value, 7 days after adrenalectomy. The administration of dexamethasone (200 micrograms/day for 7 days) started immediately after adrenalectomy lowered the ACTH/beta LPH precursor mRNA level in the anterior pituitary to 19% of the intact control value, whereas the level of prepro-CRF mRNA in the hypothalamus decreased only to 102%. These results suggest that glucocorticoids exert their feedback effect at the level of gene expression on both hypothalamic CRF neurons and pituitary corticotropes. Although the possibility that CRF neurons insensitive to glucocorticoid in the hypothalamus might blunt the change in the prepro-CRF mRNA could not be ruled out, it is also possible that the effect of glucocorticoids on the pituitary is dominant.
TL;DR: It is reported that levels of transcripts homologous to vasopressin messenger RNA increase in the PVN after adrenalectomy, in parallel with increases in vasoppressin immunoreactivity, indicating that a considerable degree of plasticity is retained by the adult neuronal genome of the rat and that this plasticity may be modulated by the endocrine environment.
Abstract: The discrete anatomical distribution of arginine vasopressin and corticotropin releasing factor (CRF) immunoreactivity in the para-ventricular nucleus (PVN) of the rat hypothalamus is altered after adrenalectomy1–3. Not only is the immunostaining of both peptides enhanced, but vasopressin immunoreactivity, normally confined to the magnocellular subdivision, becomes clear in a large percentage of CRF neurones in the parvocellular subdivision2. These changes in immunoreactivity may reflect changes in post-translational events, peptide metabolism or genomic activity that lead indirectly or directly to the enhanced expression of vasopressin. Here we report that levels of transcripts homologous to vasopressin messenger RNA increase in the PVN after adrenalectomy, in parallel with increases in vasopressin immunoreactivity. In fact, after adrenalectomy, vasopressin mRNA can be detected in CRF-immunoreactive neurones. These results indicate that a considerable degree of plasticity is retained by the adult neuronal genome of the rat and that this plasticity may be modulated by the endocrine environment.
TL;DR: In the ventral part of the spinal cord as well as in the pituitary and thyroid glands, CGRP values were higher when measured by radioreceptorassay as compared to RIA, indicating that at least two C GRP-like components are present.
Abstract: Binding sites for synthetic human 125I-labeled calcitonin gene-related peptide (125I-CGRP) have been demonstrated in membranes of the human nervous system. Binding was high in the cerebellar cortex (1.35 +/- 0.27 fmol/mg of tissue; mean +/- SEM), spinal cord (1.06 +/- 0.27 to 1.27 +/- 0.23 fmol/mg), and nucleus dentatus (1.02 +/- 0.15 fmol/mg), intermediate in the inferior colliculus (0.80 +/- 0.14 fmol/mg) and substantia nigra (0.75 +/- 0.14 fmol/mg), low in the neocortex, globus pallidus, nucleus caudatus, hippocampus, amygdala, superior colliculus, thalamus, and hypothalamus (0.15-0.32 fmol/mg), and negligible in spinal and sympathetic ganglia and pituitary (less than 0.04 fmol/mg). Autoradiography showed distinct 125I-CGRP binding over the molecular and Purkinje cell layers of the cerebellar cortex and over the substantia gelatinosa posterior of the spinal cord. The highest levels of CGRP-like components were recognized in the dorsal part of the spinal cord and the pituitary gland. In the ventral part of the spinal cord as well as in the pituitary and thyroid glands, CGRP values were higher when measured by radioreceptorassay as compared to RIA, indicating that at least two CGRP-like components are present. The predominant CGRP-like peak on HPLC had the retention time of synthetic human CGRP. Immunohistochemistry revealed the presence of a dense plexus of CGRP immunoreactive nerve fibers in the dorsal horn of the spinal cord.
TL;DR: Results provide ultrastructural evidence that GABA-ergic neurons establish symmetric (Gray II) synapses on LHRH neurons in the medial preoptic area of the rat.
Abstract: A double-label electron microscopic immunostaining procedure was employed to examine the interconnections of glutamic acid decarboxylase(GAD)- and LHRH-immunoreactive neurons in the medial preoptic area of the rat. The results provide ultrastructural evidence that GABA-ergic neurons establish symmetric (Gray II) synapses on LHRH neurons.
