Showing papers on "Area postrema published in 2004"
TL;DR: It is suggested that ghrelin acts at the nucleus of the solitary tract to suppress sympathetic activity and to decrease arterial pressure in rats.
Abstract: Ghrelin is an orexigenic peptide originally isolated from the stomach. Intracerebroventricular administration of ghrelin has been shown to elicit decreases in arterial pressure and renal sympathetic nerve activity in conscious rabbits. The aim of the present study was to determine the role of ghrelin in the brain stem in cardiovascular responses in rats. Unilateral microinjection of ghrelin into the nucleus of the solitary tract significantly decreased the mean arterial pressure and heart rate (-17.3+/-0.8 mm Hg and -13.6+/-3.5 bpm by 20 pmol). The microinjection of ghrelin into the nucleus of the solitary tract also suppressed the renal sympathetic nerve activity (-29.5+/-3.4%; P<0.0001). Pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion-blocking agent, eliminated these cardiovascular responses induced by the microinjection of ghrelin (20 pmol) into the nucleus of the solitary tract; however, pretreatment with intravenous injection of atropine sulfate (0.1 mg/kg), an antagonist of muscarinic acetylcholine receptors, failed to prevent them. In contrast, unilateral microinjection of ghrelin into the area postrema, rostral, and caudal ventrolateral medulla caused no significant changes in the mean arterial pressure and heart rate. On the other hand, immunohistochemical study revealed that the receptor for ghrelin, the growth hormone secretagogue receptor, was expressed in the neuronal cells of the nucleus of the solitary tract and the dorsal motor nucleus of the vagus, but not in the cells of the area postrema. These results suggest that ghrelin acts at the nucleus of the solitary tract to suppress sympathetic activity and to decrease arterial pressure in rats.
190 citations
TL;DR: Data provide the first evidence that feeding-induced amylin release activates AP neurons projecting to subsequent relay stations known to transmit meal-related signals to the forebrain, and Activation of this pathway seems to coincide with an inhibition of LHA neurons.
Abstract: Amylin is a peptide hormone that is cosecreted with insulin from the pancreas during and after food intake. Peripherally injected amylin potently inhibits feeding by acting on the area postrema (AP...
159 citations
TL;DR: Experimental findings do not yet provide a homogenous conception of the significance of 5‐HT3 receptors in all investigated fields; in nociception, for example, contradictory observations are still inadequately explained and complicated by bell‐shaped dose‐response curves.
Abstract: The 5-HT3 receptor is a ligand-gated cation channel located in the central and peripheral nervous system; it has also been detected on a variety of other cells. In the periphery, it is found on autonomic neurons and on neurons of the sensory and enteric nervous system. In the CNS, the 5-HT3 receptor has been localized in the area postrema, nucleus tractus solitarii, nucleus vaudatus, nucleus accumbens, amygdala, hippocampus, entorhinal, frontal, cingulate cortex, and in the dorsal horn ganglia. Further extraneuronal locations include among others lymphocytes, monocytes, and foetal tissue. 5-HT3 receptors modulate the release of neurotransmitters and neuropeptides like dopamine, cholecystokinin, acetylcholine, GABA, substance P, and serotonin itself. They have been demonstrated to be involved in sensory transmission, regulation of autonomic functions, integration of the vomiting reflex, pain processing and control of anxiety. While the physiologic functions of the 5-HT3 receptor are discrete and difficult to detect, it plays a key role in certain pathologic situations related to increased serotonin release. Clinical development of 5-HT3 receptor antagonists revealed a remarkable range of activities. 5-HT3 receptor antagonists do not modify any aspect of normal behaviour in animals or induce pronounced changes of physiological functions in healthy subjects. Clinical efficacy was shown for various forms of emesis like chemotherapy-induced, radiotherapy-induced, and postoperative emesis, diarrhoea-predominant irritable bowel syndrome, anxiety, chronic fatigue syndrome, alcohol abuse, and in pain syndromes such as fibromyalgia and migraine. Most recent data also suggest that 5-HT3 receptor antagonists are effective for the treatment of other rheumatic diseases such as rheumatoid arthritis, tendinopathies, periarthropathies, and myofascial pain. Other possible indications under discussion are chronic heart pain and bulimia. Unfortunately, experimental findings do not yet provide a homogenous conception of the significance of 5-HT3 receptors in all investigated fields; in nociception, for example, contradictory observations are still inadequately explained and complicated by bell-shaped dose-response curves. Further elucidation and better understanding of the serotonergic neuronal network remains a task for the next decade.
