Motor Nucleus Of Vagus Research Articles

Acute pulmonary edema caused by a multiple sclerosis relapse

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) [1]. In the majority of patients, MS begins with a relapsing–remitting course. It is characterized by unpredictable relapses followed by periods of months to years of clinical remission. MS relapses entail various clinical symptoms depending on the location of the inflammatory lesion within the CNS. Besides the common symptoms of optic neuritis, paresis, paraesthesia, and ataxic gait disorders, in some rare cases a relapse may alter cardiovascular and autonomic function [1]. Clinical studies have shown that acute cerebral lesions (e.g., stroke, hemorrhage) may induce changes in cardiac and respiratory function including hypertension, arrhythmias, myocardial necrosis, and sudden death [2, 3]. Moreover, experimental and clinical studies indicate that damage of the brainstem is likely to cause disturbances in either sympathetic or parasympathetic autonomic function with subsequent cardiac and respiratory dysfunction [4–6]. Neurogenic pulmonary edema (NPE) is usually defined as an acute pulmonary edema occurring shortly after various injuries of the central nervous system [7]. The most important vasomotor centers for NPE development are nuclei of the solitary tract, the dorsal motor vagus nucleus in the medulla oblongata and the medial reticulated nucleus. On the other hand, brainstem damage in the region of the solitary tract nuclei may result in a transient cardiomyopathy [8]. The exact mechanisms remain poorly understood because of the complexity of its pathophysiologic mechanisms, involving both hemodynamic and inflammatory aspects. There are two possible explanations: one presumes that neurological damage directly involves the pulmonary and cardiac vascular bed with disconnection of the central nervous system vasomotor centers. However, there are also data that brainstem dysfunction can cause changes of sympathetic vasomotor tone [7]. This case study describes a rare initial presentation of a MS relapse with pulmonary edema caused by left ventricular failure. A 48-year-old woman, diagnosed with clinically definite relapsing–remitting MS 3 years previously with a preexisting expanded disability status scale (EDSS) of 3.5, presented with increasing dyspnea and cough without chest pain to a department of internal medicine. She was on immunomodulatory treatment with glatiramer acetate. No clinically apparent atherosclerotic disease was known. On admission, laboratory testing showed that high-sensitivity troponin T was slightly elevated. An electrocardiogram showed no signs of myocardial infarction. In a coronary computed tomography angiogram, no significant changes in the coronary arteries were found. The next day, increases in high-sensitivity troponin T, C-reactive protein (CRP), and a massive increase of B-type natriuretic peptide (proBNP) were observed (Table 1). Pulmonary edema was initially not diagnosed (Fig. 1a) and according to the assumption of pneumonia the patient was treated with antibiotic therapy (amoxicillin) and furosemide. Due to the further worsening of respiratory conditions, intubation and mechanical respirator treatment became necessary. An echocardiogram showed acute left ventricular failure with apical wall motion abnormalities and a left ventricular ejection fraction of 35% in this patient without a history of cardiac disease. No abnormalities concerning the right ventricle and the atria were seen. With regard to her P. Wipfler (&) G. Pilz E. Broussalis S. M. Golaszewski A. Kunz E. Trinka J. Kraus Christian-Doppler-Klinik, University Hospital of Neurology, Paracelsus Medical University and Salzburger Landesklinken, Ignaz Harrerstrasse 79, 5020 Salzburg, Austria e-mail: p.wipfler@salk.at

Induction of apoptosis by thrombin in the cultured neurons of dorsal motor nucleus of the vagus