TL;DR: Results indicate that NPY acts on structures adjacent to the third ventricle to inhibit the secretion of LH and growth hormone but not follicle-stimulating hormone, whereas it can directly stimulate all three hormones from the cells of the anterior pituitary in vitro.
Abstract: Neuropeptide Y (NPY) has recently been localized in the rat hypothalamus. We have evaluated the effects of NPY on hypothalamic and pituitary function by injecting NPY into the third ventricle in vivo and by examining its action on perifused pituitary cells in vitro. Injections of NPY into the third ventricle of conscious ovariectomized rats led to a dramatic and highly significant reduction in plasma luteinizing hormone (LH) relative to pretreatment levels in these animals or to those of controls injected with physiological saline. Significant inhibition was obtained with doses ranging from 0.02 to 5.0 micrograms (4.7-1175 pmol) of NPY. These inhibitory effects on LH release were dose dependent and lasted for at least 120 min after injection of 5.0 micrograms of NPY. Intraventricular injection of NPY also significantly decreased plasma growth hormone; however, the threshold dose was 2.0 micrograms (470 pmol), a dose 100-fold greater than the lowest dose that inhibited LH release. Plasma follicle-stimulating hormone was unaffected by injection of NPY. NPY (10(-6) and 10(-7) M) stimulated secretion of LH, growth hormone, and follicle-stimulating hormone from perifused anterior pituitary cells loaded in a Bio-Gel P-2 column. These results indicate that NPY acts on structures adjacent to the third ventricle to inhibit the secretion of LH and growth hormone but not follicle-stimulating hormone, whereas it can directly stimulate the secretion of all three hormones from the cells of the anterior pituitary in vitro. Since NPY has been found in the hypothalamus and median eminence, it is quite likely that it plays a physiologically significant role at both hypothalamic and pituitary sites: influencing secretion of pituitary hormones.
TL;DR: An atlas of the distribution of the alpha-atrial natriuretic polypeptide-containing neuronal system in the rat brain is given and the groundwork for studying the influence of this new peptide on various brain functions is provided.
TL;DR: The results suggest the existence of at least two distinct rhGRF‐containing systems: one responsible for delivery of the peptide to portal vessels in the median eminence, and one whose relationship, if any, to hypophysiotropic function is less direct.
Abstract: Immunohistochemical methods have been used to chart the distribution of rat hypothalamic growth-hormone-releasing factor (rhGRF) immunoreactivity in the brains of normal and colchicine-treated adult albino rats. The results suggest the existence of at least two distinct rhGRF-containing systems: one responsible for delivery of the peptide to portal vessels in the median eminence, and one whose relationship, if any, to hypophysiotropic function is less direct. A dense plexus of rhGRF-stained fibers was found throughout the external lamina of the median eminence that is the route by which the peptide is delivered to the anterior pituitary. This projection appears to arise primarily from a group of rhGRF-immunoreactive neurons centered in the arcuate nucleus. Some 1,000-1,500 rhGRF-positive neurons were counted on each side of the brain in rats pretreated with colchicine. Colocalization studies, using a sequential double staining technique, indicated that a subset of rhGRF-immunoreactive neurons in the arcuate region contain neurotensin immunoreactivity. No evidence was obtained for colocalization of rhGRF with either of two pro-opiomelanocortin-derived peptides (alpha-melanocyte-stimulating hormone, adrenocorticotropic hormone (1-24)) in individual neurons in the arcuate nucleus. Much smaller groups of neurons were localized in the parvicellular division of the paraventricular nucleus of the hypothalamus and in the dorsomedial nucleus, and it is unclear whether they contribute to the plexus of rhGRF-stained fibers in the median eminence. The only other region in the rat brain in which rhGRF-stained cells were found reliably was in the area that roughly encapsulates the caudal aspect of the ventromedial nucleus of the hypothalamus. Because cells in this region are not known to project to the median eminence, they may be assumed to contribute to the extrahypophysiotropic rhGRF-stained projections outlined below. From the level of the arcuate and ventromedial nuclei, rhGRF-immunoreactive fibers could be traced along the base of the brain and through the periventricular system to discrete terminal fields limited almost exclusively to the hypothalamus and adjoining parts of the basal telencephalon. All parts of the periventricular region of the hypothalamus receive an input, including the preoptic and anterior parts in which somatostatin-containing neurons that project to the median eminence are clustered. Other prominent terminal fields were localized in discrete parts of the dorsomedial, paraventricular, suprachiasmatic, and premammillary nuclei, and in the medial preoptic and lateral hypothalamic areas.(ABSTRACT TRUNCATED AT 400 WORDS)
TL;DR: Findings indicate that a widespread network of ANF-containing neurons is present in the brain of rats and that colchicine-treated animals had a high number of immunoreactive AnF-positive cell bodies.
