Selective agonists and antagonists were employed to determine the role of indoleaminergic amacrine cells in the generation of the light-evoked responses and spontaneous activity of direction and orientation selective cells. Perfusion with 5-HT2 antagonists reduced the spontaneous activity and both the leading and trailing edge responses of ON/OFF direction selective cells. 5-HT1a agonists had a similar effect on this class of cell, namely, a reduction of light-evoked and spontaneous activity. Results from ON-center and OFF-center orientation selective cells were consistent with those obtained from direction selective cells in that no disruption of direction or orientation selectivity was observed during perfusion of these drugs. These data suggest that the indoleaminergic cells are not directly involved in the generation of the trigger features of complex ganglion cells, but may be facilitating synaptic transmission in the inner retina. This function is discussed relative to the connectivity of the rod bipolar cells and the putative indoleaminergic amacrine cells. The similarity of the effects of 5-HT1a agonists and 5-HT2 antagonists supports the hypothesis, developed during our prior studies of brisk ganglion cells, that these two receptor classes mediate antagonistic processes in the target neurons.

Background and objective: Diabetes mellitus associated with hypertension often causes perioperative complications. The α1-adrenoceptor antagonist/5-hydroxytryptamine-1A receptor agonist urapidil is an approved drug used in hypertension and hypertensive emergencies. 5-Hydroxytryptamine-1A (5-HT1A) receptor agonists impair glucose metabolism. To evaluate a possible dose-dependent hyperglycaemic effect of urapidil due to its 5-HT1A receptor agonistic properties, the effect of three doses of urapidil on hyperglycaemia in the streptozotocin diabetic rat was investigated.

Methods: Male Wistar-Kyoto rats were made diabetic by streptozotocin and randomly allocated to the following daily treatments for 7 days (n = 6 each): urapidil 6 mg kg−1, urapidil 20 mg kg−1, urapidil 60 mg kg−1, insulin 4 IU kg−1 subcutaneously. One diabetic group and one non-diabetic healthy group served as controls.

Results: Treatment for 7 days with urapidil 20 mg kg−1 and urapidil 60 mg kg−01 reduced mean glucose concentrations significantly (urapidil-20: 15.6 ± 1.1 mmol L−1P = 0.023; urapidil-60: 15.8 ± 0.8 mmol L−1, P = 0.04) compared with diabetic controls (20.9 ± 0.8 mmol L−1), whereas those after urapidil 6 mg kg−1 were similar to diabetic controls. Insulin treatment normalized blood glucose concentrations.

Conclusions: The α1-adrenoceptor antagonist/5-HT1A receptor agonist urapidil has no hyperglycaemic effect on experimental diabetes mellitus, even in high doses, despite its 5-HT1A receptor agonistic properties.