A previous study demonstrated the presence of protease-activated receptor (PAR) 1 and 2 in the dorsal motor nucleus of vagus (DMV). The aim of this study is to characterize the effect of thrombin on the apoptosis of DMV neurons. The dorsal motor nucleus of vagus neurons were isolated from neonatal rat brainstems using micro-dissection and enzymatic digestion and cultured. Apoptosis of DMV neurons were examined in cultured neurons. Apoptotic neuron was examined by TUNEL and ELISA. Data were analyzed using anova and Student's t-test. Exposure of cultured DMV neurons to thrombin (0.1 to 10 U mL(-1)) for 24 h significantly increased apoptosis. Pretreatment of DMV neurons with hirudin attenuated the apoptotic effect of thrombin. Similar induction of apoptosis was observed for the PAR1 receptor agonist SFLLR, but not for the PAR3 agonist TFRGAP, nor for the PAR4 agonist YAPGKF. Protease-activated receptors 1 receptor antagonist Mpr(Cha) abolished the apoptotic effect of thrombin, while YPGKF, a specific antagonist for PAR4, demonstrated no effect. After administration of thrombin, phosphorylation of JNK and P38 occurred as early as 15 min, and remained elevated for up to 45 min. Pretreatment of DMV neurons with SP600125, a specific inhibitor for JNK, or SB203580, a specific inhibitor for P38, significantly inhibited apoptosis induced by thrombin. Thrombin induces apoptosis in DMV neurons through a mechanism involving the JNK and P38 signaling pathways.

Vasopressin (VP) and neuropeptide FF (NPFF) systems in the normal and hypertensive human brainstem

Vasopressin (VP)-, neuropeptide FF (NPFF)-, and tyrosine hydroxylase (TH)-expressing neurons were studied by means of single and double immunocytochemistry in the human brainstem of controls who died suddenly due to trauma and of patients who suffered from essential hypertension and died due to acute myocardial infarction, while in one case there was brain hemorrhage. In the control and hypertensive groups VP fibers and NPFF neurons and fibers were the most abundantly present in the dorsal vagal complex, especially in the dorsal motor nucleus of the vagus. Numerous VP and NPFF fibers formed synaptic-like contacts with neuronal profiles in the dorsointermediate, centrointermediate, ventrointermediate, caudointermediate, and caudal parts of the dorsal motor nucleus of vagus as well as adjacent medial and intermediate subnuclei of the solitary nucleus. VP, but not NPFF, positive fibers were found to vastly contact TH-positive neuronal profiles in A2/C2, A2, and ambiguus nucleus (Amb). The density of VP fibers in the dorsal motor nucleus of the vagus and Amb did not differ between hypertensive patients and controls, whereas the density of NPFF fibers in hypertensives was 3.19 times lower in the dorsal motor nucleus of vagus and markedly decreased in the Amb. In both groups, VP and NPFF were scarcely present in the pain pathways, suggesting that these peptides are not crucially involved in nociceptive control in human. The reduction of NPFF release within the dorsal motor nucleus and Amb could serve as a possible cause of the impairment of cardiac vagal control in hypertensive patients.

Nerve cells immunoreactive for p62 in select hypothalamic and brainstem nuclei of controls and Parkinson’s disease cases

The protein p62 plays an important role in the proteasomal and/or autophagic clearance of misfolded and aggregation-prone proteins. Immunoreactivity for p62, however, not only characterizes pathological proteinaceous inclusions but also occurs in the form of homogeneous nerve cell labeling in brains of both healthy and diseased individuals, e.g., in the vagal dorsal motor nucleus and other subcortical nuclei. In sporadic Parkinson's disease (PD), the pathological process initially involves preganglionic neurons of the parasympathetic and sympathetic system and probably advances caudo-rostrally from there along the neuroaxis. Since all subsequently affected nuclei (lower raphe nuclei, magnocellular reticular formation, locus coeruleus, and central subnucleus of the amygdala) generate descending projections that terminate in the vagal dorsal motor nucleus and intermediolateral column, it has been conjectured that retrograde axonal transport and transsynaptic transmission of a pathogen contribute to the pathogenesis of PD. The hypothalamic paraventricular nucleus also sends projections to the preganglionic nuclei under consideration and, thus, should belong to the nuclei endangered by the pathological process. However, it remains uninvolved for the duration of the disorder. For this reason, we performed a retrospective study of the relevant nuclei in a cohort of 36 individuals, including 17 with clinically documented PD, one case with incidental Lewy body disease (ILBD), and 18 controls using p62-immunocytochemistry. Remarkably, the neurosecretory cells of the paraventricular nucleus were among the sites showing homogeneous p62-immunolabeling with the greatest consistency. Its p62-immunoreactive profile may indicate that the hypothalamic paraventricular nucleus is somehow capable of effectively metabolizing misfolded proteins and/or preventing their aggregation.

