SEARCH · PubMed Health

Results for “Paraventricular Hypothalamic Nucleus”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original 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

PubMed2005

Dopamine D4 receptor signaling in the rat paraventricular hypothalamic nucleus: Evidence of natural coupling involving immediate early gene induction and mitogen activated protein kinase phosphorylation.

The dopamine D4 receptor has been investigated for its potential role in several CNS disorders, notably schizophrenia and more recently, erectile dysfunction. Whereas studies have investigated dopamine D4 receptor-mediated signaling in vitro, there have been few, if any, attempts to identify dopamine D4 receptor signal transduction pathways in vivo. In the present studies, the selective dopamine D4 agonist PD168077 induces c-Fos expression and extracellular signal regulated kinase (ERK) phosphorylation in the hypothalamic paraventricular nucleus (PVN), a site known to regulate proerectile activity. The selective dopamine D4 receptor antagonist A-381393 blocked both c-Fos expression and ERK1/2 phosphorylation produced by PD168077. In addition, PD168077-induced ERK1/2 phosphorylation was prevented by SL327, an inhibitor of ERK1/2 phosphorylation. Interestingly, treatment with A-381393 alone significantly reduced the amount of Fos immunoreactivity as compared to basal expression observed in vehicle-treated controls. Dopamine D4 receptor and c-Fos coexpression in the PVN was observed using double immunohistochemical labeling, suggesting that PD168077-induced signaling may result from direct dopamine D4 receptor activation. Our results demonstrate functional dopamine D4 receptor expression and natural coupling in the PVN linked to signal transduction pathways that include immediate early gene and MAP kinase activation. Further, the ability of the selective dopamine D4 antagonist A-381393 alone to reduce c-Fos expression below control levels may imply the presence of a tonic dopamine D4 receptor activation under basal conditions in vivo. These findings provide additional evidence that the PVN may be a site of dopamine D4 receptor-mediated proerectile activity.

Aminoacetonitrile↗

PubMed2002

Lipopolysaccharide-induced oestrogen receptor regulation in the paraventricular hypothalamic nucleus of lewis and Fischer rats.

Oestrogen receptor (ER) regulation of gene transcription in neurosecretory and pituitary cells has been proposed as an important mechanism for increased hypothalamic-pituitary-adrenal (HPA) axis responses in females of several mammalian species, including humans. Inbred female Fischer (F344/N) and Lewis (LEW/N) rats have similar oestrogen levels, although Fischer rats exhibit hyper- and Lewis rats hypo-HPA axis responses. The blunted HPA axis response of Lewis rats has been associated with their blunted hypothalamic corticotropin releasing hormone (CRH) expression. To determine if the female CRH expression deficiency in Lewis rats is associated with defective ER expression and regulation, hypothalamic paraventricular nucleus (PVN) transcript levels of CRH and ER were determined under basal conditions and after immune challenge. Microdissected PVN were obtained from control and lipopolysaccharide (LPS) treated Lewis and Fischer rats and CRH, ERalpha and beta mRNA levels were determined by semiquantitative reverse-transcriptase-polymerase chain reaction. In addition, ERalpha and beta protein levels were determined by semiquantitative Western blots. ERalpha and beta mRNA and protein levels in the PVN of control Fischer rats were significantly higher than in control Lewis rats. ERalpha and beta mRNA and protein levels in Fischer rats were reduced by LPS administration at the time of maximal CRH mRNA levels but did not change in Lewis rats, an effect independent of oestrogen levels. These data indicate that defective neuroendocrine HPA axis responses are associated with defective ER expression and regulation in Lewis PVN despite oestrogen concentrations.

Animals↗

PubMed2000

Phenylethanolamine N-methyltransferase-immunoreactive neurons in the medulla oblongata of the pigeon (Columba livia) projecting to the hypothalamic paraventricular nucleus.

