GABA B depress TRPV1‐mediated glutamate release

Cranial visceral primary afferents follow the solitary tract (ST) to synapse on 2nd order solitary tract nucleus (NTS) neurons. The Transient Receptor Potential Vanilloid receptor separates afferents into C‐fibers (TRPV1+) and A‐fibers (TRPV1‐). Temperature robustly releases glutamate from a TRPV1‐controlled vesicle pool onto second‐order neurons. This additional, TRPV1‐mediated glutamate release does not occur in TRPV1−. This may provide a new site for modulation by G protein‐coupled receptors (GPCRs). In horizontal hindbrain slices, ST shocks evoked time‐invariant glutamatergic EPSCs with jitters <200 μs at 2nd order neurons. We tested whether baclofen (BAC), a specific GABA B agonist, inhibits action potential‐independent (i.e. TTX, mEPSCs), temperature‐evoked glutamate release. BAC (10 μM) inhibited mEPSCs and prevented the temperature‐induced increase (25–27°) in frequency. Our findings indicate that the ion channel TRPV1 may be a new modulation site for GPCRs like GABA B . These GPCR effects might also include additional downstream targets directly on the TRPV1 vesicle release machinery.