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 37 records · Page 2Linked to original sources

PubMed1994

Chemically defined collateral projections from the pons to the central nucleus of the amygdala and hypothalamic paraventricular nucleus in the rat.

Triple fluorescence labelling was employed to reveal the distribution of chemically identified neurons within the pontine laterodorsal tegmental nucleus and dorsal raphe nucleus which supply branching collateral input to the central nucleus of the amygdala and hypothalamic paraventricular nucleus. The chemical identity of neurons in the laterodorsal tegmental nucleus was revealed by immunocytochemical detection of choline-acetyltransferase or substance P; in the dorsal raphe nucleus, the chemical content of the neurons was revealed with antibody recognizing serotonin. The projections were defined by injections of two retrograde tracers, rhodamine- and fluorescein-labelled latex microspheres, in the central nucleus of the amygdala and paraventricular nucleus, respectively. Neurons projecting to both the central nucleus of the amygdala and the paraventricular nucleus were distributed primarily within the caudal extensions of the laterodorsal tegmental nucleus and dorsal raphe nucleus. Approximately 11% and 7% of the labelled cells in the laterodorsal tegmental nucleus and dorsal raphe nucleus projected via branching collaterals to the paraventricular nucleus and central nucleus of the amygdala. About half of these neurons in the laterodorsal tegmental nucleus were cholinergic, and one-third were substance-P-ergic; in the dorsal raphe nucleus, approximately half of the neurons containing both retrograde tracers were serotonergic. These results indicate that pontine neurons may simultaneously transmit signals to the central nucleus of the amygdala and paraventricular nucleus and that several different neuroactive substances are found in the neurons participating in these pathways. This coordinated signalling may lead to synchronized responses of the central nucleus of the amygdala and paraventricular nucleus for the maintenance of homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗

PubMed1996

Role of the hypothalamic paraventricular nucleus in cardiovascular regulation.

1. The paraventricular hypothalamic nucleus (PVH) is a complex structure with both neuroendocrine and autonomic functions. It is a major source of vasopressin and the primary source of corticotropin-releasing factor. In addition, parvicellular PVH neurons have reciprocal connections with brainstem autonomic centres and directly innervate sympathetic preganglionic neurons. Evidence is reviewed which indicates that in conscious rats PVH activation increases blood pressure, heart rate, renal nerve activity and plasma renin activity. 2. In conscious rats, a non-hypotensive haemorrhage (13 mL/kg blood loss over 24 min) results in increased numbers of Fos-immunoreactive cell nuclei within both magnocellular and parvicellular PVH neurons, including the ventral medial parvicellular regions known to contain neuronal projections to brainstem autonomic centres and spinal cord sympathetic preganglionic neurons. 3. Cell-selective ibotenate lesions of the parvicellular PVH significantly blunt the corticosterone response but do not alter blood pressure, heart rate or plasma renin concentration response to non-hypotensive or hypotensive haemorrhage. This and earlier studies indicate that, while the PVH is necessary for the corticosterone response and contributes to increased vasopressin release during blood loss, it does not play an important role in the sympathetic nervous system and renin-angiotensin responses to hypovolaemia and hypotension. 4. There is evidence to indicate that the parvicellular PVH serves as a necessary relay for cardiovascular and renin responses to certain behavioural stressors. We propose that cardiovascular information relayed to parvicellular PVH autonomic regions may be used to modulate behavioural, rather than homeostatic, effects on haemodynamics and renin release.

Animals↗

PubMed1985

Connections of neurons in the region of the nucleus tractus solitarius with the hypothalamic paraventricular nucleus: their possible involvement in neural control of the cardiovascular system in rats.

