δ-Guanidinovaleric acid as an endogenous and specific GABA-receptor antagonist: electroencephalographic study
1987; Elsevier BV; Volume: 1; Issue: 2 Linguagem: Inglês
10.1016/0920-1211(87)90016-7
ISSN1872-6844
AutoresIsao Yokoi, Keishi Tsuruta, Hiroshi Shigara, Akitane Mori,
Tópico(s)Ion channel regulation and function
ResumoSporadic spike discharges recorded on EEGs from epidural electrodes appeared 5-10 min after topical application of 0.3 nmol delta-guanidinovaleric acid (DGVA) on the pia mater of the sensorimotor cortex, on the same side as the application. Spike discharges induced by DGVA were completely suppressed within 10 min of supplementary application of GABA (50 nmol), (3R)-(-)-4-amino-3-hydroxybutanoic acid (L-GABOB) (5 nmols) or muscimol (5 nmols) on the pia mater, but the discharges were not affected by supplementing with 500 nmol of alpha-amino-DGVA, i.e., arginine (Arg). Whereas spike discharges were not induced by DGVA together with L-GABOB or muscimol, DGVA applied together with Arg induced spike discharges. Neither phenobarbital (PB) (20 mg/kg, i.m.), diazepam (DZ) (10 mg/kg, i.p.), sodium valproate (200 mg/kg, i.p.) nor diphenylhydantoin (20 mg/kg, i.p.) showed any suppressive effects on spike discharges induced by DGVA. DGVA induced spike discharges 20 min after pre-injection of PB or DZ. These electroencephalographic findings suggest that DGVA, which has one more carbon in its chain than N-amidino-GABA, might act directly on the GABA-receptor to induce spike discharges and might be a specific GABA-receptor antagonist.
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