Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPOTHALAMUS”

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

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

At least 73 records · Page 4Linked to original sources
PubMed1996

Medial amygdaloid suppression of predatory attack behavior in the cat: II. Role of a GABAergic pathway from the medial to the lateral hypothalamus.

The medial amygdala is known to powerfully suppress predatory attack behavior elicited by electrical stimulation of the lateral hypothalamus of the cat. In the preceding paper, it was shown that the initial limb of a pathway subserving suppression of predatory attack from the medial amygdala to the lateral hypothalamus projects to the ventromedial hypothalamus and its functions are mediated by substance P. The present study tested the hypothesis that the second limb of the pathway subserving medial amygdaloid suppression of predatory attack behavior projects from the medial to lateral hypothalamus and its functions are mediated by GABA. Cannula electrodes were implanted into the lateral hypothalamus for elicitation of predatory attack behavior as well as for the microinfusion of GABA compounds. Monopolar stimulating electrodes were implanted into sites within the medial amygdala from which subseizure levels of stimulation could suppress predatory attack behavior. Initially, the effects of dual stimulation of the medial amygdala and lateral hypothalamus upon response latencies for predatory attack were compared with single stimulation of the lateral hypothalamus alone. Dual stimulation was shown to significantly suppress predatory attack elicited from the lateral hypothalamus. Then, the GABAA receptor antagonist, bicuculline, was microinjected into sites within the lateral hypothalamus from which predatory attack was elicited in doses of 0.015, 0.075 and 0.15 nmol and paired trials of single and dual stimulation were again repeated in a manner identical to that applied prior to drug administration. Drug infusion produced a blockade of medial amygdaloid suppression of predatory attack in a time- and dose-dependent manner. Conversely, microinfusions of the GABAA receptor agonist, muscimol (10, 25 and 50 pmol), into the same lateral hypothalamic 'attack' site in the absence of medial amygdaloid stimulation suppressed predatory attack, thus simulating the effects of medial amygdaloid stimulation. Furthermore, pretreatment with bicuculline microinjected into the lateral hypothalamus blocked the suppressive effects of substance P, that was infused into the ventromedial hypothalamus, upon predatory attack. Receptor autoradiography demonstrated the presence of high affinity binding for GABAA receptors in the lateral hypothalamus. A combination of immunocytochemical and retrograde axonal tract tracing procedures, in which Fluoro-Gold was microinjected into the lateral hypothalamic attack sites, revealed the presence of populations of neurons labeled for both Fluoro-Gold and GABA in the ventromedial hypothalamus. These findings provide new evidence for the existence of a pathway from the medial to lateral hypothalamus whose functions are mediated by GABA. Thus, the overall findings provide support for the view that the pathway from the medial amygdala to the lateral hypothalamus underlying suppression of predatory attack behavior involves a two-neuronal arc: the first neuron projects from the medial amygdala to the medial hypothalamus and its functions are mediated by substance P: the second neuron involves a GABAergic pathway originating in the ventromedial hypothalamus and which projects to the lateral hypothalamus.

Amygdala↗
PubMed2004

[Expression of orexin A, orexin receptor-1, and Ob-R of hypothalamus in rats with chronic renal failure].

OBJECTIVE: To examine the changes of expressions of orexin A, orexin receptor-1 (OX1R), prepro-orexin (Prepro-OX) mRNA, OX1R mRNA and ob-R of hypothalamus in rats with chronic renal failure (CRF). METHODS: Sixty-two male Wister rats weighing 200-250 g were divided into three groups, including group 1 (normal, n = 5), group 2 (sham-operated, n = 25) and group 3 (CRF, n = 32). Hypothalamus orexin A was assayed by radioimmunoassay. Serum leptin was assayed by enzyme linked immunosorbent assay. The expression of Prepro-OX mRNA and OX1R mRNA of hypothalamus were measured by reverse transcription polymerase chain reaction, and expression of orexin A, OX1R and ob-R by immunohistochemistry. Automatic biochemical analyzer was used to measure the serum creatinine. RESULTS: Hypothalamus orexin A levels were negatively correlated (r = -0.63, P < 0.001) with serum leptin levels in the rats. The expression of hypothalamus Prepro-OX mRNA in CRF rats was significantly lower than that of sham-operation at week 12 (P < 0.01). Hypothalamus Prepro-OX mRNA levels were negatively correlated (r = -0.81, P < 0.001) with the levels of serum leptin and serum creatinine (r = -0.68, P < 0.05) in the rats at week 12. The expression of hypothalamus OX1R mRNA in CRF rats was lower than that of sham-operation at week 12 (P > 0.05). Specific immunoreactivity for orexin A was present in perikeryon of the hypothalamus neuron. Specific OX1R-like immunoreactivity was observed in some nerve fibres. Specific immunoreactivity for ob-R was present in membranes of the hypothalamus neuron. Hypothalamus neurons of orexin A-like specific immunoreactivity in CRF rats were significantly fewer than those in shamoperated rats at week 8. Hypothalamus neurons of OX1R-like specific immunoreactivity in CRF rats were similar to those in sham-operated rat at week 8. Hypothalamus neurons of ob-R-like specific immunoreactivity in CRF rats were significantly more than those in sham-operated rats at week 8. CONCLUSIONS: The lower hypothalamus orexin A levels may be induced by high serum leptin level in CRF rats. The lower expression of hypothalamus Prepro-OX mRNA in CRF rats may be one of the main causes inducing lower hypothalamus orexin A. The expression of OX1R in hypothalamus neurons is somewhat reduced and the expression of ob-R in hypothalamus neurons is somewhat raised in CRF rats. These remain to be studied further.

