Electrophysiological studies with a 2,3-benzodiazepine muscle relaxant: GYKI 52466

• Published in: European journal of pharmacology Vol. 167; no. 2; p. 193
• Main Authors: Tarnawa, I, Farkas, S, Berzsenyi, P, Pataki, A, Andrási, F
• Format: Journal Article
• Language: English
• Published: Netherlands 22.08.1989
• Subjects: Animals; Anti-Anxiety Agents - pharmacology; Benzodiazepines - pharmacology; Cats; Electrophysiology; Evoked Potentials - drug effects; Male; Midazolam - pharmacology; Muscle Relaxants, Central - pharmacology; Purkinje Cells - drug effects; Purkinje Cells - metabolism; Receptors, GABA-A - drug effects; Receptors, GABA-A - metabolism; Reflex, Monosynaptic - drug effects; Spinal Cord - drug effects; Spinal Cord - metabolism; Spinal Cord - physiology
• ISSN: 0014-2999
• DOI: 10.1016/0014-2999(89)90579-7

The effects of GYKI 52466, a new 2,3-benzodiazepine with muscle relaxant and anticonvulsant properties, were investigated and compared to those of midazolam in electrophysiological experiments. The effects of the drugs on the reflex potentials evoked by afferent nerve stimulation and recorded from the spinal roots in unanesthetized spinal cats were studied. GYKI 52466 exerted a strong inhibitory effect on the monosynaptic as well as the polysynaptic ventral root reflexes, while the dorsal root responses decreased slightly. In contrast, midazolam markedly enhanced the dorsal root responses, did not modify the monosynaptic reflex and partially inhibited the polysynaptic reflex. The spontaneous firing of cerebellar Purkinje cells was depressed by midazolam, but not by GYKI 52466. These results suggest strongly that, contrary to the classical 1,4-benzodiazepines, potentiation of the GABA-A receptor-mediated inhibition does not play a significant role in the pharmacological actions of GYKI 52466.