Extracellular recordings were made from 607 spontaneously firing neurons within the nucleus tractus solitarius (NTS) and its vicinity in urethane-anesthetized male rats. Following electrical stimulation of the hypothalamic paraventricular nucleus (PVN) area, 21% of the neurons were orthodromically excited, 6% were inhibited and 2.5% were antidromically activated. The antidromic spike latencies were 22-64 ms. Among those orthodromically responding neurons, 81 neurons were tested by pressure pulse stimulation of the isolated carotid sinus. The pressure stimulation produced excitation in 7 and inhibition in 13 neurons. Of the 8 tested neurons which were antidromically activated, one neuron was excited and another neuron inhibited by the pressure pulse stimulation. These results provide electrophysiological evidence for reciprocal connections between neurons in the NTS region and the PVN, and give support to the hypothesis that the PVN is involved in the neural control of the cardiovascular system.

Animals↗

PubMed1995

Effects of prolonged social isolation on responses of neurons in the bed nucleus of the stria terminalis, preoptic area, and hypothalamic paraventricular nucleus to stimulation of the medial amygdala.

The studies presented demonstrate changes in hypothalamo-pituitary-adrenocortical secretion, and in electrical activity and synaptic responses of neurons in the bed nucleus of the stria terminalis, preoptic area, and hypothalamic paraventricular nucleus of rats exposed to early, long-term social isolation. Rats isolated from all social contact from an early preweaning time showed reduced basal plasma corticosterone concentrations, compared with littermate controls raised under social conditions. Isolated animals also exhibited a selective decrease in the spontaneous electrical activity of neurons within the hypothalamic paraventricular nucleus and lateral preoptic area, but not in adjacent structures. Moreover, isolation also altered the response of neurons in certain nuclei to electrical stimulation of the medial amygdala. Thus, a reduction in excitatory responses, and an increase in inhibition and nonresponsiveness, of preoptic area and paraventricular nucleus neurons was recorded, compared with control rats. Neurons in the bed nucleus of the stria terminalis were less affected, but showed an increase in the duration of excitatory responses following medial amygdala stimulation. These results, obtained from urethane-anesthetized rats, together with the reduced basal plasma corticosterone concentrations, suggest a reduction in limbic-hypothalamo-pituitary-adrenocortical (LHPA) activity following maternal deprivation and prolonged social isolation. This may result from altered limbic activity, specifically in the amygdala and its pathways to the paraventricular nucleus (PVN). Such alterations may include the stria terminalis, in so much as increased efficacy of inhibitory components and reduced efficacy of excitatory components was observed. The neural mechanisms underlying these alterations could involve an altered synaptology of the regions examined and/or a disruption of glucocorticoid feedback events.

Amygdala↗

PubMed1993

Branching projections of catecholaminergic brainstem neurons to the paraventricular hypothalamic nucleus and the central nucleus of the amygdala in the rat.

In this study, we have employed triple fluorescent-labelling to reveal the distribution of catecholaminergic neurons within three brainstem areas which supply branching collateral input to the central nucleus of the amygdala (CNA) and the hypothalamic paraventricular nucleus (PVN): the ventrolateral medulla (VLM), the nucleus of the solitary tract (NTS) and the locus coeruleus (LC). The catecholaminergic identity of the neurons was revealed by immunocytochemical detection of the biosynthetic enzyme, tyrosine hydroxylase. The projections were defined by injections of two retrograde tracers, rhodamine- and fluorescein-labelled latex microspheres, in the CNA and PVN, respectively. In the VLM and NTS, the greatest incidence of neurons which contained both retrograde tracers was found at the level of the area postrema. These neurons were mainly located within the confines of the A1/C1 (VLM) and A2 (NTS) catecholaminergic neuronal groups. Double-projecting neurons in the LC (A6) were distributed randomly within the nucleus. It was found that 15% in the VLM, 10% in the NTS and 5% in the LC of the retrogradely labelled cells projected via branching collaterals to the PVN and CNA. One half of these neurons in the VLM and NTS were catecholaminergic, in contrast to the LC where virtually all double-retrogradely labelled neurons revealed tyrosine hydroxylase immunoreactivity. In the other brainstem catecholaminergic cell groups (A5, A7, C3), no catecholaminergic neurons were found that supplied branching collaterals to the CNA and PVN. Our results indicate that brainstem neurons may be involved in the simultaneous transmission of autonomic-related signals to the CNA and the PVN. Catecholamines are involved in these pathways as chemical messengers. Brainstem catecholaminergic and non-catecholaminergic neurons, through collateral branching inputs may provide coordinated signalling of visceral input to rostral forebrain sites. This may lead to a synchronized response of the CNA and PVN for the maintenance of homeostasis.