Animals↗
PubMed2004

Neural connections between the hypothalamus and the liver.

After receiving information from afferent nerves, the hypothalamus sends signals to peripheral organs, including the liver, to keep homeostasis. There are two ways for the hypothalamus to signal to the peripheral organs: by stimulating the autonomic nerves and by releasing hormones from the pituitary gland. In order to reveal the involvement of the autonomic nervous system in liver function, we focus in this study on autonomic nerves and neuroendocrine connections between the hypothalamus and the liver. The hypothalamus consists of three major areas: lateral, medial, and periventricular. Each area has some nuclei. There are two important nuclei and one area in the hypothalamus that send out the neural autonomic information to the peripheral organs: the ventromedial hypothalamic nucleus (VMH) in the medial area, the lateral hypothalamic area (LHA), and the periventricular hypothalamic nucleus (PVN) in the periventricular area. VMH sends sympathetic signals to the liver via the celiac ganglia, the LHA sends parasympathetic signals to the liver via the vagal nerve, and the PVN integrates information from other areas of the hypothalamus and sends both autonomic signals to the liver. As for the afferent nerves, there are two pathways: a vagal afferent and a dorsal afferent nerve pathway. Vagal afferent nerves are thought to play a role as sensors in the peripheral organs and to send signals to the brain, including the hypothalamus, via nodosa ganglia of the vagal nerve. On the other hand, dorsal afferent nerves are primary sensory nerves that send signals to the brain via lower thoracic dorsal root ganglia. In the liver, many nerves contain classical neurotransmitters (noradrenaline and acetylcholine) and neuropeptides (substance P, calcitonin gene-related peptide, neuropeptide Y, vasoactive intestinal polypeptide, somatostatin, glucagon, glucagon-like peptide, neurotensin, serotonin, and galanin). Their distribution in the liver is species-dependent. Some of these nerves are thought to be involved in the regulation of hepatic function as well as of hemodynamics. In addition to direct neural connections, the hypothalamus can affect metabolic functions by neuroendocrine connections: the hypothalamus-pancreas axis, the hypothalamus-adrenal axis, and the hypothalamus-pituitary axis. In the hypothalamus-pancreas axis, autonomic nerves release glucagon and insulin, which directly enter the liver and affect liver metabolism. In the hypothalamus-adrenal axis, autonomic nerves release catecholamines such as adrenaline and noradrenaline from the adrenal medulla, which also affects liver metabolism. In the hypothalamus-pituitary axis, release of glucocorticoids and thyroid hormones is stimulated by pituitary hormones. Both groups of hormones modulate hepatic metabolism. Taken together, the hypothalamus controls liver functions by neural and neuroendocrine connections.

Adrenal Glands↗
PubMed1996

Medial amygdaloid suppression of predatory attack behavior in the cat: I Role of a substance P pathway from the medial amygdala to the medial hypothalamus.

The medial amygdala is known to powerfully suppress predatory attack behavior in the cat, but the mechanisms underlying such modulation remain unknown. The present study tested the hypothesis that medial amygdaloid suppression of predatory attack is mediated, in part, by a pathway from the medial amygdala to the medial hypothalamus which utilizes substance P as a neurotransmitter. Stimulating electrodes were implanted into the medial amygdala and cannula electrodes were implanted into both the medial and lateral hypothalamus. Predatory attack behavior was elicited by electrical stimulation of the lateral hypothalamus. In the first phase of the study, paired trials compared attack latencies of single stimulation of the lateral hypothalamus with those following dual stimulation of the lateral hypothalamus and medial amygdala. Attack latencies were significantly elevated following dual stimulation of the medial amygdala and lateral hypothalamus. In the second phase of the study, dose and time dependent decreases in response suppression were noted following the infusion of the substance P (NK1) receptor antagonist, CP96.345 (in doses of 0.05, 0.5 and 2.5 nmol) into the medial hypothalamus. In third phase of the study, the effects of microinjections of the substance P receptor agonist, [Sar9.Met(O2)11]-substance P (in doses of 0.5, 1.0 and 2.0 nmol), directly into the medial hypothalamus upon lateral hypothalamically elicited predatory attack behavior were determined. Microinfusion of this drug elevated attack response latencies in a dose- and time-dependent manner. In addition, pretreatment with CP96,345 into the medial hypothalamus blocked the suppressive effects of subsequent delivery of [Sar9,Met(O2)11]-substance P into the same medial hypothalamic site. Other parts of the study demonstrated the presence of: (1) high densities of substance P receptors in the ventromedial hypothalamus, and (2) neurons that are positively labeled for substance P that project from the medial amygdala to the ventromedial hypothalamus as demonstrated by retrograde labeling with Fluoro-Gold. These findings provide support for the hypothesis that medial amygdaloid suppression of lateral hypothalamically elicited predatory attack behavior includes a substance P pathway from the medial amygdala to the medial hypothalamus. The findings further suggest that stimulation of the medial amygdala activates substance P receptors in the medial hypothalamus, thus triggering an inhibitory mechanism from the medial to the lateral hypothalamus, resulting in suppression of predatory attack behavior.

