Effect of depressant drugs on ECoG and on glutamate and ACh-excited cortical neurones in rats

Abstract

At moderate levels of urethane anaesthesia, spontaneously active neurones in the rat cerebral cortex fired in bursts. The bursts coincided with spontaneous surface-positive waves in the electrocorticogram (ECoG) and the number of action potentials per burst was proportional to ECoG wave area. Initially, both iontophoretically applied glutamate or acetylcholine enhanced burst firing in spontaneously active neurones, or induced bursts of firing coincident with the ECoG waves in quiescent neurones. At deeper levels of urethane anaesthesia when the ECoG wave frequency was low, larger applications of both excitants induced firing between bursts. Administered systemically, a major effect of urethane. barbiturates, benzodiazepines and halothane was to reduce endogenous excitatory drives in the cortex and hence the response to iontophoretically applied excitants. Thus, they reduced the ECoG wave frequency and the associated burst firing, whether spontaneous or induced. Thiopentone and diazepam, but not urethane and halothane, also reduced the area of the ECoG wave and the number of action potentials per burst. Under appropriate conditions, central depressants also had an apparent muscarinic anticholinergic action, as manifested by reduction or abolition of acetylcholine, but not glutamate-induced, interburst firing and facilitated burst firing.