Amygdala↗

PubMed1997

c-fos expression in the rat hypothalamic paraventricular nucleus induced by LiCl: descending projections to the dorsal vagal motor nucleus.

Anorexia inducing lithium chloride is believed to involve descending projections from hypothalamus to preganglionic autonomic output neurons. A multiple-labelling technique has presently been used to analyze the anatomical projections of lithium chloride sensitive neurons in the hypothalamus. Immunolabelling of c-fos was performed to stain neurons activated after LiCl administration, while neurons projecting toward vagal parasympathetic preganglionic levels were identified by injection of diamidino yellow in the dorsal motor nucleus of the vagus. Perikarya of descending neurons were mainly observed in the ventral and lateral areas of the paraventricular hypothalamic nucleus. In contrast, lithium chloride activated neurons were observed mainly in the magnocellular division of the paraventricular nucleus and supraoptic nucleus. Double-labelled neurons were not observed. These data provide evidence that lithium chloride sensitive neurons in the paraventricular nucleus are clearly different from those descending toward preganglionic vagal outflow neurons.

Animals↗

PubMed1996

Hypothalamic paraventricular nucleus involvement in the pressor response to N-methyl-d-aspartic acid in the periaqueductal grey matter.

The aim of this study was to demonstrate paraventricular hypothalamic nucleus (PVN) involvement in the cardiovascular changes induced by N-methyl-d-aspartic acid (NMDA) microinjections at the level of periaqueductal grey (PAG) matter. The study was carried out in anaesthetized rats and the arterial blood pressure monitored by a polygraph. NMDA injections (0.68-6.8 nmol/rat) into the PAG area induced a significant increase in blood pressure. After pretreatment by injection of the NMDA receptor antagonist dl-2-amino-5-phosphonovaleric acid (2-APV, 0.05-5 nmol/rat) into the PVN, administration of NMDA (0.68 nmol/rat) into the PAG area elicited a decrease, rather than an increase, of blood pressure. We observed a significant reduction of the pressor effect induced by 6.8 nmol/rat NMDA after 2-APV injection into the PVN. 2-APV injection into the dorsomedial hypothalamic nucleus, an area near the PVN, did not modify the increase in blood pressure induced by NMDA in the PAG area. We suggest the existence of a glutamatergic connection between the PAG area and the PVN in the cardiovascular effects of NMDA.

Animals↗

PubMed1994

Alpha-1-noradrenergic inhibition of growth hormone secretion is mediated through the paraventricular hypothalamic nucleus in male rats.

In the present work we investigated a possible role of an alpha 1-noradrenergic (NA) pathway involving the hypothalamic paraventricular nucleus (PVN) in the central regulation of growth hormone (GH) release. A week after bilateral electrolytic lesions of the PVN, pulsatile GH-secretory patterns were monitored in unanesthetized, freely moving control or lesioned male rats. While the pulsatility of GH secretion was maintained, the amplitude of the pulses and the area under the curve during an 8-hour sampling period were twice as high in PVN-lesioned than in control rats. Trough levels of GH were similar in the two groups. Inactivation of PVN alpha 1-receptors by local infusion of an alpha 1-NA antagonist, prazosin (50 ng/rat), also induced an increase in GH release. In control animals, intravenous injection of the alpha 1-NA agonist methoxamine (0.02 mg/100 g body weight) elicited a decrease in GH release but was ineffective when administered to PVN-lesioned rats. These data show that alpha 1-NA receptors, mediating GH inhibition, are located in the PVN. In light of the analogous effects observed herein on PVN-lesioned animals and, previously, after locus coeruleus (LC) lesions it is suggested that GH inhibition by the LC is relayed by the PVN via a local alpha 1-receptor population.