Visualising vagal afferent neurons and their terminals whilst silencing TRPV1

Visualising vagal afferent neurons and their terminals whilst silencing TRPV1

The effects of dose and route of administration of PSI on behavioural and biochemical indices of neuronal degeneration in the rat brain

Repeated subcutaneous administration of proteasome inhibitor 1 [PSI, Z-Ile-Glu(O tBu)-Ala-Leu-CHO] to rats causes progressive motor deficits and nigral dopaminergic cell loss in our laboratories, but this is controversial since others have not reproduced these findings. For this reason, we have investigated the role that the dose of PSI and its route of administration have on motor activity and neuronal loss in rat brain. PSI (8, 12 or 16 mg/kg, s.c.) was administered to female Wistar rats on 6 occasions on alternative days over 2 weeks. Subsequently PSI (8 mg/kg) was administered by oral, s.c. and i.p. routes on alternate days to separate groups of animals. Rats were assessed for motor function on a weekly basis up to 5 months after the end of PSI treatment. Locomotor activity was decreased following s.c. administration of 8 and 12 mg/kg PSI but not following 16 mg/kg. In subsequent experiments PSI (8 mg/kg) decreased motor activity after p.o. but not i.p. administration. PSI 8 mg/kg s.c. or p.o., but not i.p., caused neuronal loss in the substantia nigra, raphe nuclei, locus coeruleus, nucleus basalis of Meynert and dorsal motor nucleus of vagus. These data confirm that systemic administration of PSI reduces locomotor activity in rats and induces widespread neuronal degeneration in brain. However, the effects of PSI and its time course of action are dose and route dependent.

Anatomic changes in multiple brainstem nuclei after incremental, near-complete neurotoxic destruction of the pre-Bötzinger Complex in adult goats

Abrupt, bilateral destruction of the pre-Bötzinger Complex (preBötC) leads to terminal apnea in unanesthetized goats and rats. In contrast, respiratory rhythm and pattern and arterial blood gases in goats during wakefulness and sleep are normal after incremental (over a month) destruction of > 90% of the preBötC. Here, we tested the hypothesis that the difference in effects between abrupt and incremental destruction of the preBötC are a result of time-dependent plasticity, which manifests as anatomic changes at sites within the respiratory network. Accordingly, we report data from histological analyses comparing the brainstems of control goats, and goats that had undergone bilateral, incremental, ibotenic acid (IA)-induced preBötC lesioning. A major focus was on the parafacial respiratory group/retrotrapezoid nucleus (pFRG/RTN) and the pontine respiratory group (PRG), which are sites thought to contribute to respiratory rhythmogenesis. We also studied the facial (FN), rostral nucleus ambiguus (NA), medullary raphé (MRN), hypoglossal (HN), and the dorsal motor vagal (DMV) nuclei. Neuronal counts, count region area (mm²), and neuronal densities were calculated using computer-assisted analyses and/or manual microscopy to compare control and preBötC-lesioned animals. We found that within the ventral and lateral medulla 2mm rostral to the caudal pole of the FN (presumed pFRG/RTN), there were 25% and 65% more (P < 0.001) neurons, respectively, in preBötC-lesioned compared to control goats. Lesioned goats also showed 14% and 13% more (P < 0.001) neurons in the HN and medial parabrachialis nucleus, but 46%, 28%, 7%, and 17% fewer (P < 0.001) neurons in the FN, NA, DMV, and Kölliker-Fuse nuclei, respectively. In the remaining sites analyzed, there were no differences between groups. We conclude that anatomic changes at multiple sites within the respiratory network may contribute to the time-dependent plasticity in breathing following incremental and near-complete destruction of the preBötC.

