Galanin inhibits gastrin release from isolated rat gastric G-cells

Enzymatically isolated rat gastric mucosal cells (0.25% G-cells) were separated by counterflow elutriation, yielding a fraction in which the G-cell content was relatively enriched to 1.4%. In this fraction, basal gastrin release (mean ± SE) was 31.1 ± 1.3 pg · 10⁶ cells^-1 · 60 min^-1 and was stimulated by 10^-8 M neuromedin C (222.3 ± 18.1% of basal), 10^-4 M carbachol (227.5 ± 25.9%), 10^-6 M 12-O-tetradecanoylphorbol-13-acetate (TPA) (196.3 ± 14.7%), and 10^-3 M dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP) (193.9 ± 6.8%), respectively. The neuropeptide galanin was tested at 10^-10 to 10^-7 M. Galanin had no effect on basal gastrin release but reduced the responses to neuromedin C, carbachol, TPA, and DBcAMP. IC₅₀ ranged between 1 x 10^-10 and 8.6 x 10^-10 M galanin. Although in the relatively enriched G-cell fraction D-cells were not detectable by immunocytochemistry, a low rate of somatostatin release was still measured by radioimmunoassay (5.3 ± 0.5 pg · 10⁶ cells^-1 · 60 min^-1). However, galanin failed to increase this rate under basal conditions or in response to any of the stimulants tested. These results favor the assumption that galanin might exert a direct inhibitory effect on rat gastric G-cells. Galanin seems to interfere at an intracellular mechanism(s), which is induced by neuromedin C and carbachol and which is commonly activated by protein kinase C- and cAMP-mediated stimulation.