Electrocortical desynchronization after microinfusion of kainic acid into the locus coeruleus in rats.

Receptors for the endogenous excitatory amino acid, 1-glutamate, occur in the rat locus coeruleus (LC), an area of the brain involved in the control of sleep/arousal mechanisms and other behavioral functions. However, the functional role of this neurotransmitter system in the LC has yet to be clarified. Therefore, to address this question we have studied the gross behavioral changes and the effects on the electrocortical (ECoG) spectrum power in rats receiving focal injections into the LC of kainic acid, an agonist at the non-N-methyl-D-aspartate (non-NMDA) glutamate receptor subtype. Unilateral injection of kainic acid (25, 50, 100 and 200 pmol) into the rat LC produced contralateral turning, circling and stereotypes; these effects were accompanied by dose-dependent ECoG desynchronization and by a significant decrease in total voltage power and in 6-9, 9-12 and 12-16 Hz bands of the ECoG spectrum. A pretreatment (15 min before) with 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) (50 and 100 pmol), a competitive non-NMDA receptor antagonist, or with dizocilpine meleate (MK-801) (1 pmol) and 3-(2-carboxy-piperazine-4-yl)-1-propenyl-1-phosphonic acid) (CP-Pene) (10 pmol), two selective NMDA receptor antagonists, injected directly into the LC, abolished the behavioral and ECoG spectrum power effects typically elicited by kainic acid (50 pmol). Similar results were observed in rats pretreated with diazepam (0.5 mg/kg given i.p. 15 min before kainic acid).(ABSTRACT TRUNCATED AT 250 WORDS)