Central orexin-A changes the gastrointestinal motor pattern from interdigestive to postprandial in rats

Orexin-A, also described as hypocretin-I, was discovered in the extracts of the rat brain. OXA is implicated in a wide variety of physiological functions, such as feeding, arousal, behavioral activity, energy homeostasis and gastrointestinal motility. Orexin receptor type-1 is highly expressed in the dorsal motor nucleus of vagus. Although peripherally administered OXA abolishes small intestinal interdigestive contractions in rats, it still remains unclear whether central OXA affects interdigestive GI motility in rats. Two strain gauge transducers were attached on the antrum and duodenum to record circular muscle contractions. Spontaneous gastroduodenal contractions were recorded in freely moving conscious rats. OXA (1-20 µg) was administered intracerebroventricularly (icv). Atropine pretreatment (1 mg/kg, ip) and truncal vagotomy were performed to elucidate the neural pathways of central OXA. OXA (1–20 µg) dose-dependently disrupted the interdigestive phase III-like contractions and induced an irregular postprandial-like motility pattern in the stomach and duodenum. The stimulatory effect of OXA on gastroduodenal postprandial-like motility pattern was abolished by atropine and truncal vagotomy. Central administration (icv) of selective OXA receptor antagonist, SB-334867 (16 µg), enhanced gastric spontaneous phase III-like contractions. It is suggested that central OXA changes GI motor pattern from interdigestive to postprandial via the vagal cholinergic pathways. Endogenous OXA may have an inhibitory role in interdigestive GI motility in rats.

First appraisal of brain pathology owing to A30P mutant alpha‐synuclein

Familial Parkinson disease (PD) due to the A30P mutation in the SNCA gene encoding alpha-synuclein is clinically associated with PD symptoms. In this first pathoanatomical study of the brain of an A30P mutation carrier, we observed neuronal loss in the substantia nigra, locus coeruleus, and dorsal motor vagal nucleus, as well as widespread occurrence of alpha-synuclein immunopositive Lewy bodies, Lewy neurites, and glial aggregates. Alpha-synuclein aggregates ultrastructurally resembled Lewy bodies, and biochemical analyses disclosed a significant load of insoluble alpha-synuclein, indicating neuropathological similarities between A30P disease patients and idiopathic PD, with a more severe neuropathology in A30P carriers.

The human area postrema and other nuclei related to the emetic reflex express cAMP phosphodiesterases 4B and 4D

Phosphodiesterase 4 (PDE4) inhibitors, i.e. rolipram, are being extensively investigated as therapeutic agents in several diseases. Emesis is one of the most common side effects of PDE4 inhibitors. Given the fact that the area postrema is considered the chemoreceptor trigger zone for vomiting, the present study investigates the regional distribution and cellular localization of the four gene transcripts of the PDE4 subfamily (PDE4A, PDE4B, PDE4C and PDE4D) in human brainstem. In situ hybridization histochemistry was used to locate the mRNA distribution of the four PDE4 subfamilies in the area postrema and related nuclei of human postmortem brainstem. We have found that in the brainstem PDE4B and PDE4D mRNA expression is abundant and distributed not only in neuronal cells, but also in glial cells, and on blood vessels. The hybridization signals for PDE4B and PDE4D mRNAs in the area postrema were stronger than those in any other nuclei in the brainstem. They were also found in vomiting-related nuclei such as the nucleus of the solitary tract and the dorsal vagal motor nucleus. These findings suggest that cAMP signaling modification in the area postrema could mediate the emetic effects of PDE4 inhibitors in human brainstem.

