Relevant bibliographies by topics / Ventrolateral Medulla

Academic literature on the topic 'Ventrolateral Medulla'

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Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Ventrolateral Medulla"

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Mandal, Aloke K., Pingyu Zhong, Kenneth J. Kellar, and Richard A. Gillis. "Ventrolateral Medulla." Journal of Cardiovascular Pharmacology 15 (1990): S49—S60. http://dx.doi.org/10.1097/00005344-199000157-00007.

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Mandal, Aloke K., Pingyu Zhong, Kenneth J. Kellar, and Richard A. Gillis. "Ventrolateral Medulla." Journal of Cardiovascular Pharmacology 15 (January 1990): S49—S60. http://dx.doi.org/10.1097/00005344-199001001-00007.

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McCall, R. B. "GABA-mediated inhibition of sympathoexcitatory neurons by midline medullary stimulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 4 (October 1, 1988): R605—R615. http://dx.doi.org/10.1152/ajpregu.1988.255.4.r605.

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The present investigation determined whether the effects of electrical stimulation of depressor sites in midline medullary raphe nuclei were a result of inhibition of sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla of anesthetized cats. Electrical stimulation of the raphe inhibited inferior cardiac sympathetic activity. Microinjections of glutamate mimicked the effects of electrical stimulation. Electrical stimulation inhibited sympathoexcitatory neurons in the rostral ventrolateral medulla. The onset of the sympathoinhibition recorded from the inferior cardiac nerve (72 ms) was equal to the sum of the onset latency of the sympathoexcitatory response elicited from the rostral ventrolateral medulla (49 ms) plus the conduction time in the raphe to rostral ventrolateral sympathoinhibitory pathway (23 ms). Raphe stimulation excited a second set of neurons in the rostral ventrolateral medulla with an onset of 21 ms. Microiontophoretically applied bicuculline increased the discharge of sympathoexcitatory neurons and blocked the raphe-evoked inhibition. Iontophoretic glutamate excited sympathoexcitatory neurons but failed to antagonize raphe-elicited inhibition. These data suggest that neuronal elements in medullary raphe nuclei tonically inhibit sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla by activating closely adjacent gamma-aminobutyric acid (GABA) interneurons.
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Sun, Wei, and W. Michael Panneton. "The caudal pressor area of the rat: its precise location and projections to the ventrolateral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 3 (September 1, 2002): R768—R778. http://dx.doi.org/10.1152/ajpregu.00184.2002.

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Investigators have demonstrated pressor areas in the medullas of various species. The present study precisely localized the pressor area in the caudal medulla of the rat and determined its projections to the caudal and rostral ventrolateral medulla. The caudal medulla first was mapped grossly in rats with injections (30 nl) of glutamate (30-, 15-, and 7.5-nmol doses) placed 0.5, 1.0, and 1.5 mm caudal to the calamus scriptorius, 1.0, 1.5, and 2.0 mm lateral to the midline, and 1.8, 1.7, and 1.6 mm ventral to the dorsal medullary surface, respectively, and their arterial pressures were recorded. One of these nine injections showed significant increases in arterial pressure. We micromapped this area with a total of 27 injections of glutamate (10 nl; 5 nmol) placed 300 μm apart at 3 different dorsoventral levels. This micromapping study pinpointed the precise location of caudal pressor area (CPA) neurons in a restricted region lateral to the caudal end of the lateral reticular nucleus and ventromedial to the medullary dorsal horn near the level of the pyramidal decussation. Injections of glutamate into this spot, 1.0 mm caudal to the calamus scriptorius, 2.0 mm lateral to the midline, and 1.7 mm ventral from the dorsal surface of the medulla, induced significant increases in arterial pressure. The neuroanatomic connections of neurons in the CPA to the ventrolateral medulla were then investigated with iontophoretic injections of either the anterograde tracer biotinylated dextran amine (BDA) made into the CPA or the retrograde tracer FluoroGold (FG) injected into either the caudal or rostral ventrolateral medulla. BDA injections resulted in bouton-laden fibers throughout both caudal and rostral portions of the ventrolateral medulla. Either of the FG injections resulted in numerous spindle-shaped neurons interspersed between the longitudinal fiber bundles running through the CPA area. The proximity of the CPA neurons to the A1 catecholaminergic cell group is discussed.
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Bergamaschi, Cássia T., Ruy R. Campos, and Oswaldo U. Lopes. "Rostral Ventrolateral Medulla." Hypertension 34, no. 4 (October 1999): 744–47. http://dx.doi.org/10.1161/01.hyp.34.4.744.

