Uptake and release of gamma-aminobutyric acid in guinea pig gallbladder.
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.
Saito
N
N
Taniyama
K
K
Tanaka
C
C
D000818:Animals; D004558:Electric Stimulation; D005260:Female; D005704:Gallbladder / Q000201:enzymology / Q000294:innervation / Q000378:metabolism*; D005724:Ganglia / Q000166:cytology; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000378:metabolism* / Q000502:physiology
D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase