On the nature of histamine‐mediated slow hyperpolarizing synaptic potentials in identified molluscan neurones

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Abstract
Standard intracellular stimulating and recording techniques were used to test the correspondence between monosynaptic post-synaptic potentials (p.s.p.s) evoked by histamine-containing C-2 neurons and responses to focally applied histamine recorded from 2 classes of identified post-synaptic neurons in the cerebral ganglion of Aplysia californica. Two types of p.s.p.s were examined: a monophasic low hyperpolarizing potential (Isp.s.p.) lasting 1-2 s, and biphasic p.s.p. consisting of a fast depolarizing component < 0.5 in duration (Efp.s.p.) plus a slow hyperpolarizing potential (Isp.s.p.) desginated the EfIsp.s.p. Ionophoretic or pressure applied histamine mimicked both p.s.p.s. and produced conductance increases in the post-synaptic neurons similar to those associated with the evoked p.s.p.s. The reversal potentials (Erev) for the Isp.s.p. and EfIsp.s.p., estimated by extrapolation, were -85 .+-. 5.3, -35 .+-. 5.5, and -83 .+-. 8.1 mV (mean .+-. SD), respectively. The Isp.s.p.s were produced by an increase in potassium conductance because their Erevs were shifted .apprx. 16 mV by doubling or halving the concentration of extracellular potassium and they could be eliminated by cooling or by intracellular injection of TEA ions. The average Erev values for the slow hyperpolarizing histamine responses were similar to those for the Isp.s.p.s; .apprx. -83 and -86 mV in neurons receiving the monophasic Isp.s.p.s and biphasic EfIsp.s.p., respectively. Cimetidine, an antihistamine drug that selectively blocks histamine receptors associated with potassium conductances in Aplysia, reversibly abolished the Isp.s.p.s and slow hyperpolarizing responses to focally applied histamine. In similar concentrations, cimetidine had no discernible effects on the Efp.s.p. and depolarizing response to histamine or on several different types of p.s.p.s mediated by the C-2 neurons. It is proposed that the Isp.s.p.s are mediated by histamine released from the C-2 neurons.