A new function for glycine GlyT2 transporters: Stimulation of γ-aminobutyric acid release from cerebellar nerve terminals through GAT1 transporter reversal and Ca2+-dependent anion channels

2013 ◽  
Vol 92 (3) ◽  
pp. 398-408 ◽  
Author(s):  
Marco Milanese ◽  
Cristina Romei ◽  
Cesare Usai ◽  
Martina Oliveri ◽  
Luca Raiteri
Keyword(s):  
Aminobutyric Acid ◽  
Nerve Terminals ◽  
Anion Channels ◽  
Acid Release ◽  
Stimulation Of

Baclofen: effects on amino acid release

1978 ◽  
Vol 56 (1) ◽  
pp. 150-154 ◽  
Author(s):  
S. J. Potashner
Keyword(s):  
Amino Acids ◽  
Excitatory Amino Acids ◽  
The Other ◽  
Aminobutyric Acid ◽  
Nerve Terminals ◽  
Amino Butyric Acid ◽  
Acid Release ◽  
Afferent Terminals ◽  
Excitatory Transmitter ◽  
Stimulation Of

This study investigated the effects of the antispastic drug β-(p-chlorophenyl)-γ-amino-butyric acid (Baclofen) on the release of amino acids from slices of guinea pig cerebral cortex. Electrical stimulation of slices evoked the release of endogenous14C-labelled glutamate, aspartate, γ-aminobutyric acid (GABA), alanine, and threonine–serine–glutamine (labelled via metabolism of D-[U-14C]glucose), and of exogenous glutamate, aspartate, GABA, and α-aminoisobutyrate. The releases of endogenous14C-labelled glutamate, aspartate, and GABA were three to seven times larger than those of other amino acids. Baclofen (4 μM) inhibited the evoked release of endogenous 14C-labelled glutamate and aspartate by nearly 60%, that of endogenous14C-labelled threonine–serine–glutamine and alanine by 14–19%, but had no effect on that of endogenous14C-labelled GABA. The drug inhibited the evoked release of the exogenous amino acids by 25–32%. Baclofen doubled the incorporation of 14C from D-[U-14C]glucose into endogenous alanine but was without effect on either the incorporation of 14C into the other endogenous amino acids or the turnover of any of the endogenous14C-labelled amino acids. Because endogenous14C-labelled glutamate, aspartate, and GABA are probably released from nerve terminals, Baclofen selectively suppresses the release of excitatory amino acids from nerve terminals. Similarly, depression of the release of excitatory transmitter (presumably glutamate) from primary afferent terminals in the spinal cord may at least partly explain the antispastic action of Baclofen.

Stimulation of [3H]?-Aminobutyric Acid Release by Calcium Chelators in Synaptosomes

1984 ◽  
Vol 42 (6) ◽  
pp. 1507-1514 ◽  
Author(s):  
Clorinda Arias ◽  
Maria Sitges ◽  
Ricardo Tapia
Keyword(s):  
Aminobutyric Acid ◽  
Acid Release ◽  
Stimulation Of

Alkaline extracellular pH shifts generated by two transmitter-dependent mechanisms

1992 ◽  
Vol 70 (S1) ◽  
pp. S286-S292 ◽  
Author(s):  
M. Chesler ◽  
J. C. T. Chen
Keyword(s):  
Repetitive Stimulation ◽  
Extracellular Ph ◽  
Aminobutyric Acid ◽  
Anion Channels ◽  
Gaba A ◽  
Bicarbonate Ions ◽  
Alkaline Shift ◽  
Independent Process ◽  
Free Media ◽  
Stimulation Of

Recent studies of the effect of γ-aminobutyric acid (GABA) on brain extracellular pH are reviewed. Experiments were performed on isolated turtle cerebellum, using double-barrelled pH-sensitive microelectrodes. Superfusion of GABA (1 mM) caused a rapid extracellular alkaline shift accompanied by a rise in extracellular K+. Washout of GABA was often associated with an acid rebound, concomitant with an undershoot of extracellular K+. The GABA-evoked alkaline shift was blocked by picrotoxin and mimicked by the GABA-A agonists isoguvacine and muscimol. The response persisted in the nominal absence of extracellular calcium, but it was reversibly abolished in nominally bicarbonate free media. In contrast, extracellular alkaline shifts evoked by repetitive stimulation of the parallel fibers were amplified in bicarbonate-free media and were insensitive to picrotoxin. These results indicate the existence of separate, transmitter-dependent mechanisms of extracellular alkalinization: (i) a GABA-A receptor mediated process, most likely associated with efflux of bicarbonate ions across GABA-A anion channels and (ii) a bicarbonate-independent process associated with excitatory synaptic transmission.Key words: GABA, bicarbonate, extracellular pH, alkaline shift.

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