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Kubo, T., H. Amano, and Y. Misu. "Caudal ventrolateral medulla." Naunyn-Schmiedeberg's Archives of Pharmacology 328, no. 4 (February 1985): 368–72. http://dx.doi.org/10.1007/bf00692902.

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Li, Y. W., Z. J. Gieroba, R. M. McAllen, and W. W. Blessing. "Neurons in rabbit caudal ventrolateral medulla inhibit bulbospinal barosensitive neurons in rostral medulla." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 1 (July 1, 1991): R44—R51. http://dx.doi.org/10.1152/ajpregu.1991.261.1.r44.

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We made extracellular recordings from 104 spinally projecting neurons in the rostral ventrolateral medulla of urethan-anesthetized rabbits to test whether inhibitory vasomotor neurons in the caudal ventrolateral medulla act by inhibiting rostral sympathoexcitatory neurons. The median conduction velocity was 8.3 m/s, and the median discharge rate was 2.9 spikes/s. Raising arterial pressure with intravenous phenylephrine inhibited 88% of 77 neurons tested. The remaining units were excited. Lowering arterial pressure with nitroprusside excited 90% of 30 neurons tested. Remaining units were unaffected. Ninety-one percent of 58 rostral neurons inhibited by phenylephrine were also inhibited by injection of L-glutamate into the caudal ventrolateral medulla and 81% of 43 tested were excited by caudal injection of gamma-aminobutyric acid. These results confirm our suggestion [Brain Res. 253: 161-171, 1982; Am. J. Physiol. 254 (Heart Circ. Physiol. 23): H686-H692, 1988] and the findings of S. K. Agarwal, A. J. Gelsema, and F. R. Calaresu [Am. J. Physiol. 257 (Regulatory Integrative Comp. Physiol. 26): R265-R270, 1989]. The depressor neurons in the caudal medulla act substantially by inhibition of spinally projecting sympathoexcitatory neurons in the rostral medulla. All rostral units excited by phenylephrine were also excited by injections of L-glutamate into the caudal ventrolateral medulla, suggesting that some sympathoinhibition of baroreceptor and caudal medullary origin may take place in the spinal cord and be mediated by a subpopulation of rostral sympathoinhibitory neurons.
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Blessing, W. W. "Depressor neurons in rabbit caudal medulla act via GABA receptors in rostral medulla." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 4 (April 1, 1988): H686—H692. http://dx.doi.org/10.1152/ajpheart.1988.254.4.h686.