The distribution and ascending projections to the hypothalamic paraventricular nucleus of phenylethanolamine N-methyltransferase (PNMT)-immunoreactive perikaria were studied in adult pigeons using a combination of retrograde transport of Fluorogold injected into the paraventricular nucleus, and double immunohistochemical procedures for PNMT, tyrosine hydroxylase and neuropeptide Y. PNMT-immunoreactive cell bodies were found in the subtrigeminal reticular nucleus of the ventrolateral medulla and in the nucleus of the solitary tract, mainly in the subnuclei: medialis superficialis, pars posterior, and medialis ventralis, pars posterior. PNMT-immunoreactive perikaria were also tyrosine hydroxylase immunoreactive, and are located within the rostral tyrosine hydroxylase immunoreactive cell groups of these areas. No perikaria double-labeled for neuropeptide Y and PNMT were found. Retrograde labeled cell bodies were observed in the subtrigeminal reticular nucleus and in the nucleus of the solitary tract. PNMT-immunoreactive retrogradely labeled cells were mainly observed in the subtrigeminal reticular nucleus. These data suggest the presence in the pigeon of medullary adrenergic cell groups partially comparable to mammalian C1 and C2 groups. Comparison of these results with data previously obtained in amphibians and reptiles suggests that the presence of a hypothalamically-projecting C1-like group might be a plesiomorphic medullary attribute in amniotes, whereas the variable presence of C2 and C3-like groups, as well as the content of NPY in the putative adrenergic perikaria, seem to be species-specific.

Animals↗

PubMed1999

The neurotensinergic synaptic innervation of vasopressin containing neurons in the rat hypothalamic paraventricular nucleus.

A recent physiological report suggested that neurotensin could inhibit the vasopressin releasing from vasopressin-producing neurons in the hypothalamic paraventricular nucleus but not in the supraoptic nucleus. In the present study, the synaptic relationship between the neurotensin-like immunoreactive and vasopressin-like immunoreactive neurons has been examined using a pre-embedding double immunostaining technique in the rat hypothalamic paraventricular nucleus. At the light microscopic level, many neurotensin-like immunoreactive fibers were found near the vasopressin-like immunoreactive neurons. At the electron microscopic level, the neurotensin-like immunoreactive fibers were identified as axon terminals that made many synapses on the vasopressin-like immunoreactive perikarya and dendrites. The synapses were both asymmetrical and symmetrical. These findings of the present study suggest that the inhibitory effect of neurotensin on the vasopressin neurons in the hypothalamic paraventricular nucleus may be due to the direct synapses made by neurotensin-like immunoreactive axon terminals on the vasopressin-like immunoreactive neurons.

Animals↗

PubMed2000

Beta-endorphin-, adrenocorticotrophic hormone- and neuropeptide y-containing projection fibers from the arcuate hypothalamic nucleus make synaptic contacts on to nucleus preopticus medianus neurons projecting to the paraventricular hypothalamic nucleus in the rat.

The nucleus preopticus medianus is known to be situated in a key site in pathways regulating the paraventricular hypothalamic nucleus. To investigate the innervation pattern to nucleus preopticus medianus neurons by afferent fibers containing beta-endorphin, adrenocorticotrophic hormone and neuropeptide Y, a retrograde tracing method was combined with immunohistochemistry for these peptides in the rat. In the first experiment with injection of a retrograde tracer in the nucleus preopticus medianus, retrogradely labeled neurons were found in many regions throughout the brain. Among these, the arcuate hypothalamic nucleus contained a number of retrogradely labeled neurons showing immunoreactivity to the neuropeptides examined. About 20%, 20% and 40% of retrogradely labeled arcuate hypothalamic nucleus neurons showed beta-endorphin, adrenocorticotrophic hormone and neuropeptide Y immunoreactivity, respectively. About 18% and 57% of retrogradely labeled neurons in the nucleus tractus solitarius and ventrolateral medulla, respectively, were immunoreactive to neuropeptide Y. There were many more neuropeptide Y-immunoreactive projections to the nucleus preopticus medianus from the arcuate hypothalamic nucleus than those from the medulla. None of the retrogradely labeled neurons in the medulla showed immunoreactivity to beta-endorphin or adrenocorticotrophic hormone. In the second experiment with injection of a retrograde tracer in the paraventricular hypothalamic nucleus, electron microscopic observation revealed that retrogradely labeled neurons in the nucleus preopticus medianus were in synaptic contact with beta-endorphin-, adrenocorticotrophic hormone- and neuropeptide Y-immunoreactive axon terminals. The present finding indicates that nucleus preopticus medianus neurons projecting to the paraventricular hypothalamic nucleus are innervated by beta-endorphin-, adrenocorticotrophic hormone- and neuropeptide Y-containing arcuate hypothalamic nucleus neurons in addition to being innervated by neuropeptide Y-containing catecholaminergic medullary neurons which have been reported in our previous study.

