Pretreatment with 100 microM GABA of synaptosomes purified from rat brain results in an increased uptake of the labelled neurotransmitter in subsequent incubations. The effect is blocked by a GABA(B) receptor antagonist, 2-hydroxy-saclofen. The effect is mimicked by baclofen and the baclofen effect is blocked by saclofen too. Lower GABA concentrations (up to 50 microM) do not result in an increase of subsequent GABA uptake. Treatment of synaptosomes with 8-Br-cAMP results in a decreased GABA uptake. Since the uptake incubations were run with saturating concentrations of labelled GABA, the data indicates that GABA(B) receptor activation in brain synaptosomes up-regulates their GABA uptake capacity by an increase in Vmax. This mechanism appears of physiological relevance under conditions of sustained GABA release and substantial increase of its extracellular concentration.
Pretreatment of rat brain synaptosomes with GABA increases subsequent GABA uptake via GABA(B) receptor activation.
2001
Abstract
Pretreatment with 100 microM GABA of synaptosomes purified from rat brain results in an increased uptake of the labelled neurotransmitter in subsequent incubations. The effect is blocked by a GABA(B) receptor antagonist, 2-hydroxy-saclofen. The effect is mimicked by baclofen and the baclofen effect is blocked by saclofen too. Lower GABA concentrations (up to 50 microM) do not result in an increase of subsequent GABA uptake. Treatment of synaptosomes with 8-Br-cAMP results in a decreased GABA uptake. Since the uptake incubations were run with saturating concentrations of labelled GABA, the data indicates that GABA(B) receptor activation in brain synaptosomes up-regulates their GABA uptake capacity by an increase in Vmax. This mechanism appears of physiological relevance under conditions of sustained GABA release and substantial increase of its extracellular concentration.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
