Electrophysiological effects of FLFQPQRF amide, an endogenous brain morphine modulating peptide, on cultured mouse spinal-cord neurons

Intracellular recordings were made from dissociated fetal mouse spinal cord neurones in primary culture. Micropressure application of FLFQPQRFamide (10(-5) M in the delivery pipette), an endogenous mammalian brain morphine modulating peptide, onto the surface of spinal cord neurones induced, in a dose dependent manner, a transitory hyperpolarization followed by a long lasting depolarization of the membrane potential (n = 37). In contrast, no response was observed when the peptide was applied on dorsal root ganglia neurones (n = 30). The depolarizing phase of this response was underlied by an increase of the input resistance. Extrapolated reversal potential for the depolarizing phase was close to -80 mV while it was close to -40 mV for the hyperpolarizing phase. Increasing extracellular K+ concentration raised the reversal potential value of depolarizing phases to more positive values. The amplitude of the depolarizing phase was reduced by application of tetraethylammonium (50 mM) while it was enhanced by application of 4-aminopyridine (3 mM). CaCl2 application (3 mM) reversibly blocked the hyperpolarization and decreased the subsequent depolarization. In presence of Ba2+ the extrapollated reversal potential of the hyperpolarizing phase was dramatically shifted to a more positive value. Finally FLFQPQRFamide induced response can be partially mimicked by FMRFamide application. Our observations indicate that FLFQPQRFamide can have multiple effects on membrane conductance of mammalian spinal cord neurones by acting on a single class of receptor. These effects of FLFQPQRFamide were found to be mainly excitatory.