Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the role of histamine (HA) in the neuroendocrine regulation of PRL secretion in conscious male rats. Blood samples were obtained by decapitation of the animals at 0 min. Intracerebroventricular infusion of HA (34-540 nmol at -15 min) stimulated PRL secretion dose dependently with an ED50 of approximately 135 nmol. Inhibition of neuronal HA synthesis by the specific histidine decarboxylase-inhibitor (S)alpha-fluoro-methylhistidine (alpha FMH; 100 mumol/kg ip at -6 h or 400 mumol/kg ip at -20 h and -6 h) caused a 50% reduction (P less than 0.01) in the PRL response to 5 min of restraint stress. Inhibition of neuronal HA metabolism by the specific histamine-methyltransferase-inhibitor SKF-91488 (400 and 800 nmol icv at -20 min) augmented the restraint stress-induced PRL release 26% and 37%, respectively (P less than 0.05). The two enzyme inhibitors had no or only modest effect on the basal PRL secretion. Pretreatment with a specific antiserum (0.5 ml) to arginine vasopressin (AVP) or an AVP antagonist (25 nmol) administered iv at -20 min inhibited the PRL response to HA (270 nmol icv) 80% and 45%, respectively (P less than 0.01) and inhibited the PRL response to restraint stress 70% (P less than 0.01). In contrast, pretreatment with a specific oxytocin (OT) antagonist (50 nmol) had no effect on the HA- or stress-induced PRL release. The AVP antiserum showed less than 0.0003% cross-reactivity with OT, and radiolabeled OT did not bind to serial dilutions of plasma from rats treated with the AVP antiserum. The AVP antiserum or the AVP antagonist almost prevented the PRL release induced by iv infusion of 800 pmol AVP or a posterior pituitary extract. Infusion of AVP (24-800 pmol iv at -15 min) stimulated PRL secretion dose dependently. However, the dose of AVP (800 pmol) required to induce an increase in plasma PRL similar to that obtained by HA-stimulation, led to a rise in plasma AVP which was approximately 1000-fold higher than that induced by HA, which increased plasma AVP 2-fold. Restraint stress had no effect on the plasma AVP level. We conclude that neuronal HA participates in the mediation of the PRL response to stress and that the stress- and HA-induced release of PRL may involve AVP, whereas an involvement of OT seems unlikely.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mediation of the stress-induced prolactin release by hypothalamic histaminergic neurons and the possible involvement of vasopressin in this response. 198 13

The CNS cell groups that innervate the sympathoadrenal preganglionic neurons of rats were identified by a transneuronal viral cell body labeling technique combined with neurotransmitter immunohistochemistry. Pseudorabies virus was injected into the adrenal gland. This resulted in retrograde viral infections of the ipsilateral sympathetic preganglionic neurons (T4-T13) and caused retrograde transneuronal cell body infections in 5 areas of the brain: the caudal raphe nuclei, ventromedial medulla, rostral ventrolateral medulla, A5 cell group, and paraventricular hypothalamic nucleus (PVH). In the spinal cord, the segmental distribution of virally infected neurons was the same as the retrograde cell body labeling observed following Fluoro-gold injections in the adrenal gland except there was almost a 300% increase in the number of cells labeled and a shift in cell group distribution. These results imply there are local interneurons that regulate the sympathoadrenal preganglionic neurons. In the medulla oblongata, serotonin (5-HT)-, substance P (SP)-, thyrotropin-releasing hormone-, Met-enkephalin-, and somatostatin-immunoreactive neurons of the raphe pallidus and raphe obscurus nuclei and the ventromedial medulla were infected. In the ventromedial and rostral ventrolateral medulla, immunoreactive phenylethanolamine-N-methyltransferase, SP, neuropeptide Y, somatostatin, and enkephalin neurons were infected. The A5 noradrenergic cells were labeled, as were some somatostatin-immunoreactive neurons in this area. In the were infected. The A5 noradrenergic cells were labeled, as were some somatostatin-immunoreactive neurons in this area. In the hypothalamus, tyrosine hydroxylase- and SP-immunoreactive neurons of the dorsal parvocellular PVH were infected. Only a few immunoreactive vasopressin, oxytocin, Met-enkephalin, neurotensin, and somatostatin PVH neurons were labeled.
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PMID:CNS cell groups regulating the sympathetic outflow to adrenal gland as revealed by transneuronal cell body labeling with pseudorabies virus. 254 65