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Experiments were conducted in urethan-anesthetized rabbits to determine whether vasomotor effects elicited by activation or inhibition of the caudal ventrolateral medulla depend on gamma-aminobutyric acid (GABA)ergic, glycinergic, or alpha-adrenergic receptors in the region of the rostral ventrolateral medulla, which contains the bulbospinal sympathoexcitatory neurons. Bilateral injection of bicuculline methiodide into the rostral medulla caused a dose-related reduction in the fall in arterial pressure and in the inhibition of renal sympathetic nerve activity normally elicited by chemical stimulation of neurons in the caudal medulla using local injection of L-glutamate. When both bicuculline and muscimol were injected into the rostral medulla at the same time, resting arterial pressure was maintained at base-line levels, and the sympathoexcitatory neurons remained normally excitable by local injection of L-glutamate into the rostral medulla. In the presence of this mixed antagonist-agonist GABAergic blockade, both decreases and increases in arterial pressure elicited by excitation or inhibition of neuronal function in the caudal medulla were abolished. Similar effects were not observed after blockade of glycinergic or alpha-adrenergic receptors in the rostral ventrolateral medulla. Results suggest that the depressor neurons in the caudal ventrolateral medulla alter peripheral sympathetic vasomotor activity almost entirely by an action on GABAergic receptors in the rostral ventrolateral medulla.
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Naraghi, Ramin, Michael R. Gaab, Gerhard F. Walter, and Berthold Kleineberg. "Arterial hypertension and neurovascular compression at the ventrolateral medulla." Journal of Neurosurgery 77, no. 1 (July 1992): 103–12. http://dx.doi.org/10.3171/jns.1992.77.1.0103.

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✓ Intraoperative observations and animal experiments suggest that neurovascular compression at the left ventrolateral medulla is a possible etiological factor in essential hypertension. In pursuing this hypothesis, the authors examined the neurovascular relations in the posterior cranial fossa of 24 patients with essential hypertension, of 10 with renal hypertension, and of 21 normotensive control patients. Artificial perfusion of the vessels and microsurgical investigations during autopsy identified the vascular relations at the brain stem and at the root entry zone of the caudal cranial nerves. There was no evidence of neurovascular compression at the ventrolateral medulla on the left side in any patient from the control group or among those with renal hypertension. Two normotensive patients had neurovascular compression at the right ventrolateral medulla by the posterior inferior cerebellar artery. In contrast, all patients with essential hypertension had definite neurovascular compression at the left ventrolateral medulla. Additional compression of the right side was seen in three of these patients. Based on the anatomical appearance, it was possible to define three distinct types of neurovascular compression at the ventrolateral medulla. Common to all three types is the compression of the medulla oblongata at its rostral part just caudal to the pontomedullary junction and lateral to the olive in the retro-olivary sulcus. Comparative histopathological study of the microsurgically examined brain-stem specimens revealed no differences between patients with essential hypertension, those with renal hypertension, and normal controls. There was a structural integrity at the site of neurovascular compression at the ventrolateral medulla. The microanatomical findings of this study show that neurovascular relations at the ventrolateral medulla in essential hypertension give rise to pulsatile compression on the left. This supports Jannetta's hypothesis of neurovascular compression at the left ventrolateral medulla as an etiology of essential hypertension.
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Steinbacher, B. C., and B. J. Yates. "Processing of vestibular and other inputs by the caudal ventrolateral medullary reticular formation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 4 (October 1, 1996): R1070—R1077. http://dx.doi.org/10.1152/ajpregu.1996.271.4.r1070.

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Lesions of the lateral medullary reticular formation caudal to the obex abolish vestibulosympathetic and somatosympathetic responses; this area also contains neurons that mediate baroreceptor reflexes. Recordings were made from neurons in the caudal medullary reticular formation of cats that were decerebrate or anesthetized using alpha-chloralose-urethan to determine whether common neurons responded to electrical stimulation of vestibular and hindlimb afferents and had cardiac-related (i.e., baroreceptor) inputs. Many neurons in the ventrolateral portion of the caudal reticular formation received labyrinthine inputs, and they were interspersed with neurons that received baroreceptor signals. However, virtually none of the units received convergent baroreceptor and vestibular inputs, suggesting that separate pathways from the caudal ventrolateral medulla mediate baroreceptor and vestibulosympathetic reflexes. Furthermore, the neurons that received labyrinthine signals could not be antidromically activated from electrodes inserted into the rostral ventrolateral medulla, which is known to mediate vestibulosympathetic responses; thus an indirect pathway must convey vestibular inputs from the caudal to rostral medullary reticular formation. Over 75% of both neurons with baroreceptor inputs and cells with vestibular signals responded to sciatic nerve stimulation, suggesting that more than one pathway from the caudal medulla may mediate somatosympathetic responses.
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Dissertations / Theses on the topic "Ventrolateral Medulla"

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Zidon, Terese M. "Specific neuronal phenotypes within the rostral ventrolateral medulla following cardiovascular deconditioning in rats." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/6076.

