McNair Scholars Research Journal
Abstract
The current experiment aims to investigate the relationship between the early phasic portion of salt taste transduction and sodium appetite. Prior research has identified two salt transduction pathways: a sodium-selective pathway, which is inhibited by amiloride or benzamil, and a non-selective pathway, which is insensitive to these blockers (Breslin & Spector, 2008). When presented with sodium solutions, sodium-depleted mice exhibit a behavior termed the “sodium appetite,” which results in voracious sodium consumption. The prevailing theory is that this behavior depends on neural activity of sodium-selective neurons (Breza & Contreras, 2012; Roitman & Bernstein, 1999). While previous studies have demonstrated that amiloride suppresses sodium appetite, our preliminary data suggest that benzamil fails to reduce NaCl intake in sodium-depleted mice. Electrophysiological recordings from the chorda tympani nerve and single neurons in the nucleus of the solitary tract (NTS) reveal that amiloride attenuates both the early phasic and later tonic portions of the neural response to sodium, whereas benzamil selectively blocks the tonic portion. These findings suggest that the phasic response in sodium-selective neurons may be critical for initiating sodium appetite. The goal of this proposal is to record gustatory neurons in the NTS of C57BL6J (wild type) mice in response to NaCl and NH₄Cl solutions following application of varying concentrations of amiloride or benzamil. We hypothesize that amiloride will attenuate both the phasic and tonic responses in sodium-selective neurons, while benzamil will only attenuate the tonic component. Results will help determine whether the phasic sodium response is essential for driving sodium appetite.