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PubMed1998

The second messenger cAMP elicits eating by an anatomically specific action in the perifornical hypothalamus.

We have previously shown that a membrane-permeant analog of cAMP, 8-bromo-cAMP (8-br-cAMP), elicits a vigorous eating response when microinjected into the perifornical hypothalamus (PFH) or lateral hypothalamus (LH) of satiated rats, suggesting that increases in cAMP in these areas may be important in the neural control of eating. To determine the locus of this effect, we compared the ability of 8-br-cAMP (1-100 nmol/0.3 microl) to elicit eating after microinjection into the PFH, LH, or the following bracketing areas: the anterior and posterior LH, paraventricular nucleus of the hypothalamus, thalamus, and amygdala. 8-br-cAMP at 50 nmol elicited eating (>/=3.4 gm in 2 hr) exclusively in the PFH and LH. At 100 nmol, 8-br-cAMP elicited a larger response in these areas and elicited a smaller, more variable response in the thalamus. We similarly mapped the feeding-stimulatory effects of compounds that increase endogenous cellular cAMP in naive rats. Combined microinjection of matched doses (300 nmol) of 3-isobutyl-1-methylxanthine and 7-deacetyl-7-O-(N-methylpiperazino)-gamma-butyryl-forskolin was effective exclusively in the PFH, eliciting an average 2 hr food intake of 8.4 +/- 2.0 gm. Collectively, these results suggest that increases in cellular cAMP within a specific brain site, the PFH, may play a role in the neural stimulation of eating.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Hypocretin/orexin- and melanin-concentrating hormone-expressing cells form distinct populations in the rodent lateral hypothalamus: relationship to the neuropeptide Y and agouti gene-related protein systems.

Cells in the lateral hypothalamus and in the arcuate nucleus play prominent roles in the central control of food intake; however, a neurochemical link connecting these potential components of a hypothalamic circuitry regulating energy metabolism remains to be established. In the present study, the topographical relationship between cells expressing mRNAs encoding melanin-concentrating hormone and the newly discovered neuropeptide family hypocretins/orexins was studied in the rat and mouse lateral hypothalamus by using double-labeling in situ hybridization. Cells expressing the two mRNAs formed completely distinct populations, with hypocretin/orexin cells located primarily perifornically and in the magnocellular lateral hypothalamic nucleus; melanin-concentrating hormone cells extended in a wider area both laterally and periventricularly and appeared to partly surround the hypocretin/orexin population. In the arcuate nucleus, cells expressing neuropeptide Y and agouti gene-related protein were studied by routine fluorescence and/or confocal microscopy immunohistochemistry. Double staining demonstrated that a large proportion of the neuropeptide Y-positive cell bodies in this nucleus also contained agouti gene-related protein-like immunoreactivity. Moreover, these two peptides also coexisted in nerve terminals surrounding and in close relationship to perikarya and processes of both hypocretin/orexin- and melanin-concentrating hormone-immunoreactive cells in the lateral hypothalamus, whereby the former appeared to receive a more dense innervation. These results thus provide evidence for an arcuate-lateral hypothalamic neuropeptide Y/agouti gene-related protein pathway. Furthermore, the results implicate hypocretin/orexin and melanin-concentrating hormone-expressing cells as downstream targets in neuropeptide Y-induced feeding.

Agouti-Related Protein↗
PubMed1996

Progesterone receptor immunoreactivity in aromatic L-amino acid decarboxylase-containing neurons of the guinea pig hypothalamus and preoptic area.

A double-labeling immunofluorescence procedure was used to determine whether progesterone receptor (PR)-immunoreactive (IR) neurons in the preoptic area and hypothalamus of female guinea pigs also contained aromatic L-amino acid decarboxylase (AADC), an enzyme involved in the synthesis of both catecholamines and serotonin. Immunostaining was performed on cryostat sections prepared from ovariectomized guinea pigs primed by estradiol to induce PR. The nuclear presence of PR was visualized by a red fluorescence while the AADC-containing perikarya showed a yellow-green fluorescence. The topographic distribution of AADC-IR neurons was investigated by using a specific antiserum obtained by immunization of rabbits with a recombinant protein beta-galactosidase-AADC in the two regions known to contain the densest populations of estradiol-induced PR-IR cells: the preoptic area and the mediobasal hypothalamus. The localization of PR-IR and AADC-IR cell populations showed considerable overlap in these areas, mainly in the medial and periventricular preoptic nuclei and in the arcuate nucleus. A quantitative analysis of double-labeled cells estimated that about 15% to 23% of AADC-IR cells in the preoptic area and about 11% to 21% of AADC-IR cells in the arcuate nucleus possessed PR. This colocalization persisted throughout the rostrocaudal extent of these areas and represented 3% to 9% of the population of PR-IR cells. These findings provide neuroanatomical evidence that a subset of AADC neurons is directly regulated by progesterone. The exact physiological role of this enzyme in target cells for progesterone is not understood. AADC may be involved in functions other than that for the synthesis of the classical neurotransmitters.

