We studied the effect of infrared (IR) stimulation on rat sensory neurons. Primary sensory neurons were prepared by
enzymatic dissociation of the inferior (or "nodose") ganglia from the vagus nerves of rats. The 1.85-μm output of a
diode laser, delivered through a 200-μm silica fiber, was used for photostimulation. Nodose neurons express the
vanilloid receptor, TRPV1, which is a non-selective cation channel that opens in response to significant temperature
jumps above 37 C. Opening TRPV1 channels allows entry of cations, including calcium (Ca2+), into the cell to cause
membrane depolarization. Therefore, to monitor TRPV1 activation consequent to photostimulation, we used fura-2, a
fluorescent Ca2+ indicator, to monitor the rise in intracellular Ca2+ concentration ([Ca2+]i). Brief trains of 2-msec IR pulses activated TRPV1 rapidly and reversibly, as evidenced by transient rises in [Ca2+]i (referred to as Ca2+ transients). Consistent with the Ca2+ transients arising from influx of Ca2+, identical photostimulation failed to evoke Ca2+ responses in the absence of extracellular Ca2+. Furthermore, the photo-induced Ca2+ signals were abolished by capsazepine, a specific blocker of TRPV1, indicating that the responses were indeed mediated by TRPV1. We discuss the feasibility of using focal IR stimulation to probe neuronal circuit properties in intact neural tissue, and compare IR stimulation with another photostimulation technique-focal photolytic release of "caged" molecules.