Amygdala↗
PubMed1996

Evidence that brain nitric oxide synthase is the major nitric oxide synthase isoform in the hypothalamus of the adult female rat and that nitric oxide potently regulates hypothalamic cGMP levels.

Recent studies suggest that nitric oxide (NO) may function as a neurotransmitter in the hypothalamus. In order to provide further evidence supporting this contention, we examined: (1) whether the hypothalamus displays significant NO synthase (NOS) activity and whether the activity is inhibited by an NOS inhibitor, (2) whether the different NOS isoforms [brain (b)-NOS, endothelial (e)-NOS and macrophage (m)-NOS] are expressed in the various nuclei of the hypothalamus of the random cycling adult female rat, (3) whether the NO donor molecule, sodium nitroprusside (SNP), regulates the heme-containing enzyme, guanylate cyclase in the preoptic area and medial basal hypothalamus of the random cycling adult female rat as well as the ovariectomized steroid (estradiol-17 beta)-treated rat. The results of the study showed that the preoptic area (POA) and medial basal hypothalamus (MBH) of the adult female rat displays significant NOS activity which can be dose-dependently inhibited by an NOS inhibitor. All three NOS isoform mRNA transcripts were present in the hypothalamus, with the order of expression being b-NOS > e-NOS > m-NOS. Immunohistochemical localization using monoclonal antibodies to the specific NOS isoform proteins revealed that b-NOS represented the major form of NOS in the hypothalamus based on density and distribution of immunostaining. b-NOS immunostaining was especially dense in the organum vasculosum laminae terminalis (OVLT), medial preoptic area (MPOA), supraoptic nucleus, and moderately dense in the arcuate nucleus/median eminence. The pattern and density of b-NOS staining closely mirrored our previously reported pattern of NADPH-diaphorase staining in the hypothalamus, and a polyclonal antibody to b-NOS yielded a similar staining pattern as that observed for the monoclonal antibody. In contrast to the dense staining observed for b-NOS in the hypothalamus, we observed no specific staining for m-NOS in the hypothalamus. e-NOS immunostaining, on the other hand, was present in the hypothalamus, but to a much lesser extent than b-NOS. Light e-NOS staining was observed in the OVLT, MPOA, supraoptic nucleus and arcuate nucleus/median eminence. That NO can regulate guanylate cyclase as a potential mediator of its effects was demonstrated using SNP which dose-dependently elevated cGMP levels in the POA and MBH of random cycling rats and estrogen-primed ovariectomized rats. The effect of SNP was due to its NO donor ability as it was blocked by the NO scavenger molecule, hemoglobin. Interestingly, hemoglobin alone caused a 50-60% reduction in basal cGMP levels, suggesting that endogenously produced NO regulates basal guanylate cyclase activity. Taken as a whole, the present study demonstrates that b-NOS is the major NOS isoform in the hypothalamus and it also provides evidence that cGMP may be a mediator of NO effects in the female hypothalamus as evidenced by the potent ability of SNP to elevate cGMP levels in the POA and MBH.

Animals↗
PubMed2001

[Effect of Chinese herbal medicine for nourishing yin and removing fire on biosynthesis, secretion and regulative mechanism of gonadotropin-releasing hormone in hypothalamus].