パーキンソニズムを主症状としたＳＣＡ２の１剖検例

This is the first autopsy case of SCA2 with parkinsonian phenotype. At the age of 46, the patient got symptoms of parkinsonism to which anti-parkinsonian drugs were effective. He had mosaic 38, 40 CAG repeat expansions on chromosome 12q23-24, being diagnosed as SCA2, and his mother and his son also had CAG expansions on the same locus. In addition to parkinsonism, he also exhibited autonomic disturbance, dementia, and mild cerebellar ataxia Brain images revealed severe atrophy of pons and medulla oblongata, resembling MSA-C. HVA and 5-HIAA were reduced in the cerebrospinal fluid, and the heart-mediastinum (H/M) ratio in myocardial 123I-MIBG cintigram was decreased, which suggested Lewy body pathology. He died at the age of 75 and the autopsy revealed atrophy of the olivo-ponto-cerebellar (OPC) system and substantia nigra which was compatible to SCA2, although the OPC system atrophy was less severe than formerly reported SCA2 cases. The degrees of atrophy of the OPC system and substantia nigra might explain the predominancy of clinical symptoms. Anti-1C2 positive inclusions in the pontine nuclei, inferior olive nuclei, cerebellum and substantia nigra confirmed a polyglutamine disease. In addition, there were the anti-phosphorylated alpha-synuclein positive, Lewy body related pathological changes in the substantia nigra, the locus ceruleus, the dorsal motor nuclei of vagus, and the sympathetic nerve in the myocardium. Major genetic abnormalities related to Parkinson disease were not detected. As another case of SCA2 with Lewy body pathology was reported in Japan, the coexistence of SCA2 and Lewy body pathology may not be accidental. Since myocardial MIBG scincigram can predict Lewy body pathology, we should seek more clinical cases of SCA2 with Lewy body pathology.

Tonic GABAA Receptor-Mediated Inhibition in the Rat Dorsal Motor Nucleus of the Vagus

Type A gamma-aminobutyric acid (GABA(A)) receptors expressed in the dorsal motor nucleus of vagus (DMV) critically regulate the activity of vagal motor neurons and, by inference, the gastrointestinal (GI) tract. Two types of GABA(A) receptor-mediated inhibition have been identified in the brain, represented by phasic (I(phasic)) and tonic (I(tonic)) inhibitory currents. The hypothesis that I(tonic) regulates neuron activity was tested in the DMV using whole cell patch-clamp recordings in transverse brain stem slices from rats. An I(tonic) was present in a subset of DMV neurons, which was determined to be mediated by different receptors than those mediating fast, synaptic currents. Preapplication of tetrodotoxin significantly decreased the resting I(tonic) amplitude in DMV neurons, suggesting that most of the current was due to action potential (AP)-dependent GABA release. Blocking GABA transport enhanced I(tonic) and multiple GABA transporters cooperated to regulate I(tonic). The I(tonic) was composed of both a gabazine-insensitive component that was nearly saturated under basal conditions and a gabazine-sensitive component that was activated when extracellular GABA concentration was elevated. Perfusion of THIP (10 muM) significantly increased I(tonic) amplitude without increasing I(phasic) amplitude. The I(tonic) played a major role in determining the overall excitability of DMV neurons by contributing to resting membrane potential and AP frequency. Our results indicate that I(tonic) contributes to DMV neuron membrane potential and activity and is thus an important regulator of vagally mediated GI function.

Organisation of the catecholaminergic system in the vagal motor nuclei of pigs: A retrograde fluorogold tract tracing study combined with immunohistochemistry of catecholaminergic synthesizing enzymes

The vagal motor system is involved in the regulation of cardiorespiratory and gastrointestinal functions. Vagal motor neurons are localized near or adjacent to catecholaminergic neurons, but their co-localisation seems species dependent, present in the cat but absent in the rabbit. In pig, a species commonly used as an experimental model in humans brain disorders (sudden infant death syndrome, hypoxia), the relationship is poorly understood. We aimed at describing the distribution of vagal motor neurons and tyrosine hydroxylase-immunoreactive (-ir) neurons by using a double staining method in combination with retrograde tracing of vagal efferent neurons. After fluorogold impregnation of the central part of the sectioned left cervical vagal trunk, two main vagal motor neuronal populations were located in the dorsal motor nucleus of the vagus nerve (DMX) and in the area of the nucleus ambiguus (Amb). Like in the human, the DMX was composed of different subpopulations of neurons with the same morphological characteristics. Immunohistochemistry of catecholaminergic synthesizing enzymes differentiated two main sites containing vagal motor populations: the dorsomedial and the ventrolateral medulla. TH-ir was rarely seen in vagal motor neurons of the DMX, but TH-ir neurons were present around the two main vagal motor neuronal populations that contained TH-ir fibres. The anatomical organisation of the vagal motor and the catecholaminergic neuronal systems are similar to those described in humans and suggest that the involvement of the catecholamines in the control of the vagal motor system may be similar in pigs and in humans.