Adrenocorticotropic Hormone↗

PubMed1999

Psychological stress increased corticotropin-releasing hormone mRNA and content in the central nucleus of the amygdala but not in the hypothalamic paraventricular nucleus in the rat.

The central administration of corticotropin-releasing hormone (CRH) to experimental animals sets into motion a coordinated series of physiological and behavioral events that promote survival during threatening situation. A large body of evidence suggest that CRH in the central nucleus of the amygdala (CEA) induces fear-related behaviors and is essential to fear conditioning; however, evidence of CRH-mediated activation of the amygdala under physiological situation is still limited. We report here a study of the impact of a psychological stressor on hypothalamic and amygdala CRH systems in the rat. Non-footshocked rats placed in a floored compartment surrounded by footshocked rats were defined as the psychological stress group. Rats were exposed to psychological stress for 15 min, and then sacrificed 1.5 and 3 h after cessation of stress. We found that our psychological stressor induced an increase in both CRH mRNA levels, as assessed by in situ hybridization histochemistry, and CRH content, as assessed by micropunch RIA, in the CEA. Exposure to the psychological stressor also caused a significant increase in CRH mRNA levels with a trend for an increase in CRH content in the dorsolateral subdivision of the bed nucleus of the stria terminalis (BNST) which is anatomically associated with the CEA. In contrast, psychological stress induced a small, but significant increase in type-1 CRH receptor (CRHR-1) mRNA in the hypothalamic paraventricular nucleus (PVN), while it failed to elevate either PVN CRH mRNA levels or content, CRH content in the median eminence (ME), or levels of plasma ACTH or corticosterone (CORT). Thus, in the context of a psychological stressor, the activation of the amygdala CRH system can occur without robust activation of the hypothalamic CRH system. In the light of previous data that the psychological stress-induced loss of sleep was reversed by the central administration of a CRH antagonist, these data suggest that CRH in the CEA may contribute to the psychological stress-evoked fear-related behavior such as hyperarousal. These data also indicate that in response to a psychological stressor, the amygdala CRH system is much more sensitive than is the CRH system emanating from the PVN.

Adrenocorticotropic Hormone↗

PubMed1998

The arcuate nucleus is the major source for neuropeptide Y-innervation of thyrotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus.

Neuropeptide Y (NPY) immunoreactive (-ir) nerve fibers densely innervate hypophysiotropic TRH perikarya and dendrites in the hypothalamic paraventricular nucleus (PVN). To evaluate the contribution of the arcuate nucleus (Arc) to this innervation, the effect of Arc ablation by neonatal monosodium glutamate (MSG) treatment on the density of NPY-fibers contacting TRH neurons in the PVN was investigated. After the lesioned animals and vehicle-treated controls reached adulthood, the number of contacts between NPY-ir boutons and TRH-ir perikarya in the PVN was determined in double-immunostained sections. In controls, numerous contacts between NPY-ir terminals and TRH perikarya and dendrites were observed, confirming earlier findings. MSG treatment resulted in a marked reduction of the size of the Arc and also the number of NPY-perikarya with a concomitant reduction of 82.4 +/-2.1% in the relative number of NPY terminals contacting TRH perikarya and first order dendrites in the medial parvocellular and periventricular subdivisions of the PVN. In contrast, lesioning of the ascending adrenergic bundle in the brain stem caused no statistically significant change in the number of NPY-terminals in close apposition to hypophysiotropic TRH neurons in the PVN. These data confirm earlier findings that NPY-containing axon terminals innervate TRH neurons in the PVN and further demonstrate a potentially important anatomical relationship between NPY-producing neurons in the Arc and hypophysiotropic TRH neurons.

Adrenergic Fibers↗

PubMed2006

Nicotine-induced norepinephrine release in hypothalamic paraventricular nucleus and amygdala is mediated by N-methyl-D-aspartate receptors and nitric oxide in the nucleus tractus solitarius.