108 citations
TL;DR: The detailed mapping of the CTR in the rat brain has identified CTR-positive cells that will be important for subsequent characterization of behavioral functions associated with the actions of CT-related peptides.
96 citations
TL;DR: The data presented here indicate that androgens may influence numerous cell groups within the brainstem, some of these probably constitute a steroid sensitive circuit linking the MPOA to motoneurons in the spinal cord via androgen responsive cells in the caudal ventral medulla.
64 citations
TL;DR: The expression and coexpression of these CO2/pH-sensitive Kir channels suggest that they are likely to contribute to CO2 chemosensitivity of the brainstem neurons.
Abstract: Several inward rectifier K+ (Kir) channels are inhibited by hypercapnic acidosis and may be involved in CO2 central chemoreception. Among them are Kir1.1, Kir2.3, and Kir4.1. The Kir4.1 is expressed predominantly in the brainstem. Although its CO2 sensitivity is low, coexpression of Kir4.1 with Kir5.1 in Xenopus oocytes greatly enhances the CO2/pH sensitivities of the heteromeric channels. If these Kir channels play a part in the central CO2 chemosensitivity, they should be expressed in neurons of brainstem cardio-respiratory nuclei. To test this hypothesis, we performed in-situ hybridization experiments in which the expression of Kir1.1, Kir2.3, Kir4.1 and Kir5.1, and coexpression of Kir4.1 and Kir5.1 were studied in brainstem neurons using non-radioactive riboprobes. We found that mRNAs of these Kir channels were present in several brainstem nuclei, especially those involved in cardio-respiratory controls. Strong labeling was observed in the locus coeruleus, ventralateral medulla, parabrachial-Kolliker-Fuse nuclei, solitary tract nucleus, and area postrema. Strong expression was also seen in several cranial motor nuclei, including the nucleus of ambiguus, hypoglossal nucleus, facial nucleus and dorsal vagus motor nucleus. In general, the expression of Kir5.1 and Kir4.1 was much more prominent than that of Kir1.1 and Kir2.3 in all the nuclei. Evidence for the coexpression of Kir4.1 and Kir5.1 was found in a good number of neurons in these nuclei. The expression and coexpression of these CO2/pH-sensitive Kir channels suggest that they are likely to contribute to CO2 chemosensitivity of the brainstem neurons.
63 citations
TL;DR: Results suggest that STAT3‐mediated genomic activation of target gene transcription in brain cells occurred only in those cases in which sufficiently high concentrations of circulating IL‐6 were formed during systemic (i.a. or i.p. groups) or localized inflammation.
Abstract: The purpose of the present study was to investigate a possible lipopolysaccharide (LPS)-induced activation of brain cells that is mediated by the pleiotropic cytokine interleukin-6 (IL-6) and its transcription factor STAT3 during systemic or localized inflammation. In guinea pigs, intraarterial (I.A. ,1 0µ gk g −1 ) or intraperitoneal (I.P. ,3 0µ gk g −1 ) injections of bacterial LPS cause a systemic inflammatory response which is accompanied by a robust fever. A febrile response can also be induced by administration of LPS into artificial subcutaneously implanted Teflon chambers (S.C. 100 or 10 µ gk g −1 ), which reflects an experimental model that mimics local tissue inflammation. Baseline plasma levels of bioactive IL-6 determined 60 min prior to injections of LPS or vehicle amounted to 35‐80 international units (i.u.) ml −1 . Within 90 min of LPS injection, plasma IL-6 rose about 1000-fold in the groups injected I.A. .o rI.P., about 50-fold in the group injected S.C. with 100 µ gk g −1 LPS, and only 5-fold in guinea pigs injected with the lower dose of LPS (10 µ gk g −1 ). At this time point, a distinct nuclear translocation pattern of the transcription factor STAT3 became evident in several brain structures. Amongst those, the sensory circumventricular organs known to lack a tight blood‐brain barrier such as the area postrema, the vascular organ of the lamina terminalis and the subfornical organ, as well as the hypothalamic supraoptic nucleus showed intense nuclear STAT3 signals in the I.A. or I.P. injected groups. In contrast a moderate (S.C. group, 100 µ gk g −1 ), or even no (S.C. group, 10 µ gk g −1 ), nuclear STAT3 translocation occurred in response to S.C. injections of LPS. These results suggest that STAT3-mediated genomic activation of target gene transcription in brain cells occurred only in those cases in which sufficiently high concentrations of circulating IL-6 were formed during systemic (I.A.. and I.P. groups) or localized (S.C. group, 100 µ gk g −1 ) inflammation.