OBJECTIVE: To elucidate the effect of Chinese herbal medicine (CHM) for nourishing Yin and removing fire on the biosynthesis, secretion and regulative mechanism of gonadotropin-releasing hormone (GnRH) in hypothalamus. METHODS: The brain slices of medial basal hypothalamus of adolescent rats, which had been fed with CHM, were incubated. The content of GnRH in incubative liquid was determined during the slices were stimulating with high KC1 to observe the change of GnRH biosynthesis from tonic secretory center of GnRH (arcuate nucleus and ventromedial nucleus) in hypothalamus. The integrated optic density of GnRH positive immunoreactive substance in preoptic area of hypothalamus was determined by immunohistochemistry and image processing to observe the change of GnRH content in pulsative secretory center of GnRH (medial preoptic nucleus) in hypothalamus. The push-pull perfusion of medial preoptic area in hypothalamus was performed. The content of GnRH in serial perfusates was determined by radioimmunoassay (RIA) to observe the change of frequency and amplitude of GnRH pulse releasing from medial preoptic area in hypothalamus. The content of aspartic acid, glutamic acid and gamma-amino butyric acid in the perfusate was determined by high performance liquid chromatography-fluorometry, and the content of beta-endorphic in the perfusate was determined by RIA to observe the change of releasing amount of exciting aminoacid neurotransmitter and beta-endorphin from pulsative secretory center of GnRH (medial preoptic area) in hypothalamus. RESULTS: CHM could markedly reduce the content of GnRH in medial basal hypothalamus (arcuate nucleus and veatromeolial nucleus) and preoptic area (meolical preoptic nucleus) of hypothalamus, and could obviously lower the frequency and amplitude of GnRH pulse releasing from medial preoptic nucleus, It also could markedly decrease the releasing amount of aspartic acid and glutamic acid, while obviously increase the releasing amount of gamma-amino butyric acid and beta-endorphin from medial preoptic area of hypothalamus. CONCLUSION: CHM could markedly reduce the activity of GnRH neurons in hypothalamus through inhibiting the releasing of central exciting aminoacid neurotransmitter and promoting the releasing of central inhibiting aminoacid neurotransmitter and beta-endorphin, thereby, obviously decrease the biosynthesis and secretion of GnRH from tonic and pulsative secretory center of GnRH in hypothalamus. It could be one of chief effective mechanism of CHM in efficiently treating the idiopathic precocious puberty.

Animals↗
PubMedDate not supplied

Ethanol enhances medial amygdaloid induced inhibition of predatory attack behaviour in the cat: role of GABAA receptors in the lateral hypothalamus.

The present study tested the hypothesis that the suppressive effects of ethanol upon predatory attack behaviour in the cat involve a pathway from the medial amygdala to the lateral hypothalamus, and that these suppressive effects are mediated by gamma-aminobutyric acid (GABAA) receptors located in the lateral hypothalamus. Cannula electrodes were implanted into the lateral hypothalamus for elicitation of predatory attack behaviour and for microinjections of the GABAA receptor antagonist, bicuculline. Monopolar stimulating electrodes were implanted into the medial amygdala from which subseizure levels of electrical stimulation suppressed predatory attack behaviour. In the first phase of the study, we compared response latencies for predatory attack behaviour following single stimulation of the lateral hypothalamus alone with those following paired trials of dual stimulation of the medial amygdala plus lateral hypothalamus. Dual stimulation significantly suppressed predatory attack. In the second phase of the study, peripheral ethanol administration (in doses of 0.01, 0.5 and 1.0 g/kg, i.p.) enhanced the suppressive effects of medial amygdaloid stimulation in a dose- and time-dependent manner in which peak effects were obtained 60 min post-injection. In the third phase of the study, bicuculline (0.15 nmol) was microinjected into the lateral hypothalamus both prior to and following paired trials of dual stimulation. Drug infusion blocked the suppressive effects of medial amygdaloid stimulation upon predatory attack behaviour elicited from the lateral hypothalamus, indicating the importance of GABAA receptors in mediating this suppression. In the fourth phase of the study, bicuculline, microinjected into the lateral hypothalamus at the time when ethanol's effects were maximal (i.e. 60-80 min post-ethanol administration), totally blocked the suppressive effects of medial amygdaloid stimulation as well as the enhancing effects of ethanol upon medial amygdaloid suppression of this form of aggressive behaviour. In the last phase of the study, bicuculline (0.15 nmol) infusion into the lateral hypothalamus significantly reduced the suppressive effects of ethanol (1.0 g/kg, i.p.) upon predatory attack behaviour elicited from the lateral hypothalamus. These results support the hypothesis that ethanol's suppressive effects upon predatory attack behaviour in the cat are mediated, at least in part, by GABAA receptors in the lateral hypothalamus. The present and recent findings in our laboratory support the view that GABAA receptors in the lateral hypothalamus are activated, in turn, by a GABAergic pathway which arises from the medial hypothalamus whose neurons receive inputs from the medial amygdala.

Amygdala↗
PubMed1979

Neural connexions between the medial forebrain bundle, the preoptic area and the basal hypothalamus in the rat: an electrophysiological study.