The noradrenergic projections from brainstem nucleus tractus solitarius (NTS) to hypothalamic paraventricular nucleus (PVN) and amygdala (AMYG) are involved in nicotine-related stress responses and drug craving. Previous studies demonstrated that i.v. nicotine-induced norepinephrine (NE) release in the PVN and AMYG depends on nicotinic cholinergic receptors in the brainstem. However, the direct site and mechanism of nicotine's action in brainstem are unknown. The present study determined the roles of NTS ionotropic glutamate receptors and nitric oxide (NO) in the effects of both local and systemic nicotine on NE release in PVN and AMYG. In male rats, an intra-NTS microinjection of nicotine (1.2 microg free base) or i.v. nicotine infusion (0.065 or 0.09 mg/kg) significantly increased NE levels in PVN and AMYG microdialysates. Prior microinjection of the N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-amino-5-phosphonopentanoic acid (0.75 or 1.5 microg), but not an alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor antagonist, dose dependently nearly abolished both PVN and AMYG NE responses to nicotine administered into NTS or systemically. NO involvement was assessed with intra-NTS microinjections of the nonselective nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester hydrochloride (10-30 nmol), or the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (0.1-0.2 nmol); both agents dose dependently inhibited i.v. nicotine-induced NE release. These results indicate that nicotine-induced NE release in PVN and AMYG is mediated entirely through the local effects of nicotine on NTS glutamate afferents and NMDA receptors that, in part, stimulate NO production, resulting in activation of noradrenergic neurons. Therefore, nicotine acts indirectly on noradrenergic NTS neurons to elicit NE release in forebrain structures.

2-Amino-5-phosphonovalerate↗

PubMed2006

I.c.v. administration of the nonsteroidal glucocorticoid receptor antagonist, CP-472555, prevents exacerbated hypoglycemia during repeated insulin administration.

Hypoglycemia elicits an integrated array of CNS-mediated counterregulatory responses, including activation of the hypothalamic-pituitary-adrenal axis. The role of antecedent adrenocortical hypersecretion in impaired glucose counterregulation remains controversial. The present studies utilized the selective, nonsteroidal glucocorticoid receptor antagonist, CP-472555, as a pharmacological tool to investigate the hypothesis that hypoglycemic hypercorticosteronemia modulates CNS efferent autonomic and neuroendocrine motor responses to recurring insulin-induced hypoglycemia via glucocorticoid receptor-dependent mechanisms. Groups of adult male rats were injected s.c. with either one or four doses of the intermediate-acting insulin, Humulin neutral protamine Hagedorn (NPH), on as many days, while controls were injected with diluent alone. Animals injected with four doses of insulin were pretreated by i.c.v. administration of graded doses of the glucocorticoid receptor antagonist or vehicle alone prior to the first three doses of insulin. Repeated daily injection of NPH exacerbated hypoglycemia, attenuated patterns of glucagon and epinephrine secretion, and diminished neuronal transcriptional activation in discrete CNS metabolic loci, including the lateral hypothalamic area, dorsomedial hypothalamic nucleus, paraventricular hypothalamic nucleus, and nucleus of the solitary tract. While i.c.v. delivery of 25 or 100 ng doses of CP-472555 did not alter any of these parameters, animals treated with 500 ng exhibited circulating glucose, glucagon, and epinephrine levels that were similar to those in rats injected with one dose of insulin, as well as a reversal of recurring insulin-induced hypoglycemia-associated reductions in Fos immunolabeling in the lateral hypothalamic area, dorsomedial hypothalamic nucleus, and paraventricular hypothalamic nucleus. These results provide unique pharmacological evidence that antecedent activation of central glucocorticoid receptor is required for exacerbation of hypoglycemia during recurring insulin-induced hypoglycemia, and that these receptors mediate modulatory effects of hypoglycemic hypercorticosteronemia on autonomic efferent responses to recurring insulin-induced hypoglycemia. The data also suggest that neurons in central loci characterized here by antagonist-mediated overturn of recurring insulin-induced hypoglycemia-induced decreases in neuronal transcriptional activation may be direct or indirect substrates for this hormonal modulation action.

Animals↗

PubMed1990

Descending projections from the hypothalamic paraventricular nucleus to the A5 area, including the superior salivatory nucleus, in the rat.