Abstract: Immunoreactive atrial natriuretic factor- (ANF-)positive nerve fibers and cell bodies were observed in the preoptic area, hypothalamus, mesencephalon, and pons of rats. In colchicine-treated animals a large number of immunoreactive ANF-positive cell bodies were seen in the organum vasculosum of the lamina terminalis, in several hypothalamic nuclei (e.g. periventricular, arcuate, and ventral premammillary nuclei), and in the dorsolateral tegmental nuclei of the pons. Varicose nerve fibers containing ANF were generally observed in the vicinity of the cells. These findings indicate that a widespread network of ANF-containing neurons is present in the brain.
TL;DR: There is a developmental delay between the synthesis of the oxytocin prohormone (pro-oxyphysin) and its processing to form oxytoc in and NP-OT, and this was correlated with a delay in immunocytochemically detectable neurites as compared to the vasopressin cells.
Abstract: Two anti-neurophysin monoclonal antibodies (MABs), PS 36 and PS 41, described in the preceding paper (Ben-Barak, Y, J.T. Russell, M.H. Whitnall, K. Ozato, and H. Gainer (1985) J. Neurosci. 5:000–000), allowed us to specifically stain for oxytocin-associated neurophysin (NP-OT) or vasopressin-associated neurophysin (NP-AVP) in the hypothalamus of developing rats. Staining with these MABs specific for NP-OT or NP-AVP showed that both types of neurophysin appeared in cells in the developing hypothalamus as early as embryonic day (E16) and continued to increase in immunoreactivity throughout fetal life. The literature indicated that oxytocin appears in the system between E20 and E22, much later than vasopressin (E16 to E17), which we confirmed in immunocytochemical experiments using affinity-purified antisera to these hormones. Since the MABs recognize the specific prohormones as well as the specific mature neurophysins (Ben-Barak, Y., J. T. Russell, M.H. Whitnall, K. Ozato, and H. Gainer (1985) J. Neurosci. 5: 81–97), we conclude that there is a developmental delay between the synthesis of the oxytocin prohormone (pro-oxyphysin) and its processing to form oxytocin and NP-OT. The delay in prohormone processing in the oxytocin cells was correlated with a delay in immunocytochemically detectable neurites as compared to the vasopressin cells. This reduced level of axonal and dendritic immunoreactivity was still obvious in the oxytocin cells at 9 days after birth. In contrast, the clustering of cells to form adult-like hypothalamic nuclei appeared to follow similar time courses for the two types of cells. Adult-like distributions of cells staining for NP-OT and NP-AVP were already apparent in the supraoptic and paraventricular nuclei by E17.
01 Jan 1985
TL;DR: CRF immunoreactivity has been demonstrated in a discrete subset of oxytocinergic magnocellular neurosecretory neurons that project to the posterior pituitary, and in a small fraction of cells in the parvocellular division thatProject to cell groups in the brain stem and spinal cord that are associated with the control of autonomic functions.
Abstract: The generation of antiserums against a peptide that has met the criteria predicted for corticotropin-releasing factor (CRF) has allowed the immunohistochemical localization of CRF immunoreactive neurons in the rat brain. Although CRF-stained cells have been found to be widely distributed in the central nervous system, attention has focused on neurons in the paraventricular nucleus of the hypothalamus (PVH), which is now acknowledged to be the principal source for delivery of CRF to the hypophyseal portal system. Some 2000 CRF-stained neurons can be counted in the PVH of the colchicine-treated rat, and there is evidence that enkephalin, PHI, and neurotensin coexist with CRF in subsets of parvocellular neurons. Consistent with the established negative feedback effects of adrenal steroids on CRF production and release, adrenalectomy enhances CRF immunoreactivity in parvocellular neurosecretory neurons in the PVH. In addition, immunoreactive vasopressin can be demonstrated in a majority of CRF-stained parvocellular neurons after adrenalectomy, which suggests a form of plasticity that allows for synergy of the two peptides in stimulating adrenocorticotropin secretion. The effects of adrenalectomy appear to be glucocorticoid-dependent, and specific to these peptides and this cell type. A survey of neural inputs to the hypophyseotropic zone of the PVH suggests potential substrates for the control of CRF release and/or synthesis by interoceptive stimuli, by the limbic region, and by a number of cell groups in the basal forebrain. Finally, CRF may also participate in other (nonadenohypophyseal) modes of regulation that are represented in the PVH. Thus, CRF immunoreactivity has been demonstrated in a discrete subset of oxytocinergic magnocellular neurosecretory neurons that project to the posterior pituitary, and in a small fraction of cells in the parvocellular division that project to cell groups in the brain stem and spinal cord that are associated with the control of autonomic functions.