1. Electrophysiological experiments have been performed on intact cycling female rats to investigate the neural connexions that exist between the medial forebrain bundle, the anterior hypothalamic region, which included the preoptic area, and the basal hypothalamus. Recordings have been made from a total of 351 neurones in the anterior hypothalamus of which 216 were responsive to stimulation of either or both the medial forebrain bundle and basal hypothalamus (arcuate and ventromedial nuclei).2. Forty-six of these cells were responsive to a stimulus applied both to the medial forebrain bundle and the basal hypothalamus with a variety of response combinations. The majority of neurones were orthodromically activated by stimulation in both sites. Inhibition by stimulation of the medial forebrain bundle coupled with orthodromic excitation from the basal hypothalamus, or the reverse situation, was also encountered frequently.3. A few cells were antidromically invaded by the stimulation of the medial forebrain bundle and these received orthodromic or inhibitory inputs from the basal hypothalamus, although one unit outside the anterior hypothalamus was antidromically activated by both stimuli.4. Ninety per cent of all the doubly responsive units that could be antidromically activated by stimulation of the basal hypothalamus received an orthodromic input from the medial forebrain bundle, and no cells in the anterior hypothalamus that projected to the basal hypothalamus were found to receive an inhibitory input from the medial forebrain bundle.5. These results provide electrophysiological evidence for inhibitory and excitatory inputs from the medial forebrain bundle to the preoptic and anterior hypothalamic cells that either project to, or receive connexions from, the basal hypothalamus. Neurones in the preoptic area which project to the basal hypothalamus are implicated in the control of anterior pituitary function, particularly gonadotrophin secretion. These experiments, coupled with functional studies, suggest that there is an excitatory input from the medial forebrain bundle to these preoptic and anterior hypothalamic cells which may modulate adenohypophyseal secretions.

Animals↗
PubMed1988

Distribution pattern of cell bodies and fibers with neurotensin-like immunoreactivity in the cat hypothalamus.

Neurotensin is widely distributed in the central and peripheral nervous systems. Extensive radioimmunoassay and immunohistochemical studies in rats show that the neurotensin immunoreactive perikarya and fibers are most prominent in the hypothalamus. Radioimmunoassay studies have suggested that the levels of neurotensin in the hypothalamus of cats may be six times higher than that of rats. We studied the distribution pattern of neurotensin immunoreactivity within the hypothalamus of the cat by avidin-biotin modification immunohistochemical methods: (1) to define its distribution pattern within the hypothalamus, and (2) to compare our findings with the patterns that have been described in rats. Results show that neurotensin immunoreactive cell bodies and fibers are most prominent in the rostral and intermediate regions of the cat hypothalamus. Cell bodies with neurotensin-like immunoreactivity are seen maximally in the medial preoptic region, the infundibular nucleus, and the lateral hypothalamus. The neurotensin positive fibers are dense in the periventricular regions of the entire rostro-caudal extent of the hypothalamus. This pattern of distribution of neurotensin immunoreactivity is similar to that described in rats. The suprachiasmatic nuclei of the cat hypothalamus, however, contained a significant number of neurotensin immunoreactive cell bodies, an observation not noted in the rat hypothalamus. The neurotensin immunoreactive neurons were more numerous in the lateral hypothalamus than has been reported in rats, but the paraventricular nucleus of the hypothalamus in cats contained fewer neurotensin immunoreactive perikarya. The presence of neurotensin immunoreactive perikarya in the suprachiasmatic nucleus and the apparent increase in the number of neurotensin immunoreactive neurons in the lateral hypothalamus may account for the increased levels of neurotensin reported in cats. Neurotensin has been speculated to play a role in nociception, thermoregulation, and control of arterial pressure by acting as a hormone or a neurotransmitter. Details of the pattern of colocalization of neurotensin with that of other neuropeptides and neurotransmitters will aid in our understanding of its role in these functions.

Animals↗
PubMed1998

Topographic organization of connections between the hypothalamus and prefrontal cortex in the rhesus monkey.

Prefrontal cortices have been implicated in autonomic function, but their role in this activity is not well understood. Orbital and medial prefrontal cortices receive input from cortical and subcortical structures associated with emotions. Thus, the prefrontal cortex may be an essential link for autonomic responses driven by emotions. Classic studies have demonstrated the existence of projections between prefrontal cortex and the hypothalamus, a central autonomic structure, but the topographic organization of these connections in the monkey has not been clearly established. We investigated the organization of bidirectional connections between these areas in the rhesus monkey by using tracer injections in orbital, medial, and lateral prefrontal areas. All prefrontal areas investigated received projections from the hypothalamus, originating mainly in the posterior hypothalamus. Differences in the topography of hypothalamic projection neurons were related to both the location and type of the target cortical area. Injections in lateral eulaminate prefrontal areas primarily labeled neurons in the posterior hypothalamus that were equally distributed in the lateral and medial hypothalamus. In contrast, injections in orbitofrontal and medial limbic cortices labeled neurons in the anterior and tuberal regions of the hypothalamus and in the posterior region. Projection neurons targeting orbital limbic cortices were more prevalent in the lateral part of the hypothalamus, whereas those targeting medial limbic cortices were more prevalent in the medial hypothalamus. In comparison to the ascending projections, descending projections from prefrontal cortex to the hypothalamus were highly specific, originating mostly from orbital and medial prefrontal cortices. The ascending and descending connections overlapped in the hypothalamus in areas that have autonomic functions. These results suggest that specific orbitofrontal and medial prefrontal areas exert a direct influence on the hypothalamus and may be important for the autonomic responses evoked by complex emotional situations.

Animals↗
PubMed1978

Anterior and posterior hypothalamus: effects of independent temperature displacements on heat production in conscious goats.

