Receptor changes in brain tissue of rats treated as neonates with capsaicin

Capsaicin, the hot chemical in chillies, administered to neonatal rats, causes destruction of polymodal nociceptive primary afferent neurons by acting on TRPV1 receptors causing intrinsic somatosensory deprivation. Although the effects of neonatal capsaicin treatment in the periphery have been extensively investigated, less is known about the brain networks to which the capsaicin sensory neurons are relayed. In the present study the effect of neonatal capsaicin treatment on brain receptors that have been shown to interact with TRPV1 was examined. Wistar rats were treated on neonatal day 2 with capsaicin and at 15–16 weeks of age, brains were processed to measure levels of muscarinic M1/M2 and M2/M4, serotonin 5HT2A, cannabinoid CB1, dopamine D1, D2 receptors and dopamine transporter. Overall increases in levels of muscarinic M1/M4 (F = 8.219, df = 1, p = 0.005), muscarinic M2/M4 (F = 99.759, df = 1, p < 0.0001), serotonin 5HT2A (F = 28.892, df = 1, p < 0.0001), dopamine D1 (F = 8.726, df = 1, p = 0.008) and cannabinoid CB1 (F = 25.084, df = 1, p < 0.0001) receptors were found in the brains of capsaicin-treated rats, although significant regional changes occurred only in muscarinic M2/M4 and serotonin 5HT2A receptors. The results of the present study suggest that neonatal intrinsic somatosensory deprivation may have a significant impact on substrates at the central nervous system that manifest as changes in central cholinergic, monaminergic and cannabinoid systems in the adult animal.