TL;DR: Attention to the sex differences in these areas may help elucidate more precisely the neural basis for sexually dimorphic functions, as well as the basic mechanisms underlying sexual differentiation of behavior and the brain.
Abstract: Sexually dimorphic regions are described in two areas of the guinea pig brain: the medial preoptic area (MPOA) and the bed nucleus of the stria terminalis (BNST). The volume of a darkly staining portion of the MPOA is approximately 4-fold larger in male than in female guinea pigs, and the volume of a darkly staining portion of the BNST is approximately 36% larger in male than in female animals. The sex differences in both of these areas are present in animals that have been gonadectomized as adults as well as in intact animals, suggesting that they result from differences between the sexes in the hormonal environment during early development. Both the MPOA and the BNST bind high levels of gonadal steroids early in life, during the period when functional differentiation occurs. It is possible that dramatic morphological sex differences characterize such steroid-binding areas. Furthermore, these sexually dimorphic areas may form an anatomically and functionally interrelated system. Attention to these possibilities may help elucidate more precisely the neural basis for sexually dimorphic functions, as well as the basic mechanisms underlying sexual differentiation of behavior and the brain.
TL;DR: Assessment of the distribution of thyrotropin-releasing hormone (TRH) receptors in the rat CNS suggests that TRH receptors may mediate the actions of TRH in theRat CNS.
Abstract: We employed quantitative autoradiography to examine the distribution of thyrotropin-releasing hormone (TRH) receptors in the rat CNS. The binding of [3H]3-methyl-histidine-TRH [( 3H]MeTRH) to TRH receptors in frozen rat brain sections was saturable, of a high affinity (Kd = 5 nM), and specific for TRH analogs. Autoradiograms of [3H]MeTRH binding showed highest concentrations of TRH receptors in the rhinencephalon, including accessory olfactory bulb, nuclei of the amygdala, and the ventral dentate gyrus and subiculum of the hippocampus. Moderate TRH receptor concentrations were found within the thalamus and hypothalamus, in most regions of the rhombencephalon, such as the cranial nerve nuclei, and in the substantia gelatinosa of the spinal cord. Neocortex and basal ganglia contained low densities of TRH receptors. This distribution correlates well with the sensitivity of brain regions to the known effects of TRH, and suggests that TRH receptors may mediate the actions of TRH in the rat CNS.
TL;DR: The results suggest that the distribution of dopaminergic fibers in the AVPv may be sensitive to testosterone levels in the adult male, and that although the critical period for the development of this fiber distribution may begin in the prenatal period, the number of dopamine-beta-hydroxylase-(DBH-)stained fibers in this nucleus can be completely sex reversed by a single postnatal dose of TP.
