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Nonselective cation channels promote persistent spiking in many neurons from a diversity of animals. In the hermaphroditic marine-snail, Aplysia californica , synaptic input to the neuroendocrine bag cell neurons triggers various cation channels, causing an ∼30 min afterdischarge of action potentials and the secretion of egg-laying hormone. During the afterdischarge, protein kinase C is also activated, which in turn elevates hydrogen peroxide (H 2 O 2 ), likely by stimulating nicotinamide adenine dinucleotide phosphate oxidase. The present study investigated whether H 2 O 2 regulates cation channels to drive the afterdischarge. In single, cultured bag cell neurons, H 2 O 2 elicited a prolonged, concentration- and voltage-dependent inward current, associated with an increase in membrane conductance and a reversal potential of ∼+30 mV. Compared with normal saline, the presence of Ca 2+ -free, Na + -free, or Na + /Ca 2+ -free extracellular saline, lowered the current amplitude and left-shifted the reversal potential, consistent with a nonselective cationic conductance. Preventing H 2 O 2 reduction with the glutathione peroxidase inhibitor, mercaptosuccinate, enhanced the H 2 O 2 -induced current, while boosting glutathione production with its precursor, N -acetylcysteine, or adding the reducing agent, dithiothreitol, lessened the response. Moreover, the current generated by the alkylating agent, N -ethylmaleimide, occluded the effect of H 2 O 2 The H 2 O 2 -induced current was inhibited by tetrodotoxin as well as the cation channel blockers, 9-phenanthrol and clotrimazole. In current-clamp, H 2 O 2 stimulated burst firing, but this was attenuated or prevented altogether by the channel blockers. Finally, H 2 O 2 evoked an afterdischarge from whole bag cell neuron clusters recorded ex vivo by sharp-electrode. H 2 O 2 may regulate a cation channel to influence long-term changes in activity and ultimately reproduction. SIGNIFICANCE STATEMENT Hydrogen peroxide (H 2 O 2 ) is often studied in a pathological context, such as ischemia or inflammation. However, H 2 O 2 also physiologically modulates synaptic transmission and gates certain transient receptor potential channels. That stated, the effect of H 2 O 2 on neuronal excitability remains less well defined. Here, we examine how H 2 O 2 influences Aplysia bag cell neurons, which elicit ovulation by releasing hormones during an afterdischarge. These neuroendocrine cells are uniquely identifiable and amenable to recording as individual cultured neurons or a cluster from the nervous system. In both culture and the cluster, H 2 O 2 evokes prolonged, afterdischarge-like bursting by gating a nonselective voltage-dependent cationic current. Thus, H 2 O 2 , which is generated in response to afterdischarge-associated second messengers, may prompt the firing necessary for hormone secretion and procreation.

Hydrogen Peroxide Gates a Voltage-Dependent Cation Current inAplysiaNeuroendocrine Cells