59 citations
TL;DR: The magnitude of suppression produced by the greatest dose of PYY(3-36) in APX rats was significantly greater than in controls and PYY-induced suppression was still present at 24h, and APX did not diminish the potency of these effects.
58 citations
TL;DR: Evidence is presented that 5-HT3 receptor activation may be able to directly release glutamate from terminals, bypassing a requirement for voltage-dependent calcium entry into terminals, and may contribute to the chemosensitive function of area postrema neurons.
Abstract: Whole-cell voltage-clamp recordings were performed to investigate the serotonergic modulation of neurotransmitter release onto rat area postrema neurons in vitro. The bath application of serotonin (5-HT; 50 microM) or phenylbiguanide (PBA; 50 microM), a potent 5-HT3 receptor agonist, increased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) or miniature EPSCs (mEPSCs) in 35 of 83 neurons (42%). These increases occurred in all electrophysiological cell classes. No cells exhibited a decrease in EPSC frequency. The majority of responding cells showed no inward currents during the application of serotonergic agonists (n = 34/35). However, the amplitude of mEPSCs was increased in 11/11 cells with 5-HT or 3/11 cells with PBA. ICS-205,930, a potent 5-HT3 receptor antagonist, markedly suppressed the 5-HT-induced facilitation of sEPSCs (n = 5) or mEPSCs (n = 5). An increase in the frequency of mEPSCs after PBA exposure was found, even with media containing Cd2+ (50 microM) or zero Ca2+. mEPSCs and evoked EPSCs were completely blocked in media containing the non-NMDA ionotropic receptor antagonist, CNQX (10 microM), indicating that EPSCs were glutamate events. These results suggest that glutamate release is increased in the area postrema by presynaptic 5-HT3 receptor activation. Furthermore, we present evidence that 5-HT3 receptor activation may be able to directly release glutamate from terminals, bypassing a requirement for voltage-dependent calcium entry into terminals. Such a mechanism may contribute to the chemosensitive function of area postrema neurons.
54 citations
TL;DR: The results demonstrate that the laryngeal adductor pathway is contained within the broader pathways for cough and swallow in the medulla.
Abstract: Swallow and cough are complex motor patterns elicited by rapid and intense electrical stimulation of the internal branch of the superior laryngeal nerve (ISLN). The laryngeal adductor response (LAR) includes only a laryngeal response, is elicited by single stimuli to the ISLN, and is thought to represent the brain stem pathway involved in laryngospasm. To identify which regions in the medulla are activated during elicitation of the LAR alone, single electrical stimuli were presented once every 2 s to the ISLN. Two groups of five cats each were studied; an experimental group with unilateral ISLN stimulation at 0.5 Hz and a surgical control group. Three additional cats were studied to evaluate whether other oral, pharyngeal, or respiratory muscles were activated during ISLN stimulation eliciting LAR. We quantified < or = 22 sections for each of 14 structures in the medulla to determine if regions had increased Fos-like immunoreactive neurons in the experimental group. Significant increases (P < 0.0033) occurred with unilateral ISLN stimulation in the interstitial subnucleus, the ventrolateral subnucleus, the commissural subnucleus of the nucleus tractus solitarius, the lateral tegmental field of the reticular formation, the area postrema, and the nucleus ambiguus. Neither the dorsal motor nucleus of the vagus, usually active for swallow, nor the nucleus retroambiguus, retrofacial nucleus, and the lateral reticular nucleus, usually active for cough, were active with elicitation of the laryngeal adductor response alone. The results demonstrate that the laryngeal adductor pathway is contained within the broader pathways for cough and swallow in the medulla.