Animals↗
PubMed1982

The morphology and connections of the posterior hypothalamus in the cynomolgus monkey (Macaca fascicularis). I. Cytoarchitectonic organization.

The cytoarchitectonic organization of the posterior hypothalamus of the cynomolgus monkey (Macaca fascicularis) was analyzed in Nissl, Golgi, acetylcholinesterase, and reduced silver preparations. The region consists of a number of cell masses that differ considerably in their discreteness and in the homogeneity of their neuronal populations. The nuclei identified include: the medial mamillary nucleus (in which at least three distinct subdivisions can be recognized--a pars medialis, a pars lateralis, and a pars basalis); the small-celled nucleus intercalatus; the large-celled lateral mamillary nucleus; a single premamillary nucleus; the tuberomamillary nucleus; the posterior hypothalamic nucleus; the caudal extension of the lateral hypothalamic area; the supramamillary area; and the paramamillary nucleus (which appears to correspond to the nucleus of the ansa lenticularis of other workers). As a basis for the subsequent experimental study of the efferent connections of the posterior hypothalamus, the location of each of these cell masses is described and illustrated in a series of low-power photomicrographs, as are the form and distribution of the resident neuronal populations of the various components of the mamillary complex as seen in Golgi preparations.

Animals↗
PubMed1994

Gonadal hormone regulation of glial fibrillary acidic protein immunoreactivity and glial ultrastructure in the rat neuroendocrine hypothalamus.

The influence of gonadal steroids on the ultrastructure of glial cells and on the immunoreactivity for the specific astrocytic marker glial fibrillary acidic protein (GFAP) has been assessed in the neuroendocrine hypothalamus. The following parameters were analyzed in the arcuate nucleus of adult female rats: the number and the surface density of cells immunoreactive for GFAP, the number of glial profiles showing bundles of glial filaments, the size of the bundles of glial filaments, and the proportion of neuronal perikaryal membrane apposed by glial processes. These parameters were studied during the different phases of the estrous cycle, after ovariectomy, and after the administration of estradiol or progesterone to ovariectomized rats. No significant differences were detected in the number of GFAP-immunoreactive cells among the different experimental groups. The surface density of GFAP-immunoreactive material, the number of glial profiles in the neuropil, and the proportion of neuronal perikaryal membrane covered by glia were increased in the afternoon of proestrus and in the morning of estrus compared with other phases of the estrous cycle or to ovariectomized rats and showed a rapid (5 h) and reversible increase in ovariectomized rats injected with 17 beta estradiol, with a maximal effect by 24 h after the administration of the hormone. In contrast, the size of the bundles of glial filaments was decreased in the afternoon of proestrus, in the morning of estrus, and by the administration of estradiol to ovariectomized rats. The parameters studied were not affected by the administration of progesterone. However, progesterone (300 micrograms/rat) blocked the effects of 17 beta estradiol (1, 10, and 300 micrograms). The results suggest that glial cells may be actively involved in the modulation of neuroendocrine events by the hypothalamus.

Animals↗
PubMed1977

A Golgi study on the hypothalamus of amphibia. The neuronal typology.

The neuronal typology in the hypothalamus of the frog and the crested newt was studied by the Golgi technique. In the newt, piriform, multipolar or cerebrospinal fluid (CSF)-contacting neurons of relatively primitive type, according to the classification of Ramón-Moliner, are encountered in the preoptic area. Moreover, magnocellular neurons are impregnated. In the frog the preoptic area shows a more varied typology. The posterior hypothalami of the frog and the newt exhibit mainly bipolar CSF-contacting and piriform neurons. These latter are generally "tufted", but some bipolar of multipolar cells are encountered, especially in the frog. The simple anatomical organization of the amphibian hypothalamus corresponds well with the pattern of "generalized" integrative area where multimodal sensory inputs converge--including visceral information from cerebrospinal fluid by means of hypothalamic CSF-contacting sensors--to regulate the neuroendocrine outflow.

