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Caudal Ventrolateral Medulla (caudal + ventrolateral_medulla)
Selected AbstractsAnatomy of Primary Afferents and Projection Neurones in the Rat Spinal Dorsal Horn with Particular Emphasis on Substance P and the Neurokinin 1 ReceptorEXPERIMENTAL PHYSIOLOGY, Issue 2 2002A. J. Todd The dorsal horn of the spinal cord plays an important role in transmitting information from nociceptive primary afferent neurones to the brain; however, our knowledge of its neuronal and synaptic organisation is still limited. Nociceptive afferents terminate mainly in laminae I and II and some of these contain substance P. Many projection neurones are located in lamina I and these send axons to various parts of the brain, including the caudal ventrolateral medulla (CVLM), parabrachial area, periaqueductal grey matter and thalamus. The neurokinin 1 (NK1) receptor on which substance P acts is expressed by certain neurones in the dorsal horn, including approximately 80% of lamina I projection neurones. There is also a population of large NK1 receptor-immunoreactive neurones with cell bodies in laminae III and IV which project to the CVLM and parabrachial area. It has been shown that the lamina III/IV NK1 receptor-immunoreactive projection neurones are densely and selectively innervated by substance P-containing primary afferent neurones, and there is evidence that these afferents also target lamina I projection neurones with the receptor. Both types of neurone are innervated by descending serotoninergic axons from the medullary raphe nuclei. The lamina III/IV neurones also receive numerous synapses from axons of local inhibitory interneurones which contain GABA and neuropeptide Y, and again this input shows some specificity since post-synaptic dorsal column neurones which also have cell bodies in laminae III and IV receive few contacts from neuropeptide Y-containing axons. These observations indicate that there are specific patterns of synaptic connectivity within the spinal dorsal horn. [source] From neuroanatomy to gene therapy: searching for new ways to manipulate the supraspinal endogenous pain modulatory systemJOURNAL OF ANATOMY, Issue 2 2007I. Tavares Abstract The endogenous pain modulatory system is a complex network of brain areas that control nociceptive transmission at the spinal cord by inhibitory and facilitatory actions. The balance between these actions ensures effective modulation of acute pain, while during chronic pain the pronociceptive effects appear to prevail. The mechanisms underlying this imbalance were studied as to the role of two medullary components of the pain modulatory system: the dorsal reticular nucleus and the caudal ventrolateral medulla, which function primarily as pronociceptive and antinociceptive centres, respectively. Both areas are connected with the spinal dorsal horn by closed reciprocal loops. In the spino-dorsal reticular nucleus loop, the ascending branch is strongly inhibited by spinal GABAergic neurons, which may act as a buffering system of the dorsal reticular nucleus-centred amplifying effect. In the spino-caudal ventrolateral medulla loop, the ascending branch is under potent excitation of substance P (SP) released from primary afferents, which is likely to trigger the intense descending inhibition detected in acute pain. During chronic pain, the activity in the lateral reticular formation of the caudal ventrolateral medulla changes, so that the action of the caudal ventrolateral medulla upon SP-responsive spinal neurons shifts from inhibitory to excitatory. The mechanisms of this modulatory shift are unknown but probably relate to the decresed expression of µ-opioid, ,-opioid and GABAB receptors. Normalizing receptor expression in the caudal ventrolateral medulla or controlling noci-evoked activity at the dorsal reticular nucleus or caudal ventrolateral medulla by interfering with neurotransmitter release is now possible by the use of gene therapy, an approach that stands out as a unique tool to manipulate the supraspinal endogenous pain control system. [source] Right atrial stretch alters fore- and hind-brain expression of c-fos and inhibits the rapid onset of salt appetiteTHE JOURNAL OF PHYSIOLOGY, Issue 15 2008Juliana Irani Fratucci De Gobbi The inflation of an intravascular balloon positioned at the superior vena cava and right atrial junction (SVC-RAJ) reduces sodium or water intake induced by various experimental procedures (e.g. sodium depletion; hypovolaemia). In the present study we investigated if the stretch induced by a balloon at this site inhibits a rapid onset salt appetite, and if this procedure modifies the pattern of immunohistochemical labelling for Fos protein (Fos-ir) in the brain. Male Sprague,Dawley rats with SVC-RAJ balloons received a combined treatment of furosemide (Furo; 10 mg (kg bw),1) plus a low dose of the angiotensin-converting enzyme inhibitor captopril (Cap; 5 mg (kg bw),1). Balloon inflation greatly decreased the intake of 0.3 m NaCl for as long as the balloon was inflated. Balloon inflation over a 3 h period following Furo,Cap treatment decreased Fos-ir in the organum vasculosum of the lamina terminalis and the subfornical organ and increased Fos-ir in the lateral parabrachial nucleus and caudal ventrolateral medulla. The effect of balloon inflation was specific for sodium intake because it did not affect the drinking of diluted sweetened condensed milk. Balloon inflation and deflation also did not acutely change mean arterial pressure. These results suggest that activity in forebrain circumventricular organs and in hindbrain putative body fluid/cardiovascular regulatory regions is affected by loading low pressure mechanoreceptors at the SVC-RAJ, a manipulation that also attenuates salt appetite. [source] AN ALDOSTERONE-RELATED SYSTEM IN THE VENTROLATERAL MEDULLA OBLONGATA OF SPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2006Natasha N Kumar SUMMARY 1The actions of aldosterone include mediation of vasoconstriction, vascular fibrosis, endothelial dysfunction and sodium retention. These actions can contribute to hypertension. Recent studies implicate an abnormal aldosterone hormonal system in the brain in hypertension. However, the study of central aldosterone actions is still in its infancy, as the exact location and abundance of its components in the brain are uncertain. 2We aimed to detect components of the aldosterone cascade in the regions of the ventrolateral medulla oblongata (VLM)-containing neurons that regulate blood pressure and to see whether there are quantitative differences in these components between the spontaneously hypertensive rat (SHR) and normotensive Wistar-Kyoto (WKY) rat models. Tissues from four regions of the brainstem, namely, the rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively), rostral pressor area and caudal pressor area, were examined. We measured mRNA expression of aldosterone synthase, mineralocorticoid receptor (MR1), 12-lipoxygenase (12-LO), serum- and glucocorticoid- inducible kinase and K-ras in male rats. Gene expression levels were measured using real-time reverse transcription,polymerase chain reaction. 3We detected all aldosterone components in all regions of the VLM. The K-ras levels were not significantly different in any of the regions. Expression of MR1 mRNA was lower in the RVLM of SHR (n = 5) compared with WKY rats (n = 5; t = 4.590; P = 0.002) and 12-LO mRNA levels were lower in the CVLM in SHR (n = 6) compared with WKY rats (n = 7; P = 0.04). Thus, we have shown for the first time that components of the aldosterone cascade are present in the VLM. Our results suggest that there may be a differential gene expression profile in the brainstem for genetic hypertension. [source] | ||||||||||