41 citations
TL;DR: Results indicate that peripheral secretin activates catecholaminergic NTS neurons as well as neurons in medullary, pontine and limbic nuclei regulating autonomic functions and emotion through vagal-dependent capsaicin-resistant pathways.
TL;DR: The differences in c-Fos immunoreactivity induced by changing the distension patterns suggested interactions between groups of vagal and splanchnic afferents in areas of the hindbrain involved mainly in the control of gastrointestinal function.
Abstract: It has been previously shown that the walls of the stomach contain vagal and splanchnic afferents, connected to low and high threshold (LT and HT) gastric receptors, that convey physiological and noxious information to areas of the hindbrain involved mainly in the control of gastrointestinal function. Because distension of the stomach also reflexly increases the sympathetic drive to the cardiovascular system, the present study was planned to examine the pattern of activation of all nuclei encountered throughout the hindbrain in response to gastric distension. In anaesthetized rats, the stimulus was controlled by employing different transmural pressures and frequencies of distension, and c-Fos immunohistochemistry was used to characterize neuronal activation. Low intensity stimulation induced c-Fos expression in the cranial part of nucleus of solitary tract (NTS), the nucleus ambiguus (NA), the lateral reticular area (LRt) and the ventrolateral medulla (RVL/CVL). At low frequency of stimulation c-Fos positive nuclei (p.n.) were found in NTS only. At high frequency of stimulation an increase in c-Fos immunoreactivity was found. High intensity stimulation induced c-Fos expression in area postrema (AP), the lateral vestibular nucleus (LVe) and the caudal part of the NTS. At low frequency, only the number of c-Fos p.n. was increased. Increasing the frequency of stimulation induced c-Fos expression in further nuclei such as the parabrachial nucleus (PBN), the inferior olive subnuclei (IOn), the oral part of spinal trigeminal nucleus (Sp5O) and locus coeruleus (LC). At higher frequencies c-Fos immunoreactivity decreased in NTS and LRt, disappeared in VLM and increased in NA. Thus stomach distension activated several neuronal excitatory and inhibitory circuits that are involved in the control of gastrointestinal function as well as in cardiovascular, respiratory and pain regulation. The differences in c-Fos immunoreactivity induced by changing the distension patterns suggested interactions between groups of vagal and splanchnic afferents.
TL;DR: Both secretin and its receptor mRNAs were more abundant in postnatal day-7 and -14 rats as compared to postnatalDay-21, -30 and -60 rats, and both genes is developmentally regulated during the first few weeks following birth.
01 Jan 2004
TL;DR: Progress over the last two decades of research can be summarized by three major developments: (1) the discovery of leptin and its receptors, and the ensuing identification of leptin’s downstream signaling pathways via hypothalamic peptidergic neuron populations involving both anabolic and catabolic processes.
Abstract: Obesity is now recognized as a major health problem in the United States. Genes that have been selected over millions of years of human evolution to handle scarcity of food and high levels of physical activity are suddenly faced with the easy availability and low cost of calories from sugar and fat and a sedentary lifestyle (Drewnowski, 2000; Neel, 1962). In many individuals this “obesigenic” environment results in a higher defended body weight and an associated higher risk for type 2 diabetes and heart disease (Ravussin & Bogardus, 2000). As environmental changes seem unlikely in the near future, exciting recent discoveries in the field of neural regulation of food intake and energy balance may be our strongest hope to combat the obesity epidemic. Progress over the last two decades of research can be summarized by three major developments: (1) The discovery of leptin and its receptors, and the ensuing identification of leptin’s downstream signaling pathways via hypothalamic peptidergic neuron populations involving both anabolic and catabolic processes. (2) The systematic investigation of the gut–brain axis, with its humoral and neural afferent pathways to the brain, including the hindbrain, and the focus on satiety. (3) The recognition of the importance of pleasure and reward with their neurological substrates in the prefrontal cortex, nucleus accumbens, and the
TL;DR: The short- and long-lasting molecular changes in medullary and basal forebrain gene expression described here are thought to play an important role in the integration of autonomic and vestibular signals that ultimately regulate neural adaptations to space flight.