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Thesis (M.S.)--University of Missouri-Columbia, 2008.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Includes bibliographical references.
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Makeham, John Murray. "Functional neuroanatomy of tachykinins in brainstem autonomic regulation." University of Sydney, 1997. http://hdl.handle.net/2123/1960.

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Doctor of Philosophy (PhD)
Little is known about the role that tachykinins, such as substance P and its receptor, the neurokinin-1 receptor, play in the generation of sympathetic nerve activity and the integration within the ventrolateral medulla (VLM) of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The studies described in this thesis investigate these autonomic functions and the role of tachykinins through physiological (response to hypercapnoea, chapter 3), anatomical (neurokinin-1 receptor immunohistochemistry, chapter 4) and microinjection (neurokinin-1 receptor activation and blockade, chapters 5 and 6) experiments. In the first series of experiments (chapter 3) the effects of chemoreceptor activation with hyperoxic hypercapnoea (5%, 10% or 15% CO2 in O2) on splanchnic sympathetic nerve activity and sympathetic reflexes such as the baroreflex and somato-sympathetic reflex were examined in anaesthetized rats. Hypercapnoea resulted in sympatho-excitation in all groups and a small increase in arterial blood pressure in the 10 % CO2 group. Phrenic nerve amplitude and phrenic frequency were also increased, with the frequency adapting back to baseline during the CO2 exposure. Hypercapnoea selectively attenuated (5% CO2) or abolished (10% and 15% CO2) the somato-sympathetic reflex while leaving the baroreflex unaffected. This selective inhibition of the somato-sympathetic reflex while leaving the baroreflex unaffected was also seen following neurokinin-1 receptor activation in the rostral ventrolateral medulla (RVLM) (see below). Microinjection of substance P analogues into the RVLM results in a pressor response, however the anatomical basis for this response is unknown. In the second series of experiments (chapter 4), the distribution of the neurokinin-1 receptor in the RVLM was investigated in relation to catecholaminergic (putative sympatho-excitatory “C1”) and bulbospinal neurons. The neurokinin-1 receptor was demonstrated on a small percentage (5.3%) of C1 neurons, and a small percentage (4.7%) of RVLM C1 neurons also receive close appositions from neurokinin-1 receptor immunoreactive terminals. This provides a mechanism for the pressor response seen with RVLM microinjection of substance P analogues. Neurokinin-1 receptor immunoreactivity was also seen a region overlapping the preBötzinger complex (the putative respiratory rhythm generation region), however at this level a large percentage of these neurons are bulbospinal, contradicting previous work suggesting that the neurokinin-1 receptor is an exclusive anatomical marker for the propriobulbar rhythm generating neurons of the preBötzinger complex. The third series of experiments (chapter 5) investigated the effects of neurokinin-1 receptor activation and blockade in the RVLM on splanchnic sympathetic nerve activity, arterial blood pressure, and autonomic reflexes such as the baroreflex, somato-sympathetic reflex, and sympathetic chemoreflex. Activation of RVLM neurokinin-1 receptors resulted in sympatho-excitation, a pressor response, and abolition of phrenic nerve activity, all of which were blocked by RVLM pre-treatment with a neurokinin-1 receptor antagonist. As seen with hypercapnoea, RVLM neurokinin-1 receptor activation significantly attenuated the somato-sympathetic reflex but did not affect the sympathetic baroreflex. Further, blockade of RVLM neurokinin-1 receptors significantly attenuated the sympathetic chemoreflex, suggesting a role for RVLM substance P release in this pathway. The fourth series of experiments (chapter 6) investigated the role of neurokinin-1 receptors in the RVLM, caudal ventrolateral medulla (CVLM), and nucleus tractus solitarius (NTS) on regional cerebral blood flow (rCBF) and tail blood flow (TBF). Activation of RVLM neurokinin-1 receptors increased rCBF associated with a decrease in cerebral vascular resistance (CVR). Activation of CVLM neurokinin-1 receptors decreased rCBF, however no change in CVR was seen. In the NTS, activation of neurokinin-1 receptors resulted in a biphasic response in both arterial blood pressure and rCBF, but no significant change in CVR. These findings suggest that in the RVLM substance P and the neurokinin-1 receptor play a role in the regulation of cerebral blood flow, and that changes in rCBF evoked in the CVLM and NTS are most likely secondary to changes in arterial blood pressure. Substance P and neurokinin-1 receptors in the RVLM, CVLM and NTS do not appear to play a role in the brainstem regulation of tail blood flow. In the final chapter (chapter 7), a model is proposed for the role of tachykinins in the brainstem integration of the sympathetic baroreflex, sympathetic chemoreflex, cerebral vascular tone, and the sympatho-excitation seen following hypercapnoea. A further model for the somato-sympathetic reflex is proposed, providing a mechanism for the selective inhibition of this reflex seen with hypercapnoea (chapter 3) and RVLM neurokinin-1 receptor activation (chapter 5). In summary, the ventral medulla is essential for the generation of basal sympathetic tone and the integration of many vital autonomic reflexes such as the baroreflex, chemoreflex, somato-sympathetic reflex, and the regulation of cerebral blood flow. The tachykinin substance P, and its receptor, the neurokinin-1 receptor, have a role to play in many of these vital autonomic functions. This role is predominantly neuromodulatory.
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Chan, Kai-wah Raymond. "A study on the neuronal properties of the rostral ventrolateral medulla in normotensive and spontaneously hypertensive rats /." [Hong Kong] : University of Hong Kong, 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13014328.

