Formation of GABA from putrescine in the brain of fish (Salmo irideus Gibb.).

Abstract

Abstract— It was demonstrated after intraperitoneal and intracerebral injections of [1,4‐14C]‐putrescine.2 HCl that GABA is formed in vivo in the trout brain via a pathway in which glutamic acid is not an intermediate. Intraperitoneal and intracerebral injections of both thiosemicarbazide and 3‐mercaptopropionic acid had no measurable effects on GABA concentration, transformation of glutamic acid into GABA in vivo, or on glutamate de‐carboxylase activity in the brain within the first 3 h after the application of the inhibitors. Only a small decrease in concentration of pyridoxal phosphate was noticed in the fish brain after thiosemicarbazide administration. The relatively high concentrations of pyridoxal phosphate in the trout brain may be one of the reasons for the ineffectiveness of thiosemicarbazide in inhibiting glutamate decarboxylase in vivo. After intracerebral injections of [1‐14C]GABA, a half‐life of 7 h was determined for GABA. The slow turnover rate of GABA in trout brain, which can be assumed from this observation, may give a further explanation of the ineffectiveness of the glutamate decarboxylase inhibitors in lowering the GABA content ot fish brain within a few hours.