TL;DR: The results show that PrRP modulates nociception due to supraspinal rather than spinal action, and that its antinociceptive mechanism differs from that previously characterized for NPFF.
TL;DR: Data indicate that PrRP may act within the DVC to regulate gastric motor function by modulating the efficacy of conventional excitatory synaptic inputs from the NTS onto gastric‐projecting vagal motor neurones.
Abstract: Prolactin-releasing peptide (PrRP) is a recently discovered neuropeptide implicated in the central control of feeding behaviour and autonomic homeostasis. PrRP-containing neurones and PrRP receptor mRNA are found in abundance in the caudal portion of the nucleus tractus solitarius (NTS), an area which together with the dorsal motor nucleus of the vagus (DMV) comprises an integrated structure, the dorsal vagal complex (DVC) that processes visceral afferent signals from and provides parasympathetic motor innervation to the gastrointestinal tract. In this study, microinjection experiments were conducted in vivo in combination with whole-cell recording from neurones in rat medullary slices to test the hypothesis that PrRP plays a role in the central control of gastric motor function, acting within the DVC to modulate the activity of preganglionic vagal motor neurones that supply the stomach. Microinjection of PrRP (0.2 pmol (20 nl)(-1)) into the DMV at the level of the area postrema (+0.2 to +0.6 mm from the calamus scriptorius, CS) markedly stimulated gastric contractions and increased intragastric pressure (IGP). Conversely, administration of peptide into the DMV at sites caudal to the obex (0.0 to -0.3 mm from the CS) decreased IGP and reduced phasic contractions. These effects occurred without change in mean arterial pressure and were abolished by ipsilateral vagotomy, indicating mediation via a vagal-dependent mechanism(s). The pattern of gastric motor responses evoked by PrRP mimicked that produced by administration of L-glutamate at the same sites, and both the effects of L-glutamate and PrRP were abolished following local administration of NMDA and non-NMDA-type glutamate receptor antagonists. On the other hand, microinjection of PrRP into the medial or comissural nucleus of the solitary tract (mNTS and comNTS, respectively) resulted in less robust changes in IGP in a smaller percentage of animals, accompanied by marked alterations in arterial pressure. Superfusion of brain slices with PrRP (100-300 nm) produced a small depolarization and increased spontaneous firing in 10 of 30 retrogradely labelled gastric-projecting DMV neurones. The excitatory effects were blocked by administration of TTX (2 mum) or specific glutamate receptor antagonists, indicating that they resulted from interactions of PrRP at a presynaptic site. Congruent with this, PrRP increased the amplitude of excitatory postsynaptic currents (EPSCs, 154 +/- 33%, 12 of 25 neurones) evoked by electrical stimulation in mNTS or comNTS. In addition, administration of PrRP decreased the paired-pulse ratio of EPSCs evoked by two identical stimuli delivered 100 ms apart (from 0.95 +/- 0.08 to 0.71 +/- 0.11, P < 0.05), whereas it did not affect the amplitude of inward currents evoked by exogenous application of L-glutamate to the slice. The frequency, but not amplitude of spontaneous EPSCs and action potential-independent miniature EPSCs was also increased by administration of PrRP, suggesting that the peptide was acting at least in part at receptors on presynaptic nerve terminals to enhance glutamatergic transmission. In recordings obtained from a separate group of slices, we did not observe any direct effects of PrRP on spontaneous discharge or postsynaptic excitability in either mNTS or comNTS neurones (n = 31). These data indicate that PrRP may act within the DVC to regulate gastric motor function by modulating the efficacy of conventional excitatory synaptic inputs from the NTS onto gastric-projecting vagal motor neurones.
TL;DR: It is demonstrated that FosB activation is maintained for at least 24 h following an acute increase in central venous pressure and c-Fos was not significantly increased above control levels at either time point.
TL;DR: Results suggest a shift from hindbrain-initiated short-term actions to activation of hypothalamic mechanisms that could mediate the long-term anorectic responses to C75, which reduces feeding rapidly and for several days.
