Agonist and inverse agonist effects of CL 218872 on benzodiazepine receptors.
Extracellular action potentials were recorded from cerebellar Purkinje cells in urethane-anaesthetised rats. Synaptic inhibition was evoked by electrical stimulation of the nearby cortical surface and recorded using peristimulus-time histograms. A benzodiazepine agonist, RU 32007, decreased cell firing rate and increased the inhibitory response duration in parallel. beta-Carboline ethyl ester increased firing and decreased the inhibitory response. In some cases the inhibitory response was abolished, independent of the change in firing. CL 218872 decreased firing with the parallel increase in inhibitory response. However, in some cases the inhibitory response was abolished despite decreases in firing. All the effects of all three agents were blocked by Ro 15-1788.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001569:Benzodiazepines / Q000494:pharmacology; D002243:Carbolines / Q000494:pharmacology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects; D011689:Purkinje Cells / Q000187:drug effects; D011724:Pyridazines / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011963:Receptors, GABA-A / Q000187:drug effects*
D002243:Carbolines; D011724:Pyridazines; D011963:Receptors, GABA-A; D001569:Benzodiazepines; C021604:CL 218872; C024915:beta-carboline-3-carboxylic acid ethyl ester; C043990:RU 32007