A presynaptic component of the action of iontophoretically applied flurazepam on feline cortical neurones.
The effect of iontophoretically applied flurazepam on the spike activity of pericruciate cortical neurones of the cat was studied. Flurazepam increased cortical inhibition produced either by local electrical stimulation (which is known to release gamma-aminobutyric acid (GABA) or by iontophoretically applied GABA. Following intravenous treatment with thiosemicarbazide (a GABA-synthesis inhibitor), flurazepam still augmented the action of GABA but was much less effective on electrically evoked cortical inhibition. These findings suggest that part of the action of flurazepam on inhibitory cortical transmission might be at the presynaptic level.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D014151:Anti-Anxiety Agents / Q000494:pharmacology*; D002415:Cats; D002540:Cerebral Cortex / Q000187:drug effects*; D004569:Electroencephalography; D005479:Flurazepam / Q000008:administration & dosage / Q000494:pharmacology*; D005971:Glutamates / Q000494:pharmacology; D007478:Iontophoresis; D009474:Neurons / Q000187:drug effects*; D012663:Semicarbazides / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D014151:Anti-Anxiety Agents; D005971:Glutamates; D012663:Semicarbazides; D005680:gamma-Aminobutyric Acid; D005479:Flurazepam