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陳啓華 and Kai-wah Raymond Chan. "A study on the neuronal properties of the rostral ventrolateral medulla in normotensive and spontaneously hypertensive rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1991. http://hub.hku.hk/bib/B31232127.

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Bourassa, Erick Arden. "The role of the renin-angiotensin system in controlling the rostral ventrolateral medulla in normotensive and hypertensive animals /." Full text available from ProQuest UM Digital Dissertations, 2008. http://0-proquest.umi.com.umiss.lib.olemiss.edu/pqdweb?index=0&did=1850439481&SrchMode=1&sid=6&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1277483754&clientId=22256.

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Thesis (Ph.D.)--University of Mississippi, 2008.
Typescript. Vita. "August 2008." Major professor: Robert C. Speth Includes bibliographical references (leaves 110-128). Also available online via ProQuest to authorized users.
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Ott, Mackenzie M. "Functional Connectivity and Responses to Chemoreceptor Stimulation of Medullary Ventrolateral Respiratory Column Neurons." Scholar Commons, 2010. https://scholarcommons.usf.edu/etd/1734.

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Ventrolateral medullary neurons have important roles in cardiorespiratory coordination. A rostral extension of the ventral respiratory column (RVRC), including the retrotrapezoid nucleus (RTN), has neurons responsive to local perturbations of CO2 / pH. Respiratory-modulated firing patterns of RVRC neurons are attributed to influences of more caudal (CVRC) neurons. These circuits remain poorly understood. This study addressed the hypothesis that both local interactions and influences from the CVRC shape rostral neuron discharge patterns and responses. Spike trains from 294 rostral and 490 caudal neurons were recorded with multi-electrode arrays along with phrenic nerve activity in 14 decerebrate, vagotomized cats. Overall, 214 rostral and 398 caudal neurons were respiratory-modulated; 124 and 95, respectively, were cardiac-modulated. Subsets of these neurons were evaluated for responses to sequential, selective, transient stimulation of central and peripheral chemoreceptors and arterial baroreceptors. In 5 experiments, Mayer wave-related oscillations (MWROs) in neuronal firing rates were evoked, enhanced, or reduced following central chemoreceptor stimulation. Overall, 174 of the rostral neurons (59.5%) had short- time scale correlations with other RVRC neurons. Of these, 49 triggered cross-correlograms with RVRC targets yielding 330 offset features indicative of paucisynaptic actions from a total of 2,884 rostral pairs evaluated. Forty-nine of the CVRC neurons (10.0%) were triggers in 142 CVRC-RVRC correlograms - from a total of 8,490 - with offset features indicative of actions on RVRC neurons. Correlation linkage maps support the hypothesis that local circuit mechanisms contribute to the respiratory and cardiac modulation of RVRC neurons and their responses to chemoreceptor and baroreceptor challenges.
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Kumar, Natasha N. "Studies on Cholinergic and Enkephalinergic Systems in Brainstem Cardiorespiratory Control." University of Sydney, 2007. http://hdl.handle.net/2123/2014.

