My previous study suggests that the chorda tympani nerve (CT) is important in conveying fat taste information to the central nervous system, as bilateral transection of the CT (CTX) raises the taste discrimination threