CB1 Receptors in the Nucleus of the Solitary Tract Decrease the Duration of the LCR in Neonatal Rat Pups

Abstract

The laryngeal chemoreflex (LCR) is stimulated by the presence of fluid in the larynx, eliciting signal transduction in the superior laryngeal nerve to the nucleus of the solitary tract (NTS) in the brainstem. LCR activation stimulates survival reflexes to clear the airway, including apnea, bradycardia, coughing, and swallowing. Because LCR activation is pronounced in neonatal animals, the LCR has been implicated in the cessation of breathing characteristic of Sudden Infant Death Syndrome (SIDS). Transient receptor potential vanilloid 1 (TRPV1) receptors are ligand-gated ion channels in the NTS that prolong the LCR. TRPV1 receptors increase presynaptic calcium, cannabinoid1 receptors, co-expressed with TRPV1 in the NTS, reduce presynaptic calcium levels. We hypothesized that if TRPV1 is capable of elongating the LCR, then CB1 activation is capable of shortening the LCR. Therefore, the primary objective of this experiment was to characterize the role that CB1 plays to decrease the LCR. To determine if CB1 inhibition of TRPV1 was capable of shortening the LCR, the CB1 agonist arachidonyl-2′-chloroethylamide (ACEA) was microinjected into the NTS of p8 to p18 Sprague-Dawley rat pups. The LCR was recorded prior to and after injections. CB1 activation significantly (p<0.05) shortened the LCR. From these data, we can conclude that CB1 activation in the NTS, and the resulting TRPV1 inactivation in the NTS, plays a significant role in the central respiratory control of the LCR in neonatal rat pups. We are currently investigating the interaction between activation of TRPV1 and CB1 receptors.