Adrenergic alpha-Agonists↗

PubMed2005

Blockade of endogenous angiotensin-(1-7) in the hypothalamic paraventricular nucleus reduces renal sympathetic tone.

In this study, we tested the hypothesis that angiotensin-(1-7) [Ang-(1-7)] acting in the neurons of paraventricular hypothalamic nucleus (PVN) contributes to the maintenance of sympathetic activity and blood pressure. For this purpose, the effects of microinjection of the A-779, the receptor Mas antagonist, into the PVN on mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were evaluated. In rats anesthetized with urethane (1.2 to 1.4 g/kg IP), bilateral microinjections of A-779 (0.1 nmol) into the PVN resulted in a selective and significant decrease in RSNA (-26+/-6% versus -2+/-3% vehicle; saline 0.9%). The magnitude of the decrease in RSNA produced by A-779 was comparable to that observed after microinjection of muscimol (1 nmol; -26+/-4%), a powerful neuronal inhibitor. A higher dose of A-779 (1 nmol) caused a reduction in RSNA (-21+/-4%) that was comparable in magnitude to the reduction observed with the lower dose. When compared with vehicle solution, no significant changes in MAP or HR were observed with both doses of A-779 tested. A decrease in RSNA was also observed after microinjections into the PVN of the angiotensin II type 2 (AT2) receptor antagonist PD123319 (1 nmol; -18+/-4%). Microinjections of the AT1 antagonist losartan but not CV 11974 reduced MAP without changing RSNA. These results suggest that Ang-(1-7) Mas receptors and AT2 receptors in the PVN neurons play a role in mediating the tonic maintenance of RSNA.

Angiotensin I↗

PubMed1990

Peptide-amine interactions in the hypothalamic paraventricular nucleus: analysis of galanin and neuropeptide Y in relation to feeding.

The neuropeptide galanin (GAL) has been found to elicit feeding after injection into the paraventricular hypothalamic nucleus (PVN), where it coexists with norepinephrine (NE), a neurotransmitter believed to be important in the control of natural feeding behavior. Using pharmacological tools, this study investigated the possibility that PVN GAL influences food intake via its direct interaction with the noradrenergic system localized in this nucleus. Tests with alpha-adrenergic receptor blockers demonstrated that GAL-induced feeding, similar to NE-stimulated feeding, depends specifically upon functional alpha 2-receptor sites. Further, experimentation with the catecholamine synthesis inhibitors, alpha-methyl-p-tyrosine and Fla-63, suggested that GAL's action also depends upon the release of endogenous NE. This is in contrast to another hypothalamic peptide, neuropeptide Y, which is also a strong stimulant of food intake and coexists with NE in the PVN. Neuropeptide Y remains effective in eliciting feeding in the presence of alpha 2-receptor antagonists and catecholamine-synthesis inhibitors, suggesting that, unlike GAL, it can act independently of endogenous NE.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

[Reactions of the paraventricular hypothalamic nucleus and of the dorsal hippocampus in long-term adaptation to hypoxia].

In experiments on 17 Wistar rats the physiological activity was studied after stereotaxic electrode implantation according to the indices of the pulse rate and impedance, hypothalamic paraventricular nucleus and dorsal hippocamp under conditions of 30-day barochamber hypoxia (6 hours daily), at the imitated "height" of 6 km. The change recurrence was found, characterized by a prolonged period of the nucleus activation with parallel protective relieving inhibition of the dorsal hippocamp, followed by a fall in the nucleus activity and a marked hippocamp stimulation with hyporeactivity of the organism on hypoxia itself. The subsequent wave of the nucleus activation was transitory and was accompanied again by the hippocamp inhibition. The observed cyclic changes in physiological processes of the nucleus and hippocamp showed the mechanism of development of the organism adaptation to hypoxia.