Animals↗
PubMed1977

Immunohistochemical localization of somatostatin in the human hypothalamus.

In order to identify clearly the nervous structures containing somatostatin in the human hypothalamus, an immunohistochemical localization of this neurohormone was performed at light-microscopic level. Using a antiserum specific to somatostatin and the unlabeled antibody peroxidase-antiperoxidase technique, we have found somatostatin in neurons with cell bodies in an area in the anterior hypothalamus corresponding to the infundibular nucleus. Somatostatin-containing fibers were also detected in the neurovascular zone of the pituitary stalk, suggesting that somatostatin is released in that region to reach the capillaries in the pituitary portal plexus. A large bundle of somatostatin fibers extending from the anterior part of the paraventricular nucleus up to the posterior portion of the mammillary bodies has also been detected. The role of these fibers still remains to be clarified.

Adult↗
PubMed1991

Opioid binding in the rostral hypothalamus is reduced following lesion of the ventral noradrenergic tract in female rats.

Experiments were undertaken to establish whether opioid receptors exert a direct presynaptic influence on noradrenergic (NA) terminals in the preoptic/anterior hypothalamus (PO/AH) of the female rat. Thus, opioid binding studies were performed in rats with lesions of the ventral NA tract (VNAT; the main NA projection to the hypothalamus) to assess whether a loss of NA terminals may also result in a decrease in opioid binding in the PO/AH. In the first experiment, unilateral electrolytic lesions of the VNAT caused a significant reduction in both the NA content and specific [3H]-diprenorphine binding to membrane homogenates in the ipsilateral PO/AH. In the second experiment bilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the VNAT caused a significant reduction in NA levels in the PO/AH as well as significant decreases in the density of [3H]-diprenorphine binding to tissue sections of the PO/AH when compared to control animals. These results strongly suggest that the NA input to the PO/AH is regulated by endogenous opioid peptides, and provide an anatomical substrate to explain opioid-NA interactions in the control of gonadotrophin releasing hormone (GnRH) and gonadotrophin secretion.

Animals↗
PubMed1981

Inhibitory actions of amino acids in the preoptic-anterior hypothalamus of the rat.

Extracellular recordings were made from preoptic-anterior hypothalamic neurones with combined recording and iontophoresis electrodes. Short iontophoretic applications of beta-alanine, GABA, glycine and taurine inhibited the discharge of the majority of neurones tested. Bicuculline metho-chloride reversibly and selectively antagonised GABA responses. Strychnine reversibly antagonised beta-alanine, glycine and taurine but not GABA responses. These results suggest the existence of two populations of inhibitory amino acid receptors in the preoptic-anterior hypothalamus. The function of inhibitory amino acids in the rostral hypothalamus was briefly discussed.

Amino Acids↗
PubMed1994

Lateral septal projections onto tubero-infundibular neurons in the hypothalamus of the guinea pig.

Efferent projections of the lateral septal nucleus (LS) to the preoptic area and the hypothalamus were identified in 20 female guinea pigs after iontophoretic injection of the anterograde axonal tracer Fluoro-Ruby. Tubero-infundibular (TI) neurons of the preoptic area and the hypothalamus were retrogradely labeled after intracardiac injection of Granular Blue or Fluoro-Gold. Magnocellular neurons of the supraoptic and paraventricular nuclei were also labeled. The double labeling procedure allowed an estimation of the extent of the direct relationship between LS efferents and TI neurons. Contacts between lateral septal fibers and TI cell bodies were mainly observed at the light-microscopical level in the preoptic area. A group of labeled fibers coursing along the third ventricle established sparse connections with hypothalamic periventricular TI neurons. A few appositions was observed in the infundibular (arcuate) nucleus, suggestive of a monosynaptic regulation of TI neurons by a septo-arcuate tract. Close association with labeled magnocellular neurons was also noted at the edge of the supraoptic and paraventricular nuclei. The sparse but direct connections between LS and TI neurons may be involved in the neuroendocrine functions of the LS.