Abstract: The fatty acid synthase inhibitor C75 reduces feeding rapidly and for several days. We investigated brain sites potentially involved in actions of i.p. C75 in mice by examining c-Fos. At 3 h C75 increased numbers of c-Fos-immunoreactive cells in hindbrain feeding-related nuclei, and in the paraventricular nucleus (PVN), lateral aspects of the arcuate nucleus (ARC), and in the central amygdala. At 24 h C75 prevented fasting-induced c-Fos expression in the medial ARC and three of its targets: lateral magnocellular PVN, lateral hypothalamus, and dorsomedial hypothalamus. C75, but not fasting, increased c-Fos in parvocellular PVN. This pattern of results suggests a shift from hindbrain-initiated short-term actions to activation of hypothalamic mechanisms that could mediate the long-term anorectic responses to C75.
TL;DR: The results of the present study confirm that vagal afferents are distributed to the dorsomedial subnuclei of the human nucleus of the solitary tract, with particular concentrations of afferent axons in the gelatinosus subn nucleus.
Abstract: The embryonic and fetal development of the nuclear components and pathways of vagal sensorimotor circuits in the human has been studied using Nissl staining and carbocyanine dye tracing techniques. Eight fetal brains ranging from 8 to 28 weeks of development had DiI (1,1'-dioctadecyl-3,3,3',3' tetramethylindocarbocyanine perchlorate) inserted into either the thoracic vagus nerve at the level of the sternal angle (two specimens of 8 and 9 weeks of gestation) or into vagal rootlets at the surface of the medulla (at all other ages), while a further five were used for study of cytoarchitectural development. The first central labeling resulting from peripheral application of DiI to the thoracic vagus nerve was seen at 8 weeks. By 9 weeks, labeled bipolar cells at the ventricular surface around the sulcus limitans (sl) were seen after DiI application to the thoracic vagus nerve. Subnuclear organization as revealed by both Nissl staining and carbocyanine dye tracing was found to be advanced at a relatively early fetal age, with afferent segregation in the medial Sol apparent at 13 weeks and subnuclear organization of efferent magnocellular divisions of dorsal motor nucleus of vagus nerve noticeable at the same stage. The results of the present study also confirm that vagal afferents are distributed to the dorsomedial subnuclei of the human nucleus of the solitary tract, with particular concentrations of afferent axons in the gelatinosus subnucleus. These vagal afferents appeared to have a restricted zone of termination from quite early in development (13 weeks) suggesting that there is no initial exuberance in the termination field of vagal afferents in the developing human nucleus of the solitary tract. On the other hand, the first suggestion of afferents invading 10N from the medial Sol was not seen until 20 weeks and was not well developed until 24 weeks, suggesting that direct monosynaptic connections between the sensory and effector components of the vagal sensorimotor complex do not develop until this age.
TL;DR: The distribution and ultrastructure of dopaminergic neurons with double-labeling immunohistochemistry for tyrosine hydroxylase (TH) and the retrograde tracer cholera toxin subunit b (CTb) following its injection into the stomach were determined.
TL;DR: The present study suggests that purinoceptor activation may contribute to the control of several autonomic functions by area postrema neurons.
TL;DR: It is concluded that rat area postrema neurons are exquisitely sensitive to propofol, given that reductions of Ih are associated with decreased excitability in neurons, and it is believed that the known antiemetic effects of prop ofol anesthesia are at least partly a result of a direct action on area postRema neurons to lower their excitability.
TL;DR: Similar number and distribution of c‐Fos‐expressing neurons within the NTSAP and their identical chemical coding indicate that exposure of the rat stomach to backdiffusing concentrations of HCl and NH4OH activates the same vagal afferent – NTSAP pathway.