Adaptation, Physiological↗

PubMed1988

Distributions of pro-vasopressin expressing and pro-vasopressin deficient CRH neurons in the paraventricular hypothalamic nucleus of colchicine-treated normal and adrenalectomized rats.

The corticotropin-releasing hormone (CRH) neurosecretory system in normal rats consists of two major subpopulations of parvicellular neurons in the hypothalamic paraventricular nucleus distinguished by the presence or absence of coexistent vasopressin precursor (pro-AVP)-derived peptides. These neurons project to the external zone of the median eminence, where the two subtypes of axons (CRH +/AVP + and CRH+/AVP-) were previously found to be approximately equal in number. The present study was undertaken 1) to determine whether the relative numbers of pro-AVP expressing and pro-AVP deficient perikarya in the paraventricular nucleus corresponded to what we previously found for the axons in the median eminence, 2) to map the two cell types throughout the entire paraventricular nucleus to determine whether significant differences existed in their distributions, and 3) to ascertain whether or not the pro-AVP deficient subpopulation expressed pro-AVP after adrenalectomy. Postembedding electron microscopic immunocytochemistry on serial ultrathin sections was used to identify the peptide phenotypes of perikarya in the paraventricular nucleus in normal rats and 7 days after adrenalectomy with and without colchicine treatment. The peptide phenotypes of neuronal perikarya in the paraventricular nucleus were identified by using antibodies to CRH, AVP, neurophysin (NP), the C-terminal glycopeptide of pro-AVP (GP), and oxytocin-associated neurophysin (NPOT). Groups of three serial coronal ultrathin sections were analyzed at 200-micron intervals throughout the entire rostrocaudal extent of the paraventricular nucleus. The sections in each group were stained for CRH, a pro-AVP-derived peptide (AVP, NP, or GP), and NPOT, respectively. Parvicellular CRH neurons were defined as CRH-positive cells, approximately 10 micron in diameter, that did not contain detectable NPOT. Pro-AVP expressing cells were defined as staining positively for AVP, GP, or NP and negatively for NPOT. Approximately equal numbers of pro-AVP expressing ("NPAVP+") and pro-AVP deficient ("NPAVP-") parvicellular CRH neurons were found within the paraventricular nucleus of colchicine-treated normal rats, and the two subtypes were distributed differently within the paraventricular nucleus. Although the pro-AVP expressing CRH cells stained intensely for NP and GP, staining for AVP was quite variable and difficult to quantify in colchicine-treated normal animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗

PubMed1992

Differential effects of galanin and neuropeptide Y on extracellular norepinephrine levels in the paraventricular hypothalamic nucleus of the rat: a microdialysis study.

Evidence suggests that the peptides galanin (GAL) and neuropeptide Y (NPY) interact with the amine norepinephrine (NE) in the hypothalamic paraventricular nucleus (PVN) to stimulate feeding behavior. To directly investigate the nature of these interactions, extracellular levels of PVN NE were monitored in freely-moving rats using the microdialysis/HPLC technique. Following PVN administration of GAL (0.3 nmol), NPY (78 pmol) or Ringer's solution, local NE levels were measured at 20-min intervals for 2 hrs postinjection, under two feeding conditions, namely, in the presence or absence of food. The results demonstrate different effects of these peptides on endogenous NE levels. Following GAL administration, PVN NE levels were enhanced by 80 to 90%, up to 40 min postinjection, independent of food availability. In contrast, following NPY injection, NE levels were significantly reduced 20 min postinjection with food absent, and when food was available, NE levels tended to be enhanced. These results, consistent with pharmacological and biochemical studies, reveal different patterns of peptide-amine interactions in the PVN.

Animals↗

PubMed1985

Similarity between cytoplasmic inclusions in the paraventricular hypothalamic nucleus neurons of the turtle Mauremys caspica and the cytoplasmic structures as reaction to viral infections (hepatitis) and SIDA ultrastructural tracers.