Animals↗
PubMedDate not supplied

Submicroscopic localization of H3-noradrenaline in the hypothalamus.

The submicroscopic localization of H3-noradrenaline in the periventricular region of the anterior hypothalamus of the rat was investigated. It was shown that the largest concentration of the label is detected in the neuroglia of the subependymal layers, where the label is detected above the terminals of the axons with two types of vesicles and along the path of the axons above the microtubules. More rarely the label is encountered above the terminals with one type of synaptic vesicle and above cells of the neurosecretory type, similar in ultrastructure to cells of the arcuate nucleus. In the ependymal layer the label is localized above the cells and intercellular spaces. The results of the work are discussed in connection with the modern data on the fluorescence of the catecholamines of the hypothalamus.

Animals↗
PubMedDate not supplied

There are receptors for neurotensin in the caudate nucleus and posterior hypothalamus.

It was established in chronic experiments on dogs that the introduction of neurotensin in a dose of 3 or 10 micrograms in 1.5 microliters into the caudate nucleus changes the parameters of the conditioned and unconditioned food reflexes: a 31% shortening of the latent period and a 56% increase in the magnitude of the reflex. Microapplication of neurotensin in the same doses in the posterior region of the hypothalamus enhanced the secretory function of the gland caused by the introduction of histamine. It was concluded that the caudate nucleus and hypothalamus contain cells possessing receptors for neurotensin, which participate in mechanisms of formation of the conditioned reflex and central influence on the organs of the digestive system.

Animals↗
PubMed1979

Sensory neglect after lesions of substantia nigra or lateral hypothalamus: differential severity and recovery of function.

Sensory neglect was studied in cats after unilateral lesions of: lateral hypothalamus (LH); internal capsule (IC) adjacent to the LH; substantia nigra (SN) or the ventromedial hypothalamus (VMH). Special behavioral tests were employed to yield quantifiable data and also to exclude any confounding due to simple movement deficits. Lesions of SN or IC produced severe and enduring contralateral visual and somesthetic deficits and a facilitation of ipsilateral visual responsiveness. In contrast, LH lesions sparing the adjacent IC produced only weak and transient deficits and VMH lesions had no effects on sensory function. This suggests that lesions of the SN or its forebrain connections are important for producing sensory neglect and that sensory deficits after LH lesions are due to infringement on fibers of passage to or from the SN. Lesions which produced neglect often suppressed the amplitude of flash evoked responses in the ipsilateral caudate nucleus and visual and association cortex. However, these evoked potential effects were transient. There was no effect on the spontaneous EEG and this fails to support the hypothesis of a lack of hemispheric arousal in sensory neglect. The results are discussed in relation to nigrotectal projections and the process of attention. This lesion-behavior model is suggested for studies of recovery of function.

Animals↗
PubMed1980

Noradrenergic innervation of the rat hypothalamus:experimental biochemical and electron microscopic studies.

The concentrations of noradrenaline in individual hypothalamic nuclei and in the median eminence were measured 7-10 days following surgical transections of the lower brain stem or electrolytic lesions of the medullary noradrenaline-containing cell groups. Terminal degeneration in the hypothalamus was studied after the same surgical procedures. Direct, monosynaptic connections between the dorsomedial hypothalamic nucleus and all the noradrenaline-containing cell groups investigated were found. Degenerated synaptic boutons were demonstrated in the median eminence, arcuate, dorsomedial, ventromedial, periventricular and paraventricular nuclei following lesions of the solitary tract and of the lateral reticular nucleus. Biochemical measurements indicate that the pontine-medullary noradrenergic cell groups are the source of hypothalamic norepinephrine. Ascending noradrenergic fibers destined to terminate in the hypothalamus are provided by several cell groups, though the bulk of the NA-fibers seem to originate in the A1-group, in the ventrolateral part of the medullary reticular formation. Most of these fibers join the ventral NA bundle, fewer join the dorsal periventricular tract and several probably also join the dorsal NA bundle. A significant overlap was found in the hypothalamic arborization of the noradrenergic fibers, so that no strict topographical organization seems to be present either in their origin or their termination.

Adrenergic Fibers↗
PubMed1991

A study of the hypothalamic pulse-generating mechanism responsible for LH release: electrical stimulation of the medial basal hypothalamus in the ovariectomized guinea pig.

