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At least 19 recordsLinked to original sources
PubMed1989

Direct projections from the central amygdaloid nucleus to the hypothalamic paraventricular nucleus: possible role in stress-induced adrenocorticotropin release.

The amygdala, particularly the central amygdaloid nucleus, is important for the expression of adrenocorticotropin and corticosterone responses during stress. The aim of the present study was to determine if the central amygdaloid nucleus directly innervated the hypothalamic paraventricular nucleus. To accomplish this aim, the Phaseolus vulgaris leucoagglutinin lectin anterograde tracing method was used. Injections of the tracer into the medial central amygdaloid nucleus resulted in axonal and terminal labeling within the medial and lateral parvocellular parts of the caudal paraventricular nucleus. A dense patch of labeling was observed within the lateral wing of the lateral part of the parvocellular paraventricular nucleus. Only a few labeled axons were observed within the paraventricular nucleus of animals that had lectin injections localized to the lateral part of the central nucleus. Tracer injections localized to the medial amygdaloid nucleus resulted in axonal and terminal labeling primarily within the anterior parvocellular and periventricular regions of the paraventricular hypothalamic nucleus. Sparse to moderate axonal and terminal labeling was observed within the magnocellular parts of the paraventricular nucleus in animals that had injections of tracer into either the medial central nucleus or the medial nucleus. No labeling was observed within the paraventricular nucleus of animals that had injections of lectin within other amygdaloid nuclei or adjacent regions of the striatum. The results demonstrated a topographically organized projection from the amygdala to the hypothalamic paraventricular nucleus. The central nucleus mainly innervates the caudal lateral and medial parvocellular paraventricular nucleus. The medial nucleus innervates the rostral parvocellular parts of the paraventricular nucleus. These pathways could form the anatomical substrates of amygdaloid modulation of neuroendocrine responses to stressors.

Adrenocorticotropic Hormone↗
PubMed1988

Dynamism of chemoarchitecture in the hypothalamic paraventricular nucleus.

The hypothalamic paraventricular nucleus (PVN) has been implicated in a remarkable number of functions including control of pituitary-adrenocortical activity in response to stress, body fluid homeostasis, milk ejection reflex, prolactin secretion, thyroid hormone secretion, analgesia, food intake, gastrointestinal functions, cardiovascular functions, and control of pineal melatonin synthesis. Paraventricular neurons produce hormones of key importance in neuroendocrine regulation such as vasopressin (VP), oxytocin (OX), 41-residue corticotropin releasing factor (CRF), thyrotropin releasing hormone (TRH), somatostatin (SOM) and the putative prolactin releasing factor vasoactive intestinal polypeptide (VIP). Three recent advances pertinent to the organization of the PVN include: (1) the evidence that the structure of the PVN is compartmental in nature, topographically segregated cellular units seem to carry out different functions; (2) the discovery that paraventricular neurons are capable of expressing a multitude of neuromediators simultaneously, thus cellular units can be best specified by a certain combination of neuromediators; (3) evidence that the composition of the neuromediator "cocktail" in individual neurons is variable and depends on the physiological status of the animal. Hence, the PVN may be best considered as a dynamic mosaic of chemically specified subgroups of neurons. The flexibility of neurotransmitter status in paraventricular neurons may play a central role of a functional plasticity of fixed anatomical circuits.

Animals↗
PubMed1986

In vivo voltammetric monitoring of noradrenaline release and catecholamine metabolism in the hypothalamic paraventricular nucleus.

