BACKGROUND/AIMS: The inhibitory neurotransmitter gamma-aminobutyrate (GABA) has been shown to coexist with insulin in pancreatic beta-cells. We have presently investigated whether GABA also colocalizes with gastrin in G cells in rat antral mucosa. METHODS: Three alternative approaches were used: (1) gastrin in situ hybridization and GABA immunocytochemistry on consecutive cryostat sections; (2) GABA immunocytochemistry and gastrin immunocytochemistry on adjacent semithin and ultrathin sections; and (3) double-immunogold labeling of GABA and gastrin in the same ultrathin section. RESULTS: Colocalization of GABA and gastrin was observed with each of the three approaches. In the double-immunogold labeled cells, the G-cell granules displayed a high gold-particle density indicating gastrin and a low particle density indicating GABA, whereas the converse was true for the extragranular cytoplasmic matrix. The gold-particle ratios between these compartments were 11 (for gastrin) and 0.36 (for GABA), respectively. GABA labeling was also observed in two other antral endocrine cell types, classified by morphological criteria as somatostatin producing D cells and serotonin producing ECn cells. CONCLUSIONS: This is the first direct demonstration of GABA in gastrointestinal G cells. Our findings suggest that GABA may have a paracrine function in the stomach mucosa, analogous to its presumed role in the pancreatic islets.
BACKGROUND/AIMS: The inhibitory neurotransmitter gamma-aminobutyrate (GABA) has been shown to coexist with insulin in pancreatic beta-cells. We have presently investigated whether GABA also colocalizes with gastrin in G cells in rat antral mucosa. METHODS: Three alternative approaches were used: (1) gastrin in situ hybridization and GABA immunocytochemistry on consecutive cryostat sections; (2) GABA immunocytochemistry and gastrin immunocytochemistry on adjacent semithin and ultrathin sections; and (3) double-immunogold labeling of GABA and gastrin in the same ultrathin section. RESULTS: Colocalization of GABA and gastrin was observed with each of the three approaches. In the double-immunogold labeled cells, the G-cell granules displayed a high gold-particle density indicating gastrin and a low particle density indicating GABA, whereas the converse was true for the extragranular cytoplasmic matrix. The gold-particle ratios between these compartments were 11 (for gastrin) and 0.36 (for GABA), respectively. GABA labeling was also observed in two other antral endocrine cell types, classified by morphological criteria as somatostatin producing D cells and serotonin producing ECn cells. CONCLUSIONS: This is the first direct demonstration of GABA in gastrointestinal G cells. Our findings suggest that GABA may have a paracrine function in the stomach mucosa, analogous to its presumed role in the pancreatic islets.