Dorsal Motor Nucleus of Vagus protein aggregates in Lewy Body Disease with autonomic dysfunction

The Dorsal Motor Nucleus of Vagus (DMV) is degenerated in many patients with early stage Lewy Body Diseases (LBD). Many patients with LBD also develop symptomatic autonomic dysfunction prior to motor and cognitive symptoms. The DMV, along with the Nucleus Ambiguous (NA) and Raphe Obscurus (RO) regulates a variety of autonomic reflexes, suggesting that there may be an association between the degree of neurodegenerative protein aggregation in the DMV and symptomatic autonomic dysfunction in patients with LBD. Using digital in vivo pathology, we quantified αsynuclein, tau, ubiquitin and Heat Shock Protein 27 (HSP27) containing neurons in the DMV, NA, RO, in addition to the hypoglossal nucleus in 12 LBD patients. αSynuclein, ubiquitin and tau aggregates most greatly affected the DMV followed by the NA, RO, but never the hypoglossal nucleus. There was a positive correlation between DMV αsynuclein and tau aggregation ( p < 0.05) and between DMV αsynuclein and the patients' UPDRS scores ( p < 0.05) suggesting incremental DMV degeneration with disease progression. However, there was no correlation between DMV αsynuclein, tau, ubiquitin or HSP27 density and the patient's autonomic dysfunction scores. The specific incremental nature of degeneration in the DMV, suggests that by characterizing region specific molecular mechanisms underpinning DMV as opposed to NA degeneration in LBD, the pathogenesis of the disorder may be better understood. Whether DMV degeneration is causative of symptomatic autonomic dysfunction in LBD remains to be determined.

Vulnerability of macaque cranial nerve neurons to ethanol is time- and site-dependent

The present study tested the hypotheses that vulnerability to ethanol depends upon (1) population-based characteristics of the neuronal progenitors and (2) the maturation of that population by examining the effects of prenatal exposure to ethanol on brainstem nuclei derived from different rhombomeres and from the alar and basal plates. Macaca nemestrina received an ethanol-containing solution 1 day per week during the first 6 (Et6) or 24 (Et24) weeks of gestation. Control animals received an equivalent volume of saline. The treatment regime for some animals included early gastrulation (gestational day [G] 19 or G20), whereas others were treated later (on G21 or G24). Brainstems were cryosectioned and stained with cresyl violet. Stereological methods were used to determine the numbers of neurons in six different nuclei: the abducens, vagal, and hypoglossal motor nuclei and sensory components of the trigeminal brainstem nuclear complex (the principal, oral, and interpolar subnuclei). There were no differences in the numbers of neurons in any of the nuclei between controls and Et6-, or controls and Et24-treated monkeys. In contrast, the number of trigeminal sensory neurons was significantly ( P < .05) lower in animals treated on G19/G20 than in control. No differences between controls and monkeys treated on G21/G24 were detected. No motor nuclei exhibited an ethanol-induced change. These data together with data on the trigeminal motor nucleus show that vulnerability to ethanol (1) is greater in sensory nuclei than in motor nuclei and (2) is temporally restricted to the time of gastrulation.

Neuroepithelial cells require fucosylated glycans to guide the migration of vagus motor neuron progenitors in the developing zebrafish hindbrain

The molecular mechanisms by which neurons migrate and accumulate to form the neural layers and nuclei remain unclear. The formation of vagus motor nuclei in zebrafish embryos is an ideal model system in which to address this issue because of the transparency of the embryos and the availability of established genetic and molecular biological techniques. To determine the genes required for the formation of the vagus motor nuclei, we performed N-ethyl-N-nitrosourea-based mutant screening using a zebrafish line that expresses green fluorescent protein in the motor neurons. In wild-type embryos, the vagus motor neuron progenitors are born in the ventral ventricular zone, then migrate tangentially in the dorsolateral direction, forming the nuclei. However, in towhead (twd(rw685)) mutant embryos, the vagus motor neuron progenitors stray medially away from the normal migratory pathway and fail to stop in the right location. The twd(rw685) mutant has a defect in the GDP-mannose 4,6 dehydratase (gmds) gene, which encodes a key enzyme in the fucosylation pathway. Levels of fucosylated glycans were markedly and specifically reduced in twd(rw685) mutant embryos. Cell transplantation analysis revealed that GMDS is not essential in the vagus motor neuron progenitors for correct formation of the vagus motor nuclei, but is required in the neuroepithelial cells that surround the progenitors. Together, these findings suggest that fucosylated glycans expressed in neuroepithelial cells are required to guide the migration of vagus motor neuron progenitors.