The paraventricular hypothalamic nucleus receives a dense noradrenergic innervation. Electrochemically treated carbon fibre electrodes were implanted in the paraventricular nucleus of anaesthetized rats and their locations were histologically controlled after each experiment. Differential normal pulse voltammograms showed an oxidation peak at +50 mV. This peak was mainly due to 3,4-dihydroxyphenylacetic acid synthesized by noradrenergic terminals since: it appeared at the same oxidation potential as 3,4-dihydroxyphenylacetic acid in vitro; it was rapidly suppressed after inhibition of tyrosine hydroxylase by alpha-methyl-p-tyrosine or monoamine oxidase by pargyline; blockade of dopamine-beta-hydroxylase by FLA 63 induced a marked increase in this signal, whereas this drug was without effect in dopaminergic terminals fields (striatum, zona incerta); stimulation of alpha 2 noradrenergic receptors by clonidine (50 micrograms/kg) decreased the peak height and this effect was reversed by piperoxane (30 mg/kg). This oxidation peak corresponded to a 3,4-dihydroxyphenylacetic acid concentration of 2 microM. On the other hand, when recorded from rats which were treated with pargyline 3 h before recording, a small peak appeared at +100 mV. This signal was attributed to the oxidation of extracellular noradrenaline on the basis of the following arguments: it appeared at the same potential as noradrenaline in vitro; desipramine (25 mg/kg) induced a 4-fold increase in this peak height; piperoxan (2 mg/kg) enhanced this signal and reversed the decrease induced by clonidine (50 micrograms/kg); electrical stimulations (bipolar electrode, square pulses, 0.3 ms, 200 microA, 15 Hz for 40 s) in the rostral part of the A1 group were followed by an immediate, short-lasting 4-fold increase in the signal.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Adrenergic projections from the lower brainstem to the hypothalamic paraventricular nucleus, the lateral hypothalamic area and the central nucleus of the amygdala in rats.

Fine networks of phenylethanolamine N-methyltransferase (PNMT)-immunoreactive fibers are found in the hypothalamic paraventricular nucleus--mainly in the anterior, dorsal and dorso-medial parvicellular subdivisions, the lateral hypothalamus (dorsal, lateral and ventral to the fornix) and in the central amygdaloid nucleus. Coronal hemisections of the brainstem through the rostral level of the medulla oblongata show that most hypothalamic and amygdaloid PNMT fibers arise from the medullary adrenergic cell groups. Fourteen, but not 10 days after total hemisections, PNMT fibers disappeared almost completely from the hypothalamus and amygdala, ipsilateral to the knife cuts. A small decrease was also observed in the ventral, lateral hypothalamus on the contralateral side. Partial depletion of PNMT-immunoreactivity in the hypothalamus and the amygdala after medial or lateral brainstem hemisections indicates that ascending PNMT-immunoreactive fibers pass through mainly the lateral portion of the medulla, but some fibers also in its medial portion. Midsagittal transection of the diencephalon slightly reduced PNMT immunostaining in the paraventricular nucleus and the lateral hypothalamus bilaterally. The results show that the ascending PNMT system essentially is ipsilateral, but probably with a small crossing-over component, both at the diencephalic and lower brainstem level.

Adrenergic Fibers↗
PubMed1985

An enkephalinergic projection from the hypothalamic paraventricular nucleus to the hypothalamic ventromedial nucleus of the rat: an experimental immunohistochemical study.

The distribution and origins of enkephalin-like immunoreactive (ENK-IR) fibers in the nucleus ventromedialis hypothalami (vm) of the rat were examined using immunohistochemistry. A dense plexus was evenly distributed in the vm with no regional differences. A group of ENK-IR neurons was concentrated in the ventrolateral portion of the vm. The destruction of the hypothalamic paraventricular nucleus (pv) which contained numerous ENK-IR neurons, resulted in a marked decrease in ENK-IR fibers in the vm on the operated side. In addition, the destruction of the magnocellular portion of the pv, while leaving most of parvocellular portion intact, failed to substantially decrease the ENK-IR fibers in the vm, suggesting that these fibers originate from ENK-IR neurons located in the parvocellular portion of the pv. The present study further showed that the axons of these neurons first proceeded laterally to the perifornical area, next ran ventrolaterally to the ventrolateral portion of the anterior hypothalamic nucleus and finally turned medially to the vm.

Animals↗
PubMed1988

Ether stress stimulates noradrenaline release in the hypothalamic paraventricular nucleus.

