PT  - JOURNAL ARTICLE
AU  - L G Miller
AU  - W R Galpern
AU  - K Dunlap
AU  - C A Dinarello
AU  - T J Turner
TI  - Interleukin-1 augments gamma-aminobutyric acidA receptor function in brain.
DP  - 1991 Feb 01
TA  - Molecular Pharmacology
PG  - 105--108
VI  - 39
IP  - 2
4099  - http://molpharm.aspetjournals.org/content/39/2/105.short
4100  - http://molpharm.aspetjournals.org/content/39/2/105.full
SO  - Mol Pharmacol1991 Feb 01; 39
AB  - Interleukin-1 (IL-1), a cytokine involved in the acute phase reaction to injury and infection, has multiple effects in the central nervous system, including induction of fever and sleep and the release of several neuropeptides. We evaluated effects of IL-1 beta on inhibitory postsynaptic function at the gamma-aminobutyric acidA (GABAA) receptor. IL-1 (100 pg/ml to 10 ng/ml) augmented GABAA receptor function in cortical synaptic preparations. This effect of IL-1 was largely prevented by incubation with a specific IL-1 receptor antagonist. The related cytokines interleukin-6 and tumor necrosis factor did not augment GABA-dependent chloride transport. Similar enhancement of GABAA receptor function was observed in tissue prepared from mice previously injected intraperitoneally with IL-1 (1 microgram). Electrophysiological studies in cultured primary cortical neurons demonstrated that IL-1 enhanced the GABA-mediated increase in chloride permeability, whereas IL-1 alone produced no alterations in resting conductance. Behavioral studies indicated that IL-1 is similarly active in vivo; mice treated with IL-1 showed a decrease in open-field activity and an increase in the threshold for pentylenetetrazol-induced seizures. The interaction of IL-1 with GABAA receptors might account for the somnogenic and motor-depressant effects of this cytokine.