Antenatal Betamethasone Causes Alterations in Angiotensin Receptors in Sheep Brain in a Gender Specific Manner

We showed recently that antenatal betamethasone (Beta) exposure at mid gestation (80th day) elevates mean arterial pressure and attenuates baroreflex sensitivity in adult sheep of both sexes (1.8 yrs old). We now examined the effects of fetal Beta exposure on AT1, AT2, and Ang‐(1‐7) receptors in autonomic nuclei of the brain medulla in 1.8 yr old sheep using in vitro receptor autoradiography for binding with the non‐selective Ang receptor antagonist [125I‐Sar1‐Thr8]‐Ang II. Receptor subtypes were defined by competition with losartan for AT1, PD 123319 for AT2, [D‐Ala7]‐Ang‐(1‐7) for Ang‐(1‐7) in nucleus tractus solitarii (nTS), dorsal motor nucleus of vagus (dmnX) and area postrema (AP). There were no significant differences in overall binding density between Beta‐treated male or female sheep and their controls. There was a significant increase in the ratio of AT1 to A1‐7 receptors in Beta‐treated females, but not treated males, towards AT1 in nTS (0.7 ± 0.2 vs 3 ± 1), dmnX (0.6 ± 0.4 vs 4 ± 2) and AP (0.6 ± 0.2 vs 3 ± 1) versus the control group. In contrast, there was a 50‐60% reduction (p&lt;0.03) in AT2 binding in dmnX and AP of Beta‐treated male sheep compared with controls. These sex‐specific changes in receptor subtypes are consistent with different mechanisms underlying the fetal programmed hypertension in male and female animals overall favoring a greater role for Ang II via the AT1 subtype. HD47584, HL51952

Fos activation in the lower brainstem after feeding and refeeding in gold thioglucose-treated mice

Event Abstract Back to Event Fos activation in the lower brainstem after feeding and refeeding in gold thioglucose-treated mice Péter Kurucz1*, Kinga Ibolya1, Meltzer K. Szabó1 and Miklos Palkovits1 1 Hungarian Academy of Sciences and Semmelweis University, Hungary Single injection of gold thioglucose (GTG) lesions the hypothalamic ventromedial nucleus in mice and increases food intake and obesity. It is also known that GTG treatment produces lesions in the lower brainstem as well: in the nucleus of the solitary tract (NTS), the dorsal motor nucleus of vagus (DMV) and the area postrema (AP). In the present study, acute responses to fasting and refeeding were investigated by immunohistochemical detection of Fos expression in neurons located in these brain areas of GTG lesioned and control mice. Very strong Fos activity was seen in the DMV and AP in control mice after 2 days fasting, while the NTS was silent. GTG-treated, fasted animals showed similar pattern of Fos distribution but with reduced number of immunoreactive neurons in all three investigated nuclei. In control mice, refeeding increased Fos activity in the NTS and AP while the DMV remained silent. In GTG-treated mice, feeding produced Fos immunoreactivity in the same areas but the intensity was lower than that in saline-injected control mice. In summary, refeeding elicited activity in the nucleus of the solitary tract and the area postrema neurons was reduced by GTG. In GTG-treated animals fasting produced lower intensity changes in the activity of the preganglionic dorsal motor vagal neurons but not in the viscerosensory NTS. These results are similar to our previous findings concerning on the effect of fasting and refeeding in the vagal nuclei of monosodium glutamate treated rats. Supported by OTKA K 62893. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Homeostatic regulatory mechanisms Citation: Kurucz P, Ibolya K, Szabó MK and Palkovits M (2009). Fos activation in the lower brainstem after feeding and refeeding in gold thioglucose-treated mice. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.114 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Mar 2009; Published Online: 04 Mar 2009. * Correspondence: Péter Kurucz, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary, kuruczp@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Péter Kurucz Kinga Ibolya Meltzer K Szabó Miklos Palkovits Google Péter Kurucz Kinga Ibolya Meltzer K Szabó Miklos Palkovits Google Scholar Péter Kurucz Kinga Ibolya Meltzer K Szabó Miklos Palkovits PubMed Péter Kurucz Kinga Ibolya Meltzer K Szabó Miklos Palkovits Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Infralimbic/anterior cingulate/amygdala projections to the gastrointestinal preganglionic vagal neurons in the medulla