Abstract: Recently we reported that the anteroventral periventricular nucleus (AVPv) of the preoptic region contains a dramatic sexual dimorphism in the distribution of tyrosine hydroxylase- (TH-)immunoreactive cells and fibers in the rat. This sexual dimorphism appears to be due to a greater density of dopaminergic fibers, and a larger number of dopaminergic cell bodies, in the AVPv of the female. In the present study we used an indirect immunohistochemical method to evaluate the distribution of TH-immunoreactive cell bodies and fibers, and of dopamine-β-hydroxylase-(DBH-)stained fibers, in the AVPv of female rats that were treated with testosterone propionate (TP) perinatally or postnatally, or were left untreated. All of the postnatally TP-treated animals failed to show a phasic pattern of luteinizing hormone (LH) secretion in response to estrogen and progesterone injections. Both the perinatally and postnatally TP-treated females had polyfollicular ovaries that lacked corpora lutea at the time of gonadectomy. Perinatal TP exposure resulted in what appears to be a complete masculinization of both the number of TH-stained cells and the density of TH-stained fibers in the AVPv. The number of TH-stained cells in the postnatally TP-treated females was also completely masculinized, although the density of TH-stained fibers did not appear to be altered significantly. Gonadectomy resulted in a moderate increase in the density of TH-stained fibers in adult males, and did not significantly affect the fiber density in females, or the number of TH-stained cells in either sex. The distribution of DBH-stained fibers in the AVPv did not appear to be altered in any of the treatment groups. These results suggest that the distribution of dopaminergic fibers in the AVPv may be sensitive to testosterone levels in the adult male, and that although the critical period for the development of this fiber distribution may begin in the prenatal period, the number of dopaminergic cells in the AVPv can be completely sex reversed by a single postnatal dose of TP that appears to correlate with a permanent disruption of the normal pattern of gonadotropin secretion.
TL;DR: Data from the combined steroid autoradiography-immunocytochemical method are consistent with the hypothesis of a genomic effect of estradiol on a particular subset of medial basal hypothalamic neurons that produce endogenous opioid peptides.
Abstract: We used the combined steroid autoradiography-immunocytochemical method to determine whether estradiol- or dexamethasone-concentrating cells contain endogenous opioid peptides. Ovariectomized-adrenalectomized female rats were given highly radioactive doses of 3H-estradiol or 3H-dexamethasone, then sacrificed to demonstrate nuclear steroid binding. Autoradiograms were prepared, exposed for 2-12 months, photodeveloped, and fixed; immunocytochemistry was carried out on the same sections using antibodies to beta-endorphin or dynorphin A (1-17). In the medial basal hypothalamus, many estradiol- and some dexamethasone-concentrating neurons were found intermingled with beta-endorphin or dynorphin-immunoreactive neurons. Of the beta-endorphin-immunoreactive neurons in the medial basal hypothalamus, 4% concentrated estradiol in their nuclei. In addition, a subset of beta-endorphin-immunoreactive cells in the anterior pituitary concentrated estradiol in their nuclei. Although none of the beta-endorphin-immunoreactive neurons in the medial basal hypothalamus concentrated dexamethasone in their nuclei, many of the beta-endorphin-immunoreactive cells in the anterior pituitary did. Of the dynorphin-immunoreactive neurons in the medial basal hypothalamus, 10% concentrated estradiol in their nuclei. These data are consistent with the hypothesis of a genomic effect of estradiol on a particular subset of medial basal hypothalamic neurons that produce endogenous opioid peptides.
TL;DR: High levels of aromatase in the neuroendocrine tissues of teleosts recommend them as animal models for further studying the enzyme, its regulation, and its role in governing androgen-dependent responses in central targets.
TL;DR: The data specifically implicate the hippocampus in modulating feedback sensitivity, as down-regulation was extensive in this structure, and did not occur in the septum, amygdala, hypothalamus or pituitary.
TL;DR: The results suggest that the supraoptic nucleus is influenced by the same brain areas which project to its companion within the magnocellular system, the paraventricular nucleus.
TL;DR: The present findings suggest that neurons containing corticotropin-releasing factor are pathologically altered in SDAT, in addition to the previously described cholinergic and somatostatinergic neuronal degeneration.
Abstract: The concentration of corticotropin-releasing factor-like immunoreactivity (CRF-LI) in the human central nervous system was measured by radioimmunoassay in postmortem tissue of control patients and in those with histologically confirmed senile dementia of the Alzheimer type (SDAT) In the controls, CRF-LI was found in high concentrations in the hypothalamus and frontal cortex (Brodmann's area 10), in moderate concentrations in amygdala, substantia innominata, temporal and parietal cortex (Brodmann's areas 38 and 7), and the caudate nucleus, and in low concentrations in posterior hippocampus and nucleus accumbens A marked reduction in the concentration of CRF-LI was observed in the frontal and temporal cortex (approximately 50%) as well as in the caudate nucleus (approximately 70%) in the SDAT group The present findings suggest that neurons containing corticotropinreleasing factor are pathologically altered in SDAT, in addition to the previously described cholinergic and somatostatinergic neuronal degeneration ( JAMA 1985;254:3067-3069)