Two types of "inclusions" observed in the neurons of the hypothalamic paraventricular nucleus of the turtle Mauremys caspica, "tubular systems" and "fingerprint-like" structures, may be added to the inventory of those described in apparently normal neurons. Despite their enigmatic significance, we are inclined to think that they could be a morphological expression of viral diseases in the neuron cytoplasm. These structures have a striking similarity with those observed on pathological cells (hepatitis and SIDA).

Animals↗

PubMed2002

Multiple NPY receptors Inhibit GABA(A) synaptic responses of rat medial parvocellular effector neurons in the hypothalamic paraventricular nucleus.

We have recently shown that NPY and alpha-melanocyte-stimulating hormone, which potently induce or inhibit feeding, respectively, have opposing modulatory actions on GABAergic synapses in the medial parvocellular region of the paraventricular hypothalamic nucleus (mpPVN). Because this action might underlie the effects of NPY on feeding, we have examined the pharmacology of NPY responses using electrophysiological recordings. Focal electrical stimulation within the PVN elicited a GABA(A) synaptic response in some mpPVN neurons, which was reversibly inhibited by NPY in a concentration-dependent manner (EC(50) = 28 nM). NPY did not alter the response to the GABA(A) agonist, muscimol. Agonist responses to NPY analogs were not consistent with a single NPY receptor subtype; the most subtype selective agonists were less effective than the more broadly selective ones. Antagonist blockade of individual receptor subtypes partly inhibited NPY action, while fully blocking effects of selective agonists. Combining Y1 and Y5 antagonists blocked actions of NPY entirely, but the Y2 antagonist also completely blocked actions of NPY in some neurons. NPY inhibits GABA(A) synaptic transmission onto mpPVN neurons, but this can be mediated by three different NPY receptors. Controversy regarding the receptor or receptor subtypes involved in NPY-mediated feeding may arise from the multiple NPY receptors present.

Animals↗

PubMed1991

Bombesin immunoreactive neurons in the hypothalamic paraventricular nucleus innervate the dorsal vagal complex in the rat.

Bombesin-like immunoreactivity has been localized within neuronal cell bodies of the hypothalamus and nerve terminals within the dorsal vagal complex. The possibility that the hypothalamus is a source for bombesin-like immunoreactive terminals within the dorsal vagal complex was examined using the combined retrograde tracing and immunohistochemical technique. After injections of retrograde tracer were made into the dorsal vagal complex, cells in the hypothalamus labeled with both retrograde tracer and bombesin immunoreactivity were localized in the parvocellular part of the paraventricular nucleus. In the paraventricular nucleus most of the vagal projecting bombesin immunoreactive neurons were located within the medial parvocellular subdivision. Approximately 30% of the bombesin immunoreactive neurons in this subnucleus projected to the dorsal vagal complex. The results suggest that the paraventricular hypothalamic nucleus is a major source of bombesin terminals within the dorsal vagal complex. This pathway may mediate some of the autonomic nervous system changes that are observed when bombesin is injected within the central nervous system. Additionally, this data adds to a growing amount of evidence supporting the role of bombesin as a peptide neurotransmitter.

Amidines↗

PubMed1987

Analysis of peptide histidine-isoleucine/vasoactive intestinal polypeptide-immunoreactive neurons in the central nervous system with special reference to their relation to corticotropin releasing factor- and enkephalin-like immunoreactivities in the paraventricular hypothalamic nucleus.

