Biochemical and physiological evidence that histamine is the transmitter of barnacle photoreceptors

Abstract

AbstractWe tested the hypothesis that histamine is the transmitter released by barnacle photoreceptors. Median and lateral ocelli were incubated with3H-histidine and found to synthesize3H-histamine, identified by high-voltage electrophoresis. Synthesis could be blocked by the histidine decarboxylase inhibitor (S)-α-fluoromethylhistidine. Histamine was applied to 1-cells either by superfusion or by pressure ejection from a pipette (100 µM or 1 mM histamine) positioned close to the I-cell's soma. When bath-applied at concentrations ranging from 5–100 µM, histamine hyperpolarized the I-cell in a dose-dependent fashion and increased its conductance. At 100 µM, histamine abolished the I-cell's response to light. The response to a pulse of pressure-applied histamine was a hyperpolarization whose amplitude was graded with dose (determined by the duration of the pulse). This response persisted in concentrations of Co2+and Cd2+that blocked synaptic transmission from the photoreceptors. Cimetidine, an antagonist of mammalian H2 receptors, markedly decreased the cell's responses both to HA and to light at 100 µM and blocked both responses at 1 mM. Pyrilamine and triprolidine, H1 antagonists, had a complex effect on the I-cell's responses to histamine and to light. Neither H1 nor H2 antagonists, nor histamine itself, affected the voltage or light responses recorded in the presynaptic terminal region, or any phase of calcium-dependent action potentials induced in the terminal in the presence of tetraethylammonium ion. Thus, biochemical, immunocytochemical, and physiological evidence suggests that HA is the transmitter from these photoreceptors to the I-cells. Although gammaaminobutyric acid (GABA) is also present in the photoreceptors, it did not affect the I-cell's responses to light or to histamine when bath-applied at 100 µM. Thus, GABA does not appear to modulate transmission from the photoreceptor to the I-cell.