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Doctor of Philosophy(PhD)
This thesis addresses the neurochemistry and function of specific nuclei in the autonomic nervous system that are crucial mediators of cardiorespiratory regulation. The primary aim is to build on previous knowledge about muscarinic cholinergic mechanisms within cardiorespiratory nuclei located in the ventrolateral medulla oblongata. The general focus is characterisation of gene expression patterns of specific muscarinic receptor subtypes in central nuclei involved in blood pressure control and respiratory control in normal rats. The findings were subsequently extended by characterisation of muscarinic receptor gene expression patterns in 1) a rat model of abnormal blood pressure control (hypertension) (Chapter 3) 2) a rat model of cholinergic sensitivity (Chapter 5) 3) the rat ventral respiratory group (Chapter 6) The results of a series of related investigations that ensued from the initial aims more finely characterise the neurocircuitry of the ventrolateral medulla, from a specifically cholinoceptive approach. All five muscarinic receptor subtypes are globally expressed in the ventrolateral medulla but only the M2R mRNA was significantly elevated in the VLM of hypertensive animals compared to their normotensive controls and in the VLM of animals displaying cholinergic hypersensitivity compared to their resistant controls. Surprisingly, M2R mRNA is absent in catecholaminergic cell groups but abundant in certain respiratory nuclei. Two smaller projects involving gene expression of other neurotransmitter / neuromodulators expressed in cardiorespiratory nuclei were also completed during my candidature. Firstly, the neurochemical characterisation of enkephalinergic neurons in the RVLM, and their relationship with bulbospinal, catecholaminergic neurons in hypertensive compared to normotensive animals was carried out (Chapter 4). A substantial proportion of sympathoexcitatory neurons located in the RVLM were enkephalinergic in nature. However, there was no significant difference in preproenkephalin expression in the RVLM in hypertensive compared to normotensive animals. Secondly, the identification and distribution of components of the renin-angiotensin aldosterone system (RAAS) within the brainstem, and differences in gene expression levels between hypertensive and normotensive animals was also investigated. The RAAS data was not included in this thesis, since the topic digresses substantially from other chapters and since it is published (Kumar et al., 2006). The mRNA expression aldosterone synthase, mineralocorticoid receptor (MR1), 12-lipoxygenase (12-LO), serum- and glucocorticoid- inducible kinase and K-ras) were found to be present at all rostrocaudal levels of the ventrolateral medulla. Expression of MR1 mRNA was lower in the RVLM of SHR compared with WKY rats and 12-LO mRNA levels were lower in the CVLM in SHR compared with WKY rats. Otherwise, there was no difference in gene expression level, or the method of detection was not sensitive enough to detect differences in low copy transcripts between hypertensive and normotensive animals.
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Bardgett, Megan Elyse. "NEURAL MECHANISMS OF SYMPATHETIC ACTIVATION DURING HYPERINSULINEMIA AND OBESITY-INDUCED HYPERTENSION." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/46.