The distribution of peptide histidine-isoleucine (PHI) and vasoactive intestinal polypeptide (VIP), two peptides derived from the same precursor molecule, was analysed with immunohistochemistry in the central nervous system of the rat, and to a limited extent in some other species including sheep, monkey and man. Special attention was focused on possible cross-reactivity between PHI antisera and corticotropin releasing factor in parvocellular neurons in the hypothalamic paraventricular nucleus projecting to the external layer of the median eminence. (1) Characterization of the PHI and VIP antisera revealed that they recognized different sequences of the peptide molecules. One of the PHI antisera (PHI-N), although mainly N-terminally directed, also probably contained an antibody population directed against the C-terminal amino acid in PHI which is an amidated isoleucine. Rat and human corticotropin releasing factor but not ovine also have an amidated isoleucine in C-terminal position. (2) PHI- and VIP-like immunoreactivity were found with parallel and overlapping distribution in all areas investigated in the rat central nervous system. In many cases coexistence of the two immunoreactivities could be directly demonstrated. PHI neurons were found in some areas so far not know to contain PHI/VIP neurons, including the dorsal septum, the septofimbrial nucleus, the stria terminalis and lamina V of the spinal cord. (3) Using an antiserum directed against the amino acid sequence 111-122 of the VIP/PHI precursor, immunoreactive cell bodies were seen in some areas containing VIP and PHI neurons. PHI- and VIP-like immunoreactivity were expressed in parallel in increasing amounts in the superficial laminae of the dorsal horn after transection of the sciatic nerve [G. P. McGregor et al. (1984) Neuroscience 13, 207-216; S. A. S. Shehab and M. E. Atkinson (1984) J. Anat. 139, 725; S. A. S. Shehab and M. E. Atkinson (1986) Expl Brain Res. 62, 422-430]. (5) The PHI-N antiserum stains large numbers of immunoreactive cells in the parvocellular part of the paraventricular nucleus and these cells are mostly identical with corticotropin releasing factor-positive neurons. Absorption experiments suggested that this PHI-N-like immunoreactivity to a large extent represented cross-reactivity with rat CRF and that earlier demonstration of many PHI-positive neurons in the paraventricular nucleus probably represents an artefact as proposed by F. Berkenbosch et al. (Neuroendocrinology 44, 338-346). However, some cells did, in fact, contain VIP- as well as PHI-like immunoreactivity as was shown with antisera not cross-reacting with corticotropin releasing factor.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1986

Effects of mu-opioid receptor stimulation in the hypothalamic paraventricular nucleus on basal and stress-induced catecholamine secretion and cardiovascular responses.

Previous work from this laboratory has demonstrated that opioid peptides, acting at mu-receptors in the brain, stimulate central sympathetic outflow thereby increasing plasma catecholamine concentrations in unstressed rats. Brain sites involved in opioid-mediated catecholamine secretion have not been characterized fully. Additionally, brain opioid effects on sympathoadrenal catecholamine secretion during stress have not been defined. Because the paraventricular hypothalamic nucleus (PVN) plays a central role in autonomic and cardiovascular regulation, we administered the mu-selective enkephalin analog, D-Ala2-NMe-Phe4-Gly(ol)5enkephalin (DAGO), directly into PVN in conscious, unstressed rats and determined the changes in plasma catecholamine concentrations, blood pressure and heart rate. Then, during the peak response, rats were subjected to restraint stress and the same parameters were again measured. Under basal conditions, picomolar doses of DAGO injected into PVN increased plasma concentrations of catecholamines, especially epinephrine, and raised blood pressure. These effects were dose-related (0.01-0.3 nmol) and antagonized by naloxone given either systemically or directly into PVN. Tachycardia was also observed except at the highest dose of DAGO (0.3 nmol). Thus, mu-receptor stimulation in PVN increases central sympathetic outflow in nonstressful situations, producing increased adreno-medullary catecholamine secretion, blood pressure and heart rate. During restraint stress, PVN microinjections of DAGO blunted stress-induced tachycardia, apparently by a vagal mechanism as this effect was blocked by atropine methyl nitrate. PVN DAGO had no significant effect on the plasma catecholamine responses to restraint stress. In contrast, naloxone injected into PVN augmented stress-induced epinephrine secretion. Thus, PVN mu-receptors may regulate heart rate during stress, and an endogenous opioid released during restraint stress may modulate adrenomedullary responses to stress.

Animals↗