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Foetal rat pancreatic rudiments, explanted on day 14 of gestation and grown for 7 days in organ culture, were highly sensitive to the stimulatory effect of glucose on insulin secretion. The autonomic innervation of the cultivated explant was investigated as a possible explanation of this phenomenon. No sign of sympathetic innervation was detected in the pancreas explanted on day 14; the uptake of alpha-methyl-noradrenaline was not detectable by fluorescence microscopy, the concentration of noradrenaline/pancreatic rudiment was less than 7 pg and no nerve-endings containing granular vesicles were visible by electron microscopy. It was concluded that sympathetic innervation of the pancreas occurs after day 14 of gestation. Sympathetic receptors developed independently of innervation since phentolamine, and, to a lesser extent, phenoxybenzamine, potentiated the glucose-induced insulin release from cultured explants. The beta-agonists isoproterenol or salbutamol were inactive alone, but in combination with phentolamine, they potentiated the effect of glucose. Alpha-antagonists reversed the inhibitory effect of adrenaline in a dose-dependent manner. Intrapancreatic neurones were demonstrated microscopically as cholinesterase-positive cells; parasympathetic receptors were shown to be present after potentiation of glucose-stimulated insulin release by carbamylcholine and its reversal by atropine. The preservation of parasympathetic innervation and the absence of sympathetic innervation in the cultured pancreatic rudiment may explain in part the high sensitivity of the tissue to the stimulatory effect of glucose on the release of insulin.