In order to examine the neurophysiological properties of the hypothalamus responsible for the pulsatile release of luteinizing hormone (LH) the medial basal hypothalamus (MBH) of the ovariectomized adult female guinea pig was stimulated electrically through an implanted electrode and LH release was monitored as an indication of luteinizing hormone-releasing hormone (LHRH) release. Electrical stimulation (ES) consisting of monophasic square wave pulses with 0.5 ms pulse duration was applied for 2 min at 60, 40, 20, or 10 min intervals. Current intensity (80, 200, 500 microA) and frequency (8, 50, 100 Hz) were varied to determine the parameters of ES which resulted in an LH pulse with amplitude similar to that of a pulse induced by the endogenous pulse-generating mechanism. Blood samples were collected at 5 or 10 min intervals through an indwelling catheter, and LH was measured by RIA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Galanin neurons exhibit estrogen receptor immunoreactivity in the female rat mediobasal hypothalamus.

Galanin has been shown to augment the hypothalamic luteinizing hormone releasing hormone and pituitary luteinizing hormone release and to play an important role in the feedback effects of ovarian steroids on pituitary hormone secretion. To further characterize estrogen effects on galanin, we tested for the existence of estrogen receptors in arcuate nucleus galanin-producing cells. Hypothalamic vibratome sections from colchicine-pretreated female rats were double immunolabeled for estrogen receptor and galanin. Neurons which exhibited immunoreactivity for either estrogen receptor or galanin were distributed throughout the hypothalamus; and a population of neurons, located predominantly in the mediobasal hypothalamus, displayed immunoreactivity for both galanin and estrogen receptor. These results raise the possibility that estrogen may act directly on galanin-producing arcuate nucleus neurons to regulate pituitary hormone secretion.

Animals↗
PubMed1990

The fos proto-oncogene protein:regulation by morphine in the rat hypothalamus.

Mechanisms by which opiates alter neuronal functions, including neuroendocrine functions, are not well defined. We have previously demonstrated that morphine rapidly and transiently increases expression of the proto-oncogene c-fos in the rat caudate-putamen. This regulation of the c-fos gene by morphine may represent a portion of the intracellular cascade coupling activation of opiate receptors on the cell surface to subsequent alterations in neuropeptide gene expression. In the present study, we have focussed on effects of morphine on c-fos expression in the ventromedial hypothalamus, which contains estrogen-concentrating neurons and a large number of neurons expressing the opioid proenkephalin and Proopiomelanocortin. The hypothalamus has been identified as a "final common pathway" between the remainder of the central nervous system and the pituitary gland. As a marker for c-fos expression, we have detected pp50 c-fos (FOS) protein immunocytochemically, using a polyclonal antibody to the M peptide of FOS, and revealed an intense nuclear stain in many neurons. Labeled nuclei were drawn by camera lucida from 12 matched sections (one side only) covering the rostral and middle levels of the ventromedial nucleus of six rats given morphine and six given phosphate buffered saline. Morphine treatment significantly increased the number and density of immuno-labeled nuclei in the ventromedial nucleus, but not in the arcuate nucleus. These results suggest effects of morphine (directly or indirectly) on neurons in the ventromedial hypothalamic nucleus, despite the relative absence of morphine receptors in this nucleus. These results may also provide an anatomical basis for neuroendocrine alterations following morphine treatment.

Animals↗
PubMed1982

Cortical control of neurally-mediated arrhythmogenic properties of desacetyl lanatoside C: the role of the posterior hypothalamus.

Functional ablation of the cerebral cortex by cortical spreading depression (CSD) significantly increased the dose of desacetyl lanatoside C required to induce A-V block and ventricular fibrillation. To examine the role of the posterior hypothalamus in the increased resistance of decorticated rats to arrhythmia induced by toxic doses of desacetyl lanatoside C, four groups of animals were injected with this drug: group 1 rats had a craniotomy; group 2 rats had a craniotomy and functional decortication; group 3 rats had a craniotomy and a hypothalamic lesion; and group 4 rats had a craniotomy, hypothalamic lesion and functional decortication. The dose of drug required to induce A-V block and ventricular fibrillation was significantly less in group 1, than in groups 2,3 and 4, and there was no statistically significant difference between these last three groups. These results are consistent with the hypothesis that the increased resistance to arrhythmia induced by desacetyl lanatoside C in decorticated rats is mediated by the posterior hypothalamus.

Animals↗