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10.1371/journal.pone.0000001 http://scihub22266oqcxt.onion/10.1371/journal.pone.0000001 17183631!1762328!17183631     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=17183631&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       PLoS+One 2006 ; 1 (1): e1 Nephropedia Template TP {{tp|p=17183631|t=2006. Neural substrate of cold-seeking behavior in endotoxin shock |pdf=|usr=}}{{17183631}} gab.com Text Neural substrate of cold-seeking behavior in endotoxin shock JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=17183631 #FOAvip Systemic inflammation is a leading cause of hospital death. Mild systemic inflammation is accompanied by warmth-seeking behavior (and fever), whereas severe inflammation is associated with cold-seeking behavior (and hypothermia). Both behaviors are adaptive. Which brain structures mediate which behavior is unknown. The involvement of hypothalamic structures, namely, the preoptic area (POA), paraventricular nucleus (PVH), or dorsomedial nucleus (DMH), in thermoregulatory behaviors associated with endotoxin (lipopolysaccharide [LPS])-induced systemic inflammation was studied in rats. The rats were allowed to select their thermal environment by freely moving in a thermogradient apparatus. A low intravenous dose of Escherichia coli LPS (10 microg/kg) caused warmth-seeking behavior, whereas a high, shock-inducing dose (5,000 microg/kg) caused cold-seeking behavior. Bilateral electrocoagulation of the PVH or DMH, but not of the POA, prevented this cold-seeking response. Lesioning the DMH with ibotenic acid, an excitotoxin that destroys neuronal bodies but spares fibers of passage, also prevented LPS-induced cold-seeking behavior; lesioning the PVH with ibotenate did not affect it. Lesion of no structure affected cold-seeking behavior induced by heat exposure or by pharmacological stimulation of the transient receptor potential (TRP) vanilloid-1 channel ("warmth receptor"). Nor did any lesion affect warmth-seeking behavior induced by a low dose of LPS, cold exposure, or pharmacological stimulation of the TRP melastatin-8 ("cold receptor"). We conclude that LPS-induced cold-seeking response is mediated by neuronal bodies located in the DMH and neural fibers passing through the PVH. These are the first two landmarks on the map of the circuitry of cold-seeking behavior associated with endotoxin shock. Twit Text FOAVip Neural substrate of cold-seeking behavior in endotoxin shock ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=17183631 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17183631 #FOAvip English Wikipedia <ref>{{Cite pmid|17183631}}</ref> Neural substrate of cold-seeking behavior in endotoxin shock #MMPMID17183631 Almeida MC; Steiner AA; Branco LG; Romanovsky AA PLoS One 2006[Dec]; 1 (1): e1 PMID17183631show ga Systemic inflammation is a leading cause of hospital death. Mild systemic inflammation is accompanied by warmth-seeking behavior (and fever), whereas severe inflammation is associated with cold-seeking behavior (and hypothermia). Both behaviors are adaptive. Which brain structures mediate which behavior is unknown. The involvement of hypothalamic structures, namely, the preoptic area (POA), paraventricular nucleus (PVH), or dorsomedial nucleus (DMH), in thermoregulatory behaviors associated with endotoxin (lipopolysaccharide [LPS])-induced systemic inflammation was studied in rats. The rats were allowed to select their thermal environment by freely moving in a thermogradient apparatus. A low intravenous dose of Escherichia coli LPS (10 microg/kg) caused warmth-seeking behavior, whereas a high, shock-inducing dose (5,000 microg/kg) caused cold-seeking behavior. Bilateral electrocoagulation of the PVH or DMH, but not of the POA, prevented this cold-seeking response. Lesioning the DMH with ibotenic acid, an excitotoxin that destroys neuronal bodies but spares fibers of passage, also prevented LPS-induced cold-seeking behavior; lesioning the PVH with ibotenate did not affect it. Lesion of no structure affected cold-seeking behavior induced by heat exposure or by pharmacological stimulation of the transient receptor potential (TRP) vanilloid-1 channel ("warmth receptor"). Nor did any lesion affect warmth-seeking behavior induced by a low dose of LPS, cold exposure, or pharmacological stimulation of the TRP melastatin-8 ("cold receptor"). We conclude that LPS-induced cold-seeking response is mediated by neuronal bodies located in the DMH and neural fibers passing through the PVH. These are the first two landmarks on the map of the circuitry of cold-seeking behavior associated with endotoxin shock. |Animals[MESH] |Autonomic Nervous System/drug effects/physiopathology[MESH] |Behavior, Animal/drug effects/physiology[MESH] |Body Temperature Regulation/drug effects/physiology[MESH] |Cold Temperature[MESH] |Dorsomedial Hypothalamic Nucleus/drug effects/injuries/pathology/physiopathology[MESH] |Dose-Response Relationship, Drug[MESH] |Hot Temperature[MESH] |Humans[MESH] |Hypothalamus/*drug effects/injuries/pathology/*physiopathology[MESH] |Lipopolysaccharides/administration & dosage/toxicity[MESH] |Male[MESH] |Paraventricular Hypothalamic Nucleus/drug effects/injuries/pathology/physiopathology[MESH] |Preoptic Area/drug effects/injuries/pathology/physiopathology[MESH] |Rats[MESH] |Rats, Wistar[MESH]Neural substrate of cold-seeking behavior in endotoxin shock (epmc).pdf DeepDyve Pubget Overpricing