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Neuronal calcium (Ca2+) signaling represents a molecular trigger for diversecentral nervous system adaptations and maladaptions. The altered function ofdorsal spinal inhibitory interneurons is strongly implicated in the mechanismsunderlying central sensitization in chronic pain. Surprisingly little is known,however, about the characteristics and consequences of Ca2+ signaling in thesecells, including whether and how they are changed following a peripheral insultor injury and how such alterations might influence maladaptive pain plasticity.As a first step towards clarifying the precise role of Ca2+ signaling in dorsalspinal inhibitory neurons for central sensitization, we established methods forcharacterizing Ca2+ signals in genetically defined populations of these cells.In particular, we employed recombinant adeno-associated viral vectors todeliver subcellularly targeted, genetically encoded Ca2+ indicators intoparvalbumin-positive spinal inhibitory neurons. Using wide-field microscopy, weobserved both spontaneous and afferent fiber activity triggered Ca2+ signals inthese cells. We propose that these methods may be adapted in future studies forthe precise characterization and manipulation of Ca2+ signaling in diversespinal inhibitory neuron subtypes, thereby enabling the clarification of itsrole in the mechanisms underlying pain chronicity and opening the door forpossibly novel treatment directions.

Afferent Fiber Activity-Induced Cytoplasmic Calcium Signaling in Parvalbumin-Positive Inhibitory Interneurons of the Spinal Cord Dorsal Horn