Rektor I, Silva-Barrat C, Barthuel P, Ménini C
Laboratoire de Physiologie Nerveuse, C.N.R.S., Gif-sur-Yvette, France.
Electroencephalogr Clin Neurophysiol. 1991 Aug;79(2):148-52. doi: 10.1016/0013-4694(91)90053-7.
In Papio papio baboons benzodiazepines can facilitate the appearance of a naturally occurring non-epileptic myoclonus, suggesting a possible role of GABAergic transmission in their physiopathology. Nevertheless, as this myoclonus is blocked by physostigmine, the effect of benzodiazepines is probably due to their indirect action on the cholinergic system. Therefore, in this study, we report the effects on the non-epileptic myoclonus of drugs influencing GABAergic transmission. Systemic injections of progabide (GABA precursor), baclofen (GABAB receptor agonist) and allylglycine (glutamic acid decarboxylase inhibitor) did not modify or induce the non-epileptic myoclonus. In the same way, localized chronic injections of GABA into various cerebral structures (prefrontal and motor cortical areas, reticular magnocellular nucleus and substantia nigra) had no effect. When the two types of myoclonus were present in the same photosensitive animal, the epileptic myoclonus induced by photic stimulation was blocked by benzodiazepines but was not influenced by physostigmine, thus differing from the non-epileptic myoclonus. This suggests that different neurochemical mechanisms are involved in the two types of myoclonus, the non-epileptic myoclonus not being directly influenced by the GABAergic transmission.