Three goats were chronically implanted with thermodes to alter the temperatures of the anterior and posterior hypothalamus independently of each other. At an air temperature of +14 degrees C the anterior hypothalamus was cooled with different intensities, while the posterior hypothalamus was simultaneously either warmed (39 degrees C) or cooled (29 degrees C). In both conditions cooling anterior hypothalamus increased heat production. However, the increase was smaller, when the posterior hypothalamus was cooled. The inhibiting effect was most pronounced during the first parts of the periods and diminished with time. Nevertheless, in a separate series of experiments, the effects of posterior hypothalamic cooling were found to persist over periods of 3 h. At an air temperature of +3 degrees C the posterior hypothalamus temperature was altered between 28 and 42 degrees C, while anterior hypothalamus temperature was kept close to its control level. Shivering and heat production decreased with cooling and increased with warming of the posterior hypothalamus. The results suggest that those neurons which reside in the posterior hypothalamus and mediate shivering, are sensitive to temperature. Thermosensitivity of these allegedly integrative neurons affects shivering and heat production in a way inverse to the thermosensitivity of the temperature sensing neurons in the anterior hypothalamus.

Animals↗
PubMed1988

Alzheimer's disease. Aminergic-cholinergic alterations in hypothalamus.

To better understand the role of the hypothalamus in Alzheimer's disease (AD), we have measured dopamine, norepinephrine (NE), and serotonin (5HT) levels, tritiated spiperone and tritiated serotonin blinding, and choline acetyltransferase (ChAT) and acetylcholinesterase activity in seven subregions of the hypothalamus from 18 normal control subjects and ten patients with AD. We have found a significant reduction of 5HT in the anterior hypothalamus, lateral hypothalamus, and posterior lateral hypothalamus and a decline in spiperone binding in the anterior hypothalamus of patients with AD. The ChAT activity was found to be diminished only in the posterior lateral hypothalamus of patients with AD. No NE or dopamine alterations were found in any region of the AD hypothalamus. In the normal hypothalamus, dopamine, NE, and 5HT were found to be regionally distributed. Our study documents region-specific neurotransmitter abnormalities in the AD hypothalamus and raises the question of the relationship of these changes, especially in 5HT, to some of the noncognitive clinical alterations observed in AD.

Acetylcholinesterase↗
PubMed1994

Ionotropic glutamate-receptor gene expression in hypothalamus: localization of AMPA, kainate, and NMDA receptor RNA with in situ hybridization.

In situ hybridization and Northern blots were used to study the ionotropic subtypes of the glutamate receptor in the rat hypothalamus. Widespread expression of AMPA, kainate, and NMDA receptor RNA was found in the hypothalamus with the transcripts the same size and number as found in other regions of the brain. Most of the glutamate-receptor subunits studied were expressed in greater amounts in hippocampus than in hypothalamus; GluR5, on the other hand, showed a greater expression in hypothalamus than in hippocampus. On the basis of Northern blot analysis, all regions of the brain examined, including hypothalamus, cerebral cortex, cerebellum, olfactory bulb, and hippocampus, expressed all eight of the subunits studied. Each subunit showed different relative expressions in the different regions. In the hypothalamus, GluR1 and GluR2 were among the most widely expressed of the non-NMDA ionotropic receptors. Other AMPA-preferring receptors, GluR3 and -R4, were also found, but to a lesser extent. Scattered cells expressed the kainate-preferring receptors GluR5, -R6, and -R7. The NMDA receptor NMDAR1 was detected throughout the hypothalamus. In many regions of the hypothalamus, only scattered cells showed detectable expression of the glutamate-receptor mRNA as detected by autoradiographic silver grains over neurons; unlabeled cells were mixed among labeled cells. Every region of the hypothalamus had several different glutamate receptors. The expression of many different types of ionotropic glutamate receptors throughout the hypothalamus suggests that multiple modes of ion channel regulation by glutamate probably operate here and provides further support for the importance of the excitatory transmitter glutamate in hypothalamic regulation.

Animals↗
PubMed1995

Opioid precursor gene expression in the human hypothalamus.

