AJP - Gastrointestinal and Liver Physiology, Vol 249, Issue 2 192-G196, Copyright © 1985 by American Physiological Society
Uptake and release of gamma-aminobutyric acid in guinea pig gallbladder
N. Saito, K. Taniyama and C. Tanaka
The presence of gamma-aminobutyric acid (GABA)-ergic neuron in guinea pig
gallbladder was investigated by measuring GABA contents and glutamate
decarboxylase (GAD) activity and by demonstrating the uptake and release of
[3H]GABA. GABA and GAD are both present in the gallbladder, and a positive
correlation in regional distribution was observed among GABA, GAD, and the
number of ganglion cells. The uptake of [3H]GABA by the gallbladder showed
two saturable components; a high-affinity component (Km = 23.3 microM, Vmax
= 7.63 nmol X g-1 X 10 min-1) and a low-affinity component (Km = 515
microM, Vmax = 57.1 nmol X g-1 X 10 min-1). These high-affinity and
low-affinity transport systems corresponded to those obtained in the
presence of beta-alanine and L-2,4-diaminobutyric acid, respectively,
thereby suggesting the presence of neuronal and nonneuronal GABA transport
systems in this tissue. Electrical transmural stimulation produced an
increase in [3H]-GABA release from the isolated gallbladder preloaded with
[3H]GABA, in the presence of beta-alanine. The stimulation-evoked release
of [3H]GABA was prevented by calcium-free medium containing 1 mM EGTA and
tetrodotoxin, thereby indicating that the released GABA originates from the
nerve terminals. These results provide evidence for the presence of
GABA-ergic neurons in the guinea pig gallbladder.
