Neonatal capsaicin treatment permanently eliminates most rat C-type baroreceptors but baroreflex function is preserved

Applied acutely, capsaicin (CAP) potently excites and then depresses the function of sensory neurons with slowly conducting axons. In previous studies, we found that arterial baroreceptor C-type axons are sensitive as well. Early in postnatal development, application of CAP destroys sensitive sensory neurons. Here we tested the effects of neonatal CAP treatment on the aortic depressor nerve (ADN) which in the rat contains large numbers of C-fiber baroreceptors. Low magnification electron micrographs of ADN from adult rats treated with subcutaneous CAP (50 mg/kg) within 24 hrs of birth (nCAP) showed remarkable losses of unmyelinated axon profiles compared to normal (about an 85% loss, n=5). Counts of myelinated axons in ADN were not changed by neonatal CAP. Previously, we found that reflex blood pressure and heart rate responses to low frequency, high intensity activation of ADN electrical stimulation depend on C-fibers. In adult nCAP rats, we have found similar frequency response relations for blood pressure and heart rate for electrical activation of ADN in normal (n=11) and nCAP (n=13) rats. Since the 1-5 Hz range normally requires C-fiber baroreceptor activation, the results present a paradoxical anatomic loss of C-type aortic baroreceptors with no apparent functional baroreflex deficit.