Hypersynchronisation and sedation produced by GABA-transaminase inhibitors and picrotoxin: does GABA participate in sleep control?
Systemic administration of GABA-transaminase inhibitors, gamma-acetylenic GABA (100 mg/kg) or gamma-vanylic GABA (1200 mg/kg) produces behavioral picture of somnolence accompanied by EEG hypersynchronisation reminiscent of electrographic signs of petit mal epilepsy. Similarly, systemic administration of GABA antagonist, Picrotoxin (3--4 mg/kg) produces a short lasting period of sedation preceding the development of myoclonic jerks which is also accompanied by Wave-spike discharges. The role of GABA in sleep control is discussed. Although the area is not ready for firm conclusions, the results suggest that hyperactivity of GABA-ergic system as well as its hypoactivity could mediate pathological somnolence associated with different forms of epilepsy.
D000612:4-Aminobutyrate Transaminase / Q000037:antagonists & inhibitors*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D002540:Cerebral Cortex / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004569:Electroencephalography; D008297:Male; D010852:Picrotoxin / Q000494:pharmacology*; D051381:Rats; D012640:Seizures / Q000139:chemically induced; D012894:Sleep Stages / Q000187:drug effects* / Q000502:physiology; D000637:Transaminases / Q000037:antagonists & inhibitors*; D005680:gamma-Aminobutyric Acid / Q000031:analogs & derivatives / Q000494:pharmacology / Q000502:physiology*
D000612:4-Aminobutyrate Transaminase; D010852:Picrotoxin; D000637:Transaminases; D005680:gamma-Aminobutyric Acid