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Obesity afflicts more than 30% of the U.S. population and is a major risk factor for the development of hypertension, type II diabetes, and cardiovascular disease. Studies in humans and animals indicate that obesity is associated with increased sympathetic outflow to the vasculature and kidneys. One mechanism postulated to underlie the increase in sympathetic nerve activity (SNA) in obesity is hyperinsulinemia. Little is known regarding the central circuitry underlying elevated SNA and arterial blood pressure (ABP) during hyperinsulinemia and obesity or if sympathoexcitatory circuits are still responsive to insulin in obesity. Hyperinsulinemic-euglycemic clamps elevate SNA to the hind limb vasculature in lean rodents but obesity is associated with resistance to the peripheral and anorexic effects of insulin. Therefore, the first aim was to determine whether diet-induced obesity causes development of insulin resistance in the central circuits mediating SNA. The sympathoexcitatory response to insulin was still intact in diet-induced obese rats indicating a role for insulin in the elevation in SNA and ABP in obesity. The second aim of this project was to identify the specific receptors in the rostral ventrolateral medulla (RVLM) that mediate the elevated SNA during hyperinsulinemia. The RVLM provides basal sympathetic tone and maintains baseline ABP. Glutamate is the major excitatory neurotransmitter and glutamate receptors of the RVLM are known to mediate multiple forms of hypertension. Blockade of RVLM NMDA-specific glutamatergic receptors reverses the increased lumbar SNA associated with hyperinsulinemia. In contrast, blockade of angiotensin II type 1 or melanocortin receptors in the RVLM had no effect on the sympathoexcitatory response to insulin. The goal of the third aim was to identify the cellular mechanisms within RVLM that mediate the elevated SNA and ABP in diet-induced obesity. Blockade of RVLM glutamate receptors reversed the elevated ABP and lumbar SNA associated with diet-induced obesity while it had no effect on rats on a low fat diet or those resistant to weight gain on the high fat diet. Similar to the findings during hyperinsulinemia, blockade of RVLM angiotensin II type 1 or melanocortin receptors had no effect on lumbar SNA or ABP during diet-induced obesity.
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黃德彬 and Tak-pan Wong. "An electrophysiological study of the projection from the paraventricular nucleus of hypothalamus to the cardiovascular neuronsin the rostral ventrolateral medulla of the rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31212724.

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Wong, Tak-pan. "An electrophysiological study of the projection from the paraventricular nucleus of hypothalamus to the cardiovascular neurons in the rostral ventrolateral medulla of the rat /." Hong Kong : University of Hong Kong, 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B14709120.

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Books on the topic "Ventrolateral Medulla"

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Yang, Zhuo. The influence of the paraventricular nucleus of the hypothalamus on cardiovascular neurones in the ventrolateral medulla in normotensive and hypertensive rats. Birmingham: University of Birmingham, 1999.

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Luppi, Pierre-Hervé, Olivier Clément, Christelle Peyron, and Patrice Fort. Neurobiology of REM sleep. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0003.

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REM (paradoxical) sleep is a state characterized by rapid eye movements, EEG activation, and muscle atonia. REM sleep behavior disorder (RBD) is a parasomnia characterized by loss of muscle atonia during REM sleep. Cataplexy, a key symptom of narcolepsy, is a striking sudden episode of muscle weakness comparable to REM sleep atonia triggered by emotions during wakefulness. This chapter presents recent results on the neuronal network responsible for REM sleep and explores hypotheses explaining RBD and cataplexy. RBD could be due to a specific degeneration of glutamatergic neurons responsible for muscle atonia, localized in the pontine sublaterodorsal tegmental nucleus (SLD) or the glycinergic/GABAergic premotoneurons localized in the ventral medullary reticular nuclei. Cataplexy in narcoleptics could be due to activation during waking of SLD neurons. In normal conditions, activation of SLD neurons would be blocked by simultaneous excitation by hypocretins of REM sleep-off GABAergic neurons localized in the ventrolateral periaqueductal gray.
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Book chapters on the topic "Ventrolateral Medulla"

