Research articleOptoactivation of parvalbumin neurons in the spinal dorsal horn evokes GABA release that is regulated by presynaptic GABAB receptors

•PV interneurons in the spinal dorsal horn can be optogenetically labeled and activated.•Selective activation of PV neurons induces GABA release.•Activation of GABAB receptors on PV neuron terminals depresses GABA release.•Baclofen activity on GABA release is mainly mediated by P/Q type Ca2+ channels.

Among heterogeneous neural cells in the spinal dorsal horn, parvalbumin (PV)-positive neurons are one subtype of GABA (γ-aminobutyric acid)-containing interneurons. Using an optogenetic approach, we expressed blue light-sensitive cation channel channelrhodopsin-2 (ChR2) via a viral vector on PV neurons in the spinal dorsal horn. Combined with in vitro whole-cell recordings, we activated ChR2 expressed on PV neurons by blue light and recorded GABAA receptor-mediated light-evoked inhibitory postsynaptic currents (L-IPSCs). The L-IPSCs were action potential-dependent and abolished by the GABAA receptor antagonist picrotoxin, indicating a synchronic GABA release from presynaptic terminals. Activation of GABAB receptors (the metabotropic receptors of GABA) on presynaptic terminals by a putative agonist, baclofen, depressed the amplitude of L-IPSCs. This depression was largely occluded by pretreatment with the highly selective Cav2.1 (P/Q-type) Ca2+ channel blocker ω-agatoxin IVA. N-type Ca2+ channel blocker ω-conotoxin GVIA showed less effects on either L-IPSCs or baclofen depression. We conclude that optoactivation of PV-ChR2 neurons in the spinal dorsal horn induces GABA release from presynaptic terminals, which is modulated by presynaptic GABAB receptors that are coupled to P/Q-type Ca2+ channels. Importantly, our studies provide a simple and reliable optogenetic approach to study dorsal horn neural circuits.