Abstract: Exposure of the gastric mucosa to backdiffusing acid is signalled to the brainstem via vagal afferents. This study examined whether exposure of the Sprague-Dawley rat stomach to hydrochloric acid (HCI) or ammonium hydroxide (NH 4 OH), a noxious chemical produced by Helicobacter pylori, activates different vagal afferent pathways as reflected by different circuitries in the medullary brainstem. Two hours after intragastric treatment with HCI or NH 4 OH the activation of neurons in the nucleus tractus solitarii at the rostrocaudal extension of the area postrema (NTS A P ) was visualized by c-Fos immunohistochemistry and their chemical coding characterized by double-labelling immunohistochemistry. Exposure of the rat gastric mucosa to HCI (0.15-0.5 M) or NH 4 OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTS A P The number and distribution of NTS A P neurons activated by 0.35 M HCI and 0.3 M NH 4 OH were similar; the highest number of activated neurons occurring in the medial part of the NTS A P Some 60% of the NTS A P neurons activated by intragastric HCI and NH 4 OH stained for the high affinity glutamate transporter EAAC1, while some 30% contained calbindin or neuropeptide Y. Glutamate receptors of the N-methyl-D-aspartate type were found on approximately 50% of the c-Fos-positive cells in the NTS A R whereas tachykinin NK 1 , NK 2 and NK 3 receptors were present on 5-10% of the activated neurons. The similar number and distribution of c-Fos-expressing neurons within the NTS A P and their identical chemical coding indicate that exposure of the rat stomach to backdiffusing concentrations of HCI and NH 4 OH activates the same vagal afferent - NTS A P pathway.
TL;DR: Data suggest that the CNS control of the uterine horn varies depending on reproductive status, and the low frequency of brain labeling in pregnant rats may be related to the almost complete lack of sympathetic fibers in the uterus prior to parturition and the very high frequency of labeling in lactating animals to the postpartum hyperinnervation of the uterus.
Abstract: Using the transneuronal viral tracing method, the central nervous system (CNS) connections of the uterine horn were studied in virgin, pregnant, and in lactating rats. The frequency of viral labeling in the brain and the distribution of virus-infected neurons from the uterine horn were compared among groups. There was a marked difference in the frequency of viral labeling in the brain stem. In virgin rats more than half of the brain stems (5 out of 9) were labeled. In contrast, in pregnant animals viral-labeled neurons were detected in only a few cases (3 out of 16) and almost each brain stem of the lactating group was labeled (12 out of 13). A similar, less marked difference was observed in the hypothalamus. The pattern of distribution of infected neurons was similar in each group. In the brain stem, the nucleus of the solitary tract, dorsal motor nucleus of the vagus, area postrema, gigantocellular and paragigantocellular nucleus, ventrolateral medulla, A5 cell group, and caudal raphe nuclei were the most frequently labeled structures. In the diencephalon, viral-infected neurons were detected primarily in the hypothalamic paraventricular nucleus. The telencephalon was devoid of infected cells. Data suggest that the CNS control of the uterine horn varies depending on reproductive status. The low frequency of brain labeling in pregnant rats may be related to the almost complete lack of sympathetic fibers in the uterus prior to parturition and the very high frequency of labeling in lactating animals to the postpartum hyperinnervation of the uterus.
TL;DR: The results suggest that central and peripheral angiotensin II-induced fetal pressor responses may be mediated by separate mechanisms, and these regulatory mechanisms start to function by near-term or early.
01 Jan 2004
TL;DR: The circumventricular organs of the human brain comprises of the subfornical organ (SFO), vascular organ of the lamina terminalis (OVLT), median eminence, neurohypophysis, pineal gland, subcommissural organ, area postrema, and choroid plexus.
Abstract: The circumventricular organs (CVOs) of the human brain comprises of the subfornical organ (SFO), vascular organ of the lamina terminalis (OVLT), median eminence, neurohypophysis, pineal gland, subcommissural organ, area postrema, and choroid plexus. They are a group of specialized structures within the brain, so named because they occupy strategic positions along the surface of the brain ventricles. In lower vertebrates, a number of other structures, including the saccus vasculosus, paraventricular organ, and paraphysis, have also been classified in this grouping of CVOs, but are not found in adult mammalian brain. The mammalian CVOs are subdivided into two groups—namely, paraependymal CVOs and ependymal CVOs. The paraependymal CVOs are the subfornical organ, OVLT, neurohypophysis, median eminence, pineal gland, and area postrema. They are characterized in regard to their neuroectodermal component by subependymal elements that differ considerably from the ependymal cells. The paraependymal CVOs have been further categorized into sensory and secretory circumventricular organs.