Light and electron microscopic immunocytochemistry was used to study the fine structural organization of the catecholaminergic and hypothalamic peptidergic innervation of the dorsal vagal complex of the medulla oblongata in the rat and guinea pig, the latter of which is known to lack central adrenergic neurons. In the rat, adrenergic fibers immunoreactive to phenylethanolamine-N-methyltransferase were concentrated in the dorsal motor nucleus of the vagus, where they established frequent symmetric synapses with dendrites and perikarya. On the other hand, the density of both oxytocin- and corticotropin-immunoreactive fibers appeared far lower in this nucleus than in the dorsal regions of the nucleus of the tractus solitarius, where they formed asymmetric synapses with small dendrites. In tissue treated for the dual labeling of two neuronal antigens, oxytocin- or corticotropin-reactive fibers were in close contact with adrenergic neurons in this dorsal medullary region. In the guinea pig, unlike the rat, the dorsal motor nucleus of the vagus contained large amounts of oxytocin- and corticotropin-reactive fibers, which formed many symmetric synapses with perikarya and dendrites. Taken together, these data suggest that the control of vagal preganglionic neurons by hypothalamic peptidergic neurons involves a bisynaptic neuronal pathway including adrenergic medullary neurons in the rat, whereas it is direct in the guinea pig, which lacks this adrenergic relay.
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PMID:Comparative immunocytochemical study of the catecholaminergic and peptidergic afferent innervation to the dorsal vagal complex in rat and guinea pig. 257 99

The presence of neurohypophyseal nonapeptides in the adrenal gland of nonmammalian vertebrates and the possible action of these regulatory peptides on corticosteroid secretion have never been investigated. We have applied the indirect immunofluorescence technique to examine whether vasotocin (AVT) and/or mesotocin (MT) are located in frog adrenal (interrenal) tissue. Using antisera against AVT and tyrosine hydroxylase, we found that all chromaffin cells contain an AVT-like peptide. Labeling of consecutive sections with phenylethanolamine-N-methyltransferase or AVT antibodies showed that both noradrenaline- and adrenaline-storing cells contain AVT-like immunoreactivity. In contrast no labeling of frog adrenal slices was observed using a MT antiserum. At the ultrastructural level, the immunogold technique revealed that the AVT-immunoreactive peptide is sequestered in chromaffin granules with varying electron densities. Filtration of frog adrenal tissue extracts on Sep-Pak C-18 cartridges showed that the elution profile of the AVT-like peptide was similar to that of synthetic AVT. The apparent concentration of AVT in the adrenal was 2.7 ng/g tissue. Since chromaffin cells represent approximately one third of all interrenal cells, the actual concentration of AVT in chromaffin tissue was about 8 ng/g tissue. The role of AVT in the regulation of frog adrenal steroidogenesis was studied in vitro using perifused frog interrenal slices. Graded doses of AVT (10(-10)-10(-7) M) induced a dose-dependent stimulation of both corticosterone and aldosterone secretion. The other neurohypophyseal peptides (vasopressin, oxytocin, and MT) were also able to enhance corticosteroid secretion, but AVT was by far the most potent stimulator of steroidogenesis. Prolonged administration (4 h) of AVT induced a rapid increase in corticosterone and aldosterone output, followed by a gradual decline of corticosteroid secretion. These results show that an AVT-like peptide is stored in chromaffin granules of frog adrenal gland. Our data also indicate that synthetic AVT is a potent stimulator of corticosteroid secretion by frog interrenal cells. Since in amphibians adrenocortical and chromaffin cells are intimately intermingled, these results suggest that AVT produced by chromaffin cells may regulate corticosteroid release locally, through a cell to cell mode of communication.
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PMID:Identification of vasotocin-like immunoreactivity in chromaffin cells of the frog adrenal gland: effect of vasotocin on corticosteroid secretion. 267 89

Retrograde, transneuronal viral tracing technique combined with neurotransmitter immunohistochemistry was used to identify the type of neurons in spinal cord and brain that project to the rat's kidney. Pseudorabies virus (PRV) injections were made into the left kidney. After an incubation of 4 days postinjection, PRV-infected neurons were located immunocytochemically in the ipsilateral intermediolateral (IML) cell column of the spinal cord and several brainstem cell groups: medullary raphe nuclei, ventromedial medulla (VMM), rostral ventrolateral medulla (RVLM), A5 cell group and the hypothalamic paraventricular nucleus (PVH). In the medulla, serotonin (5-HT)-immunoreactive neurons of the caudal raphe nuclei, substance P (SP)-immunoreactive neurons of the raphe obscurus (ROb) nuclei and tyrosine hydroxylase (TH)-immunoreactive neurons of A5 cells were infected. In the VMM and RVLM, immunoreactive phenylethanolamine-N-methyltransferase (PNMT) neurons were infected. Some PRV-infected neurons in VMM contain 5-HT immunoreactivity. In the hypothalamus, immunoreactive vasopressin (VP) and oxytocin (OT) neurons were infected with PRV. This work indicates that sympathetic outflow to kidney is regulated by different types of neurons and the bulbospinal pathways regulating sympathetic outflow to the kidney are not obviously different from those regulating the other visceral, e.g., adrenal, heart, etc.
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PMID:Characterization of the central cell groups regulating the kidney in the rat. 1052 46