Differential normal-pulse voltammetry was combined with treated carbon fibre electrodes for monitoring in vivo extracellular catechols synthesized by noradrenergic terminals innervating the paraventricular hypothalamic nucleus. From urethane-anaesthetized rats, pretreated with a monoamine oxidase inhibitor, pargyline, we were able to monitor a catechol signal which unequivocally corresponded to extracellular noradrenaline, and we observed that ether inhalation for 2 min induced an immediate increase in this signal. Electrical stimulation of the ventral noradrenergic pathway (10 Hz for 40 s) induced a similar effect. On the other hand, from freely moving rats which were not treated with pargyline, we recorded a catechol peak which mainly corresponded to 3,4-dihydroxyphenylacetic acid which was synthesized by noradrenergic terminals. However, electrochemical and biochemical evidence strongly suggested that the increase in this signal induced by a 2-min ether stress does not correspond to 3,4-dihydroxyphenylacetic acid, but to an increase in the extracellular noradrenaline concentration. In both experimental situations the time course of the effects was identical: ether stress induced an immediate and pronounced increase in norepinephrine release, and this effect lasted as long as the stimulus duration. This effect appeared specific for noradrenergic terminals, since no effect on dopamine release was observed when recorded from the striatum or behind the paraventricular hypothalamic nucleus from the A13 dopaminergic group. In conclusion, our data are consistent with those which suggest a facilitatory action of norepinephrine on neurosecretory neurons whose cell bodies are located in the paraventricular hypothalamic nucleus and which play a major role in the hormonal response to stress.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Ontogeny of expression of the corticotropin-releasing factor gene in the hypothalamic paraventricular nucleus and of the proopiomelanocortin gene in rat pituitary.

The ontogeny of expression of the CRF gene in the paraventricular hypothalamic nucleus and POMC gene in the pituitary was studied in rats using in situ hybridization histochemistry and Northern blotting techniques, respectively. CRF mRNA was first detected on day 17 of gestation (E17) in the paraventricular nucleus of the hypothalamus. The levels of hypothalamic CRF mRNA increased progressively from E17 to E19-E20, decreased during the perinatal period, and increased thereafter. The levels of POMC mRNA in the pituitary paralleled the variations in hypothalamic CRF mRNA, showing a peak on E20-E21. POMC mRNA levels in the anterior pituitary were decreased on days 4-7 after birth (P4-P7) and increased steadily thereafter. In contrast to levels in the anterior pituitary, POMC mRNA levels increased steadily from P1 to P21 in the neurointermediate lobe of the pituitary. These data indicate that the expression of both the CRF and POMC genes in the paraventricular nucleus and anterior pituitary, respectively, are reduced during the first week of life, i.e. within the so-called stress nonresponsive period. Our observations suggest that an impaired regulation of ACTH and CRF synthesis due to an immature neuronal pathway within the brain or increased glucocorticoid feedback may account for the stress nonresponsive period.

Animals↗
PubMed1990

Stress-induced renin and corticosterone secretion is mediated by catecholaminergic nerve terminals in the hypothalamic paraventricular nucleus.

Cell bodies in the hypothalamic paraventricular nucleus (PVN) mediate stress-induced increases in renin and corticosterone secretion. Since the PVN has an extensive catecholaminergic innervation, we wanted to determine the role of catecholamines in the neuroendocrine response to stress. The stressor was a conditioned emotional (fear) response paradigm (CER). The catecholamine neurotoxin, 6-hydroxydopamine (6-OHDA), was injected into the PVN 14 days before the rats were subjected to the CER procedure. Damage to noradrenergic nerve terminals was verified immunocytochemically, using an antibody against dopamine beta-hydroxylase. Injection of 6-OHDa into the PVN prevented the stress-induced increase in plasma renin activity (PRA), plasma renin concentration (PRC) and plasma corticosterone concentration, suggesting that intact catecholaminergic innervation of neurons in the PVN is necessary for the stress-induced increase in renin and corticosterone secretion. To determine if beta-adrenoceptors in the PVN mediate the effect of stress on renin and corticosterone secretion, the beta-adrenoceptor antagonist sotalol was injected into the PVN through chronically implanted bilateral cannulae. The injection was performed on the 4th day of the CER paradigm, just before the rats were placed into the CER chamber. Sotalol prevented the stress-induced increase in corticosterone concentration, but did not diminish the stress-induced increase in PRA and PRC. These results suggest that the stress-induced increase in corticosterone concentration is influenced by beta-adrenoceptors in the PVN. The stress-induced increase in PRA and PRC is mediated by different receptors whose ligands might be catecholamines acting at non-beta-receptors or other neuroactive substances colocalized in catecholaminergic nerve terminals.

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↗
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↗
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↗
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↗
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↗