GLUTAMATE RELEASE IN THE NUCLEUS-TRACTUS-SOLITARIUS INDUCED BY PERIPHERAL LIPOPOLYSACCHARIDE AND INTERLEUKIN-1-BETA

The involvement of vagal afferents in the communication pathway from t he immune system to the brain was studied. Glutamate was measured in t he nucleus tractus solitarius, the brain area receiving glutamatergic vagal afferents, after peripheral injection of lipopolysaccharide or i nterleukin-1 beta. Intraperitoneal or intravenous saline or intraperit oneal heat-inactivated inlerleukin-1 beta increased glutamate release, measured by brain microdialysis in freely-moving rats at 20 min (137 +/- 19%, 126 +/- 10% and 133 +/- 6%, respectively), without inducing a ny other change up to 3 h after injection. Intraperitoneal lipopolysac charide (10 mu g/rat) increased glutamate at 20 min (132 +/- 10%) and at 60 min (208 +/- 26%). To compare lipopolysaccharide effectiveness b y the two routes, serum levels of interieukin-1 beta, interleukin-6 an d tumour necrosis factor-alpha were measured. Intravenous lipopolysacc haride induced each cytokine more rapidly and efficiently than intrape ritoneal lipopolysaccharide. Perfusion with tetrodotoxin (1 mu M) in t he dialysis probe decreased glutamate basal levels by approximately 20 % and completely prevented lipopolysaccharide effects, showing the neu ronal component of the glutamate measured. Except for the 20-min incre ase, intravenous lipopolysaccharide (10 mu g/rat) did not affect gluta mate release. Intraperitoneal interleukin-1 beta (4 mu g/rat) increase d glutamate release at 20 min (126 +/- 6%) and at 40 min (150 +/- 18%) . These data indicate that vagal glutamatergic system in the nucleus t ractus solitarius is activated by intraperitoneal injections of immuno active compounds. (C) 1998 IBRO. Published by Elsevier Science Ltd.