Using in situ hybridization histochemistry, we studied the distribution of neurons that express preproopiomelanocortin (pre-POMC), preprodynorphin (pre-PDYN), and preproenkephalin (pre-PENK) gene transcripts within the human hypothalamus and surrounding structures. Of the three opioid systems, pre-POMC neurons have the most restricted distribution. Pre-POMC cells are most numerous in the infundibular nucleus and retrochiasmatic area of the mediobasal hypothalamus; a few labeled cells are present within the boundaries of the ventromedial nucleus and infundibular stalk. Pre-POMC message was not found in the limited samples of structures adjacent to the hypothalamus. In contrast to neurons that express pre-POMC, neurons expressing pre-PDYN and pre-PENK are more widely represented throughout the hypothalamus and extrahypothalamic structures. However, pre-PDYN and pre-PENK cells differ from one another in distribution. Pre-PDYN message is especially abundant in neurons of the tuberal and mammillary regions, with a distinct population of labeled cells in the premammillary nucleus and dorsal posterior hypothalamus. Pre-PDYN gene expression also is found in neurons of the dorsomedial nucleus, ventromedial nucleus, caudal magnocellular portion of the paraventricular nucleus, dorsolateral supraoptic nucleus, tuberomammillary nucleus, caudal lateral hypothalamus, and retrochiasmatic area. In structures immediately adjacent to the hypothalamus, pre-PDYN neurons were observed in the caudate nucleus, putamen, cortical nucleus of the amygdala, and bed nucleus of the stria terminalis. Pre-PENK neurons occur in varying numbers in all hypothalamic nuclei except the mammillary bodies. The chiasmatic region is particularly rich in pre-PENK neurons, with the highest packing density in the intermediate nucleus [the intermediate nucleus (Braak and Braak [1987] Anat. Embryol. 176:315-330) has also been termed the sexually dimorphic nucleus of the preoptic area (SDA-POA; Swaab and Fliers [1985] Science 228:1112-1115) or the interstitial nucleus of the anterior hypothalamus 1 (Allen et al. [1989] J. Neurosci. 9:497-506)], dorsal suprachiasmatic nucleus, medial preoptic area, and rostral lateral hypothalamic area. Pre-PENK neurons are numerous in the infundibular nucleus, ventromedial nucleus, dorsomedial nucleus, caudal parvicellular portion of the paraventricular nucleus, tuberomammillary nucleus, lateral hypothalamus, and retrochiasmatic area. Only a few lightly labeled cells were found in the periphery of the supraoptic nucleus and lateral tuberal nucleus. In areas adjacent to the hypothalamus, cells that contain pre-PENK message occur in the nucleus basalis of Meynert, central nucleus of amygdala, bed nucleus of the stria terminalis, caudate nucleus, and putamen.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1982

Characterization of high affinity dopamine uptake into the dopamine neurons of the hypothalamus.

The study of hypothalamic dopamine (DA) neurons is complicated by the difficulty in distinguishing DA neurons from norepinephrine (NE) neurons and by the fact that they comprise only a small proportion of the catecholamine neuron population of the hypothalamus. We have studied DA uptake into nerve terminals of hypothalamic DA neurons using a synaptosomal preparation. Desmethylimipramine (DMI) was used to prevent uptake into synaptosomes from NE neurons, thus pharmacologically isolating dopaminergic from noradrenergic nerve terminals. This DMI-insensitive DA uptake in hypothalamus had all the properties of a high affinity uptake process; it was saturable, dependent on incubation time and incubation temperature, increased linearly with increasing amounts of tissue and was completely abolished by excess unlabeled DA. Also, it was completely abolished by benztropine, an inhibitor of amine uptake into DA neurons. We believe that DMI-insensitive DA uptake into hypothalamic synaptosomes represents uptake into DA nerve terminals. The DMI-insensitive DA accumulation in discrete areas of hypothalamus correlated well with the known prevalence of DA neurons relative to NE neurons in these areas: median eminence greater than median eminence-arcuate nucleus greater than mediobasal hypothalamus greater than whole hypothalamus. Comparison of the affinity constants for DA uptake into synaptosomes incubated without DMI revealed a 2-fold higher affinity constant for DA uptake in median eminence compared with striatum, but affinity constants in all the other hypothalamic regions examined (mediobasal hypothalamus, hypothalamus minus median eminence, whole hypothalamus) were identical to that of striatum. In contrast, comparison on the affinity constants for DA uptake in the presence of DMI revealed a 2-3-fold higher affinity constant for DA uptake in all these hypothalamic regions compared with striatum. It appears the tuberoinfundibular DA neurons and the other DA neurons of the hypothalamus have a high affinity uptake system for DA, although affinity for DA in all of these hypothalamic DA neurons appears to be 2-3-fold lower than that in striatal DA neurons. The data also suggest that the much larger mediobasal hypothalamus may serve as a model for studies of DA uptake into tuberoinfundibular DA neurons of the median eminence.

Animals↗
PubMed2000

Visceral inputs to neurons in the anterior hypothalamus including those that project to the periaqueductal gray: a functional anatomical and electrophysiological study.