Event Abstract Back to Event Infralimbic/anterior cingulate/amygdala projections to the gastrointestinal preganglionic vagal neurons in the medulla Éva Rebeka Szabó1*, Aniko Reichart1, Rege Sugárka Papp1 and Miklos Palkovits1 1 Department of Anatomy, Histology and Embryology, Semmelweis University, Hungary The possible role of the medial prefrontal cortex (mPFC) in the regulation of gastric activity has been suggested, and direct (monosynaptic) and indirect (multisynaptic) projections from the prefrontal cortex have been documented to the gastrointestinal projecting preganglionic neurons in the dorsal motor vagal nucleus in the dorsomedial medulla. Signals from prelimbic, infralimbic and dorsal peduncular cortical neurons may be relayed by hypothalamic or amygdaloid neurons. In our previous study, by using pseudorabies virus, a retrograde multisynaptic tracer, the existence of axonal projections from all of the compartments of the mPFC to the central amygdala (CeA) has been proved. The fine topography of an infralimbic – anterior cingulate – central amygdala neuronal circuit was investigated in the present study. To localize the individual compartment of this neuronal circuit biotinylated dextran amine (BDA) was deployed into the anterior cingulate cortex (ACi) and the infralimbic cortex, separately. Bilateral and unilateral surgicals transections through the caudal portion of the ACi, and BDA administrations into the ACi and the infralimbic cortex lead to identify one of the possible routes from the mPFC to the CeA. In intact rats, unilateral labeling was seen in the anterior amygdaloid area, the basolateral amygdala, and in the basolateral intercalate cells close to the CeA. Along the external capsule, BDA-labeled fibers were followed from the ACi into the amygdala. These fibers were eliminated by the surgical transections. Although, retrograde viral labeling suggested a direct anterior cingulate – central amygdala connections, the monosynaptic BDA tracing indicated the existence an intraamygdaloid (basolateral – central amygdala) relay of the prefrontal projections by GABAergic intercalate neurons. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Developmental neurobiology and subcortical functions Citation: Szabó É, Reichart A, Papp R and Palkovits M (2009). Infralimbic/anterior cingulate/amygdala projections to the gastrointestinal preganglionic vagal neurons in the medulla. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.078 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 02 Mar 2009; Published Online: 02 Mar 2009. * Correspondence: Éva Rebeka Szabó, Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary, szabo.eva.rebeka@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Éva Rebeka Szabó Aniko Reichart Rege Sugárka Papp Miklos Palkovits Google Éva Rebeka Szabó Aniko Reichart Rege Sugárka Papp Miklos Palkovits Google Scholar Éva Rebeka Szabó Aniko Reichart Rege Sugárka Papp Miklos Palkovits PubMed Éva Rebeka Szabó Aniko Reichart Rege Sugárka Papp Miklos Palkovits Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Histological study of the Vagus, Accessory and Hypoglossal nerves nuclei in one humped camel Camelus Dromedarius

The present work making histological studies of certain part of medullaoblongata on seven one humped camel ( Camelus Dromedarius ) of differentages and sexes. The location of Vagus X, accessory XI and hypoglossal XIInerve nuclei. The hypoglossal nerve XII nucleus consist of two nuclei dorsalgreater and ventral smaller and the dorsal nuclei observed. Connected withdorsal motor vagal nucleus X by specific arch of fiber in many sections andanother observation the root fiber of hypoglossal nucleus XII pass along thelateral border of inferior olivary nucleus and some sections the root fiberpenetrate lateral part of inferior olivary nucleus.