The descending projection of the hypothalamic paraventricular nucleus (PVN) to the A5 area was elucidated using a technique that combines retrograde labeling with horseradish peroxidase (HRP), anterograde labeling with PHA-L (Phaseolus vulgaris leucoagglutinin and immunohistochemistry for dopamine-beta-hydroxylase (DBH). Following an iontophoretic injection of PHA-L into the PVN, HRP was applied to the greater petrosal nerve. Frozen sections of the hypothalamus and the caudal pons were first treated according to a protocol for HRP histochemistry using tetramethylbenzidine with cobalt-enhanced diaminobenzidine, and then they were processed for displaying PHA-L, and then for DBH immunohistochemistry. PHA-L labeled fibers from the PVN were observed in a ventrolateral part of the pontine reticular formation corresponding to the A5 area, where they give rise to a dense network around the cells of origin of the greater petrosal nerve (GPN cells) and DBH-positive cells. Terminals or varicosities labeled with PHA-L were preferentially observed around the somata of GPN cells, suggesting direct contact. However, apparent contact between both elements was hardly ever observed. On the other hand, terminals or varicosities were occasionally observed in close relation to DBH-positive cells. These results suggest that descending fibers of the PVN project more strongly to GPN cells than to DBH-positive cells. The relationship of this fiber pathway to control of the secretomotor or cardiovascular systems is discussed.

Animals↗

PubMed1998

Area postrema removal abolishes stimulatory effects of intravenous interleukin-1beta on hypothalamic-pituitary-adrenal axis activity and c-fos mRNA in the hypothalamic paraventricular nucleus.

This study examined the role of the area postrema (AP) in transducing peripheral immune signals, represented by intravenous (i.v.) interleukin-1beta (IL-1), into neuroendocrine responses. The AP, a circumventricular organ with a leaky blood-brain barrier, lies adjacent to the nucleus of the solitary tract (NTS) in the medulla. The AP was removed by aspiration, and 2 weeks later, AP-lesioned or sham-lesioned rats were injected i.v. with 0.5 microg/kg IL-1 or sterile saline. After 30 min, brains were removed and analyzed for c-fos mRNA levels in various structures implicated in the hypothalamic-pituitary-adrenal axis response to peripheral cytokine challenge. The sham-lesioned animals responded to IL-1 with large elevations in adrenocorticotropic hormone (ACTH) and corticosterone levels in the plasma and c-fos mRNA levels in cells of the AP, NTS, central nucleus of the amygdala, bed nucleus of the stria terminalis, hypothalamic paraventricular nucleus (PVN), and meninges. Prior AP removal abolished the IL-1 -induced increases in ACTH and corticosterone in the plasma and c-fos mRNA levels in the NTS and PVN. However, AP removal had no effect on IL-1-induced increases in c-fos mRNA levels in the other areas examined. The selective AP lesion effects suggest that the AP and adjacent NTS play a pivotal role in transducing a circulating IL-1 signal into hypothalamic-pituitary-adrenal axis activation by a pathway that may be comprised of known anatomical links between the AP, NTS, and corticotropin-releasing hormone neurons of the PVN.

Adrenocorticotropic Hormone↗

PubMed2005

Median preoptic neurones projecting to the hypothalamic paraventricular nucleus respond to osmotic, circulating Ang II and baroreceptor input in the rat.

