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Metabotropic glutamate receptors mediate lipopolysaccharide-induced fever and sickness behavior

Metabotropic glutamate receptors mediate lipopolysaccharide-induced fever and sickness behavior,10.1016/j.bbi.2005.08.007,Brain Behavior and Immunity,

Metabotropic glutamate receptors mediate lipopolysaccharide-induced fever and sickness behavior   (Citations: 5)
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Several mechanisms have been proposed for neuroimmune communication supporting the sickness syndrome (fever, anorexia, inactivity, and cachexia) following infection. We examined the role of glutamate as a neurochemical intermediary of sickness behavior induced by intraperitoneal lipopolysaccharide (LPS). Mice implanted with biotelemetry devices capable of detecting body temperature (Tb) were administered LPS (50 or 500μg/kg i.p., serotype 0111:B4) with or without i.p. pretreatment with vehicle or broad-spectrum antagonists selective for N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic (AMPA)/kainite, or metabotropic glutamate (mGlu) receptors. While NMDA and AMPA/kainate receptor antagonism failed to attenuate LPS-induced sickness behavior, antagonism of metabotropic receptors with l(+)-AP3 reduced the febrile (0–11h: control: 37.32±0.16°C, l(+)-AP3: 36.66±0.27), anorexic (control: −87±5%, l(+)-AP3: 48±12% scotophase food intake), and cachexic (control: −8.9±0.4%, l(+)-AP3: −6.1±1.3% body weight) effects of 500μg/kg LPS, and produced a biphasic Tb effect in response to 50μg/kg LPS (1h: −0.90±0.26; 6h: 1.78±0.35°C relative to baseline). At this dose the Tb of l(+)-AP3-treated mice was 1.18°C lower than controls 2h post-injection, and 0.68°C greater that controls 8h post-injection. These results suggest a role for mGlu receptors in mediating fever, anorexia, and cachexia possibly via activation of extra-vagal pathways, since the attenuating effect of l(+)-AP3 increased with increasing dosages of LPS. Given the critical role ascribed to mGlu receptors in neurotransmitter release and astrocytic processes, it is possible that these observations reflect an l(+)-AP3-induced attenuation of these systems.
Journal: Brain Behavior and Immunity - BRAIN BEHAV IMMUN , vol. 20, no. 3, pp. 233-245, 2006
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