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Chalmers, John P., Emilio Badoer, David Morilak, Guy Drolet, Jane B. Minson, Ida J. Llewellyn-Smith, Peter Somogyi, Vimal Kapoor, and Paul Pilowsky. "Afferent Inputs to Ventrolateral Medulla." In Central Neural Mechanisms in Cardiovascular Regulation, 3–13. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4615-9834-3_1.

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Allen, Andrew M., Shuichi Sasaki, Roger A. L. Dampney, Frederick A. O. Mendelsohn, and William W. Blessing. "Actions of Angiotensin II in the Ventrolateral Medulla Oblongata." In Central Neural Mechanisms in Cardiovascular Regulation, 95–103. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4615-9834-3_8.

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Averill, David B., Hiromi Muratani, Karla J. Madalin, and Carlos M. Ferrario. "Cardiovascular Actions of Angiotensin II in the Ventrolateral Medulla." In Central Neural Mechanisms in Cardiovascular Regulation, 104–21. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4615-9834-3_9.

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Ruggiero, D. A., R. E. Gomez, S. L. Cravo, E. Mtui, M. Anwar, and D. J. Reis. "The Rostral Ventrolateral Medulla: Anatomical Substrates of Cardiopulmonary Integration." In Cardiorespiratory and Motor Coordination, 89–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75507-1_11.

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Macrae, I. M., and J. L. Reid. "Cardiovascular effects of Neuropeptide Y in the Caudal Ventrolateral Medulla." In Opioid Peptides and Blood Pressure Control, 112–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73429-8_12.

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Nolan, P. C., G. H. Dillon, and T. G. Waldrop. "Central Hypoxic Chemoreceptors in the Ventrolateral Medulla and Caudal Hypothalamus." In Advances in Experimental Medicine and Biology, 261–66. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1933-1_49.

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Van Bockstaele, Elisabeth J., and Gary Aston-Jones. "Widespread Autonomic Afferents to the Nucleus Paragigantocellularis of the Rostral Ventrolateral Medulla." In Central Neural Mechanisms in Cardiovascular Regulation, 14–28. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4615-9834-3_2.

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McMullan, Simon. "Identification of Spinally Projecting Neurons in the Rostral Ventrolateral Medulla In Vivo." In Stimulation and Inhibition of Neurons, 123–40. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-233-9_7.

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Haxhiu, M. A., B. Erokwu, and I. A. Dreshaj. "Selective Hypoxic Loading of the Ventrolateral Medulla Inhibits Cholinergic Outflow to the Airways." In Oxygen Transport to Tissue XX, 467–73. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4863-8_57.

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Sapru, Hreday N. "Control of Blood Pressure by Muscarinic and Nicotinic Receptors in the Ventrolateral Medulla." In Tobacco Smoking and Nicotine, 287–300. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1911-5_18.

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Conference papers on the topic "Ventrolateral Medulla"

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Agarwala, Priya, Oanh Le-Hoang, Judith A. Neubauer, and Jagadeeshan Sunderram. "TIME COURSE OF INDUCTION OF HEME OXYGENASE –1 (HO-1) IN THE CENTRAL CARDIORESPIRATORY REGION OF THE ROSTRAL VENTROLATERAL MEDULLA (RVLM) IN MICE FOLLOWING CHRONIC INTERMITTENT HYPOXIA." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4203.

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You might also be interested in the extended bibliographies on the topic 'Ventrolateral Medulla' for particular source types:
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