The present study sought to determine whether individual neurones of the median preoptic nucleus (MnPO) with axonal projections to the hypothalamic paraventricular nucleus (MnPO-PVN) respond to osmotic, circulating angiotensin II (Ang II), and baroreceptor stimulation. Hypertonic NaCl (0.75 or 1.5 osmol l(-1)) or Ang II (150 ng) was injected into the internal carotid artery (ICA). Baroreceptor stimulation was performed by i.v. injection of phenylephrine or sodium nitroprusside to increase or decrease arterial blood pressure, respectively. Of 65 MnPO neurones, 50 units were antidromically activated from the PVN with an average onset latency of 11.3 +/- 0.7 ms. Only 9.5% of MnPO-PVN neurones were antidromically activated from the PVN bilaterally. Type I MnPO-PVN neurones (n = 14) responded to osmotic but not Ang II stimulation. In 79% (11/14) of these type I neurones, the response was an increase in cell discharge. Type II MnPO-PVN neurones (n = 7) displayed a significant increase in cell discharge in response to ICA injection of Ang II but not hypertonic NaCl. Type III MnPO-PVN neurones (n = 16) responded to both ICA injection of hypertonic NaCl and Ang II. In 88% (14/16) of type III neurones, osmotic and Ang II stimulation each increased cell discharge. Type IV MnPO-PVN neurones (n = 13) displayed no change in cell discharge in response to ICA injection of hypertonic NaCl or Ang II. Baroreceptor stimulation altered the discharge in subpopulations of type I, II and III MnPO-PVN neurones (43-63% depending on neuronal type). Only one MnPO-PVN neurone responded solely to baroreceptor stimulation (type IV). In addition, a subset of type I, II and III neurones displayed a significant correlation with sympathetic nerve activity and/or the cardiac cycle. These findings suggest that a significant population of MnPO-PVN neurones respond to osmotic and circulating Ang II stimulation and thereby represents a neural substrate through which neurohumoral inputs are integrated within the forebrain lamina terminalis.

Action Potentials↗

PubMed2006

Effects of spinal cord injury on c-fos expression in hypothalamic paraventricular nucleus and supraoptic nucleus in rats.

The effects of spinal cord injury (SCI) on c-fos expression in hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON) in rats were investigated. As hypothesized, SCI has a significant effect on neuronal responses in the PVN and SON. A significant increase in c-fos in the PVN was found at 1, 6, 12 and 24 h following SCI, implying that the neurons in the PVN can be activated soon after SCI and persist for at least 24 h. However, in contrast to the PVN, SCI did not induce a significant increase in c-fos expression in the SON until 12 h following SCI. The highest expression of c-fos in the SON was found at the end point of this study (24 h) following SCI. The data demonstrated that SCI can significantly activate neurons in the PVN and SON. The activated neurons might involve in the initiation of a variety biochemical, ischemic and other injury processes. The area-specific effects of SCI on the PVN and SON suggest that these nuclei might play their roles in different stages in the prolonged time course following SCI.

Analysis of Variance↗

PubMed1993

Median preoptic neurons projecting to the hypothalamic paraventricular nucleus are sensitive to blood pressure changes.

Twenty-one neurons in the median preoptic nucleus (MnPO) were antidromically activated by electrical stimulation of the hypothalamic paraventricular nucleus (PVN) in male rats under urethane anesthesia. The activity of these identified neurons was tested for a response to activation of peripheral baroreceptors, achieved by rising arterial blood pressure with an intravenous administration of the alpha-agonist metaraminol. Of the neurons tested, 14 displayed a reduction and 2 exhibited an increase in neuronal excitability that accompanied a 30- to 50-mmHg elevation in mean arterial pressure, while 5 were unresponsive. The results show that efferent pathways from the MnPO to the PVN may receive neural inputs from the peripheral baroreceptors, suggesting the involvement of the pathways in the control of cardiovascular function.

Action Potentials↗

PubMed1987

Subfornical organ and hypothalamic paraventricular nucleus connections with median preoptic nucleus neurons: an electrophysiological study in the rat.

The role of pathways from the subfornical organ (SFO) to the hypothalamic paraventricular nucleus (PVN) through the median preoptic nucleus (MnPO) in regulating the activity of putative vasopressin (VP)-secreting neurons in the PVN was examined in urethane-anesthetized male rats. The activity of the majority (79%) of SFO neurons antidromically identified as projecting to the MnPO was excited by microiontophoretically (MIPh) applied angiotensin II (ANG II) and the effect was blocked by MIPh-applied saralasin (Sar), an ANG II antagonist. Identified SFO neurons that were excited by MIPh-applied ANG II were also excited by intravenously administered ANG II. Electrical stimulation of the SFO produced orthodromic excitation (48%) or inhibition (24%) of the activity of MnPO neurons antidromically identified as projecting to the PVN. Identified MnPO neurons that were excited by SFO stimulation were also excited by MIPh-applied ANG II, while the remaining neurons were not affected. The excitatory responses to SFO stimulation and to MIPh-applied ANG II were both blocked by MIPh-applied Sar, whereas the inhibitory responses to SFO stimulation were not affected. ANG II injected into the region of the SFO produced either an excitation (55%) or no effect (45%) on the activity of identified MnPO neurons. Electrical stimulation of the MnPO produced orthodromic excitation (27%) or inhibition (23%) of the activity of putative VP-secreting PVN neurons. ANG II injected into the region of the MnPO produced either an excitation (31%) or no effect (69%) on the activity of putative VP-secreting PVN neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1999

Neuropeptide Y innervation and neuropeptide-Y-Y1-receptor-expressing neurons in the paraventricular hypothalamic nucleus of the mouse.