TL;DR: Dorsal vagal motoneurons of neonatal swine likely projected primarily to the enteric nervous system, exerting excitatory influence over gastrointestinal activity, with special focus on the origins of cardiomotor neurons.
Abstract: Pediatric disorders frequently exhibit dysregulation of sympatho-vagal activity, and impaired control of cardiovascular vagal networks. Factors influencing the maturation of vagal networks are of special interest because they normally protect the heart and circulation, facilitate digestion, and preserve visceral metabolism. At present, scant literature exists regarding the development of vagal innervation of the heart. This study in neonatal swine, Sus scrofa, mapped the normal anatomy of vagal motor cell groups, with special focus on the origins of cardiomotor neurons. Right cardiac nerve branches, or the right thoracic vagal trunk were resected, inserted into capillary glass vials filled with 2% FluoroGold (FG) tracer solutions, and sealed to prevent leakage (false positives). Dorsal and ventral vagal complexes were identified on cross-sectioned tissues incubated in a well-characterized specific FG antibody. Thoracic and abdominal vagal motoneurons were cytologically heterogeneous, and predominantly medium-sized, polygonal cell bodies. Discrete longitudinal cell columns were observed, as well as organized arrays of elongate spindle-shaped cells in formation. Long axes and dendrites appeared to orient toward incoming peripheral sensory and central afferents, and were juxtaposed to cerebral microvasculature. The piglets' dorsal vagal complex is: (i) thick and long, comparable to ruminants, in contrast to much shorter lengths in non-ruminants, and (ii) the chief source of vagal motoneurons, forming discrete, topographically organized parasympathetic cell groups with distinct dendritic arbors. The cardiac motor subnucleus is localized to a highly restricted areal subunit of nucleus ambiguus' external formation in the vicinity of the obex. On the other hand, dorsal cardiac vagal motoneurons were few in number and diffusely distributed. Dorsal vagal motoneurons of neonatal swine likely projected primarily to the enteric nervous system, exerting excitatory influence over gastrointestinal activity.
Journal Article•
TL;DR: It is suggested that centrally administered ADM may increase the expression of c-fos in the forebrain, the hypothalamus and the brainstem and activate nitric oxide-producing neurons in the PVN, SON, NTS and PGL and may be partly mediated by CGRP receptors.
Abstract: To define the action sites of adrenomedullin (ADM) in the rat brain, and to examine whether neuronal NO may participate in the actions of ADM, the present study was undertaken to examine the effects of icv administration of ADM on the induction of Fos protein and on nitric oxide-producing neurons in rat brain nuclei involved in cardiovascular regulation, using double immunohistochemical method for Fos and neuronal nitric oxide synthase (nNOS) Following icv administration of ADM (1 nmol/kg, 3 nmol/kg), Fos-like immunoreactivity neurons were markedly increased in several brain areas of the rat, including the nucleus of the solitary tract (NTS), the area postrema, the locus coeruleus, the parabrachial nucleus and the nucleus paragigantocelluaris laterialis (PGL) in the brainstem, the paraventricular nucleus (PVN), the supraoptic nucleus (SON) and the ventromedial hypothalamic nucleus in the hypothalamus, as well as the central amygdaloid nucleus and the lateral habenular nucleus in the forebrain Following icv injection of ADM (1 nmol/kg, 3 nmol/kg), the number of double-labeled neurons for Fos and nNOS was increased in the PVN and SON Small numbers of double-labeled neurons were also found in the NTS and PGL following icv injection of ADM (3 nmol/kg), while icv injection of ADM (1 nmol/kg) did not change the number of double-labeled neurons in the NTS and PGL Pretreatment with calcitonin gene-related peptide receptor antagonist CGRP(8-37) (30 nmol/kg) significantly reduced the action of ADM (3 nmol/kg) in the brain These results suggest that centrally administered ADM may increase the expression of c-fos in the forebrain, the hypothalamus and the brainstem and activate nitric oxide-producing neurons in the PVN, SON, NTS and PGL These effects may be partly mediated by CGRP receptors
TL;DR: The results suggest that the peripheral vasopressin system participates in negative feedback to modulate neuronal activities in the PVN, probably through the AP or direct action at the PVn in response to central osmotic and/or Na(+) stimulation.