The present study was designed to examine peripheral, in particular noxious visceral, inputs to neurons in the hypothalamus that project to the midbrain periaqueductal gray. The induction of Fos protein was used to localize hypothalamic neurons that were activated by noxious visceral stimulation. This was combined with retrograde transport of fluorescent latex microspheres from identified "pressor" and "depressor" sites in the dorsolateral/lateral or ventrolateral columns of the periaqueductal gray. A second series of electrophysiological experiments examined the receptive field characteristics, including the incidence of viscerosomatic convergence, of neurons in the ventral part of the anterior hypothalamus. Noxious visceral stimulation (intraperitoneal acetic acid) induced Fos-like immunoreactivity in significantly more neurons in the hypothalamus than control stimuli (intraperitoneal saline and intravenous phenylephrine). Particularly high numbers of Fos-positive neurons were found in the paraventricular nucleus, the supraoptic nucleus and ventral regions of the anterior hypothalamus. When combined with retrograde tracing from "depressor" sites in the ventrolateral periaqueductal gray, the highest numbers of double-labelled neurons were localized in the paraventricular nucleus and the lateral area of the anterior hypothalamus. However, the regions that contained the greatest proportions of Fos-positive neurons that projected to "depressor" sites in the ventrolateral periaqueductal gray were the lateral area of the anterior hypothalamus and its rostral extension, the lateral preoptic area. Fewer double-labelled neurons were localized in the hypothalamus after retrograde transport from sites in the dorsolateral/lateral periaqueductal gray compared to the results obtained from injections of tracer in the ventrolateral periaqueductal gray. Furthermore, the numbers of Fos-positive hypothalamic neurons that projected to the dorsolateral/lateral periaqueductal gray were very similar in experimental and control animals. The electrophysiological study confirmed that a large proportion of neurons in and around the lateral area of the anterior hypothalamus can be driven by noxious visceral stimulation and demonstrated a high incidence of viscerosomatic convergence in these cells (66% of cells driven from somatic structures were also driven by electrical stimulation of the splanchnic nerve). Somatic receptive fields of these neurons were generally large, often including all four limbs and the face. The results of the functional anatomical and electrophysiological studies have identified neurons in an area of the ventral anterior hypothalamus that are a focus of nociceptive visceral input and which project to the midbrain periaqueductal gray, in particular to its ventrolateral column. These results are discussed in relation to the roles of the anterior hypothalamus and the different longitudinal columns of the periaqueductal gray in co-ordinating autonomic and sensory functions in response to visceral pain.

Animals↗
PubMed2002

Acute effects of acephate and methamidophos and interleukin-1 on corticotropin-releasing factor (CRF) synthesis in and release from the hypothalamus in vitro.

Acute effects of Ace, Meth and IL-1 on AChE activity, ACh and CRF mRNA levels in, and CRF-release from the hypothalamus were studied in vitro. The hypothalamus samples were dissected from the rat brain and were incubated in vitro with IL-1, Ace or Meth in the presence or absence of Dex, Atrop, PTL, PROP and GABA. Ace and Meth, but not IL-1, inhibited AChE activity, while all three compounds; (1) increased ACh and CRF mRNA levels in and CRF release from; (2) activated the CRE promoter region of CRF-gene in: and (3) increased cFos binding to the AP-1 region of the CRF-gene in the hypothalamus. Dex suppressed the effects of IL-1, possibly by inducing the nGRE regulatory sites of the CRF-gene. Dex, however, did not modulate the effects of Ace and Meth on the hypothalamus, which may be attributed to the failure of Dex to modulate the CRF-gene's nGRE regulatory sites. Atrop caused 80-90% inhibition of the effects of IL-1, but caused only 50-65% inhibition of the effects of Ace or Meth on CRF mRNA levels in and CRF release from the hypothalamus. PTL did not affect, while PROP slightly attenuated the effects of IL-1 and the insecticides on the hypothalamus. GABA attenuated the effects of the insecticides but not the effects of IL-1 on the hypothalamus. This suggests that the IL-1-induced augmentation of CRF synthesis in and release from the hypothalamus is mediated through a cholinergic pathway, while the insecticide-induced augmentation of CRF synthesis in and release from the hypothalamus is mediated through the cholinergic and GABAergic pathways. The insecticides, but not IL-1, disrupt feedback regulation of CRF synthesis in and release from the hypothalamus.

Acetylcholine↗
PubMed1981

In situ estradiol and progestin (R5020) localization in the vascularly separated and isolated hypothalamus of the rhesus monkey.

A neurosurgical procedure has been developed for vascular isolation of the hypothalamus-thalamus region of the rhesus monkey brain. Utilizing this preparation, the left and right halves of the hypothalamus were perfused simultaneously, but separately, with a dextran-blood solution. Radiolabeled steroids were directly perfused in the dextran-blood into either the left or right half of the hypothalamus. Studies with radiolabeled gonadal steroids indicate that the majority of the carotid circulation is confined to the hypothalamus-thalamus area in this brain preparation and the cross-circulation of labelled steroids between the left and right sides of the hypothalamus is less than 10%. The usefulness of the preparation is illustrated by an autoradiographic study of the in situ hypothalamic distribution of (3H)estradiol in ovariectomized rhesus monkeys and of the synthetic progestin(3H)R5020 in estrogen-primed, ovariectomized rhesus monkeys. The direct perfusion of the (3H) steroids into the hypothalamus greatly increases the sensitivity of such compared to systemic administration of the (3H) steroids. The perfusion of one-half of the hypothalamus with )3H) steroid and the other half with (3H) steroids. The perfusion of one-half of the hypothalamus with (3H) steroid and the other half with (3H) steroids. The perfusion of one-half of the hypothalamus with (3H) steroid and the other half with (3H)steroid plus radioinert steroids permits in 1 animal, acting as its own control, the examination of a saturable distribution of a gonadal steroid in the rhesus monkey hypothalamus.

Animals↗