The paraventricular hypothalamic nucleus (PVH) serves as integrator and link between the neuroendocrine and autonomic nervous systems. Neuropeptide-Y (NPY)-producing neurons in the arcuate nucleus project to the PVH, where neurons expressing NPY Y1 receptor (Y1R) have been demonstrated. This projection has been suggested to be involved in the regulation of parameters related to energy metabolism, e.g. food intake and thermoregulation. The present study aimed at characterizing this pathway and chemically defining Y1R-expressing neurons by means of immunohistochemistry. The densely distributed NPY-immunoreactive (ir) terminals in the PVH co-stained for agouti gene-related protein (AGRP) mainly in the medial parvocellular regions, indicating an origin in the arcuate nucleus. This was in contrast to noradrenergic/adrenergic terminals in the PVH, which were less frequently seen to contain NPY-like immunoreactivity. Furthermore, AGRP-ir terminals were seen forming abundant close appositions on Y1R-ir cell bodies. Double staining revealed co-existence of Y1R-like immunoreactivity and immunoreactivities for thyrotropin-releasing hormone (TRH) and, to a minor extent, cocaine- and amphetamine-regulated transcript peptide in parvocellular neurons. No Y1R-like immunoreactivity was noted in parvocellular neurons expressing corticotropin-releasing hormone or in magnocellular neurons expressing vasopressin or oxytocin. The present results suggest that the arcuatoparaventricular NPY projection targets the TRH neurons preferentially via the Y1R, whereas the NPYergic regulation of corticotropinergic and magnocellular neurons may be relayed through other subtypes of NPY receptors. This study further defines the link between NPY-induced feeding and the hypothalamus-pituitary-thyroid axis.

Agouti-Related Protein↗

PubMed1992

Met-enkephalin-Arg6-Gly7-Leu8- and substance P-containing projections from the nucleus preopticus medianus to the paraventricular hypothalamic nucleus.

The nucleus preopticus medianus (POMe) is known to be important for the regulation of fluid balance and cardiovascular control. Direct projections from the POMe to the paraventricular hypothalamic nucleus (PVN), where vasopressin-containing neurons exist, were examined in the rat using immunohistochemistry combined with a retrograde tract tracing method. After injection of WGA-HRP-colloidal gold into the PVN, many neurons were retrogradely labeled in the POMe; some of them were immunoreactive to Met-enkephalin-Arg6-Gly7-Leu8 (mE8) or substance P (SP). The results indicate that mE8- and SP-immunoreactive neurons in the POMe send their axons to the PVN.

Animals↗

PubMed2004

Centrally administered orexin-A activates corticotropin-releasing factor-containing neurons in the hypothalamic paraventricular nucleus and central amygdaloid nucleus of rats: possible involvement of central orexins on stress-activated central CRF neurons.

We examined the effects of centrally administered orexin-A on corticotropin-releasing factor (CRF)-containing neurons in the hypothalamic paraventricular nucleus (PVN) and the central amygdaloid nucleus (CeA) of rats, using dual immunostaining for CRF and Fos. Ninety minutes after intracerebroventricular administration of orexin-A, approximately 96% and 45% of CRF-containing neurons expressed Fos-like immunoreactivity (LI) in the PVN and the CeA, respectively. We also examined the effects of immobilized stress and cold exposure on orexin-A-containing neurons in the rat hypothalamus using dual immunostaining for orexin-A and Fos. After immobilized stress for 20 min and cold exposure at 4 degrees C for 30 min, approximately 24% and 15% of orexin-A-containing neurons expressed Fos-LI, respectively. These results suggest that orexins in the central nervous system may be involved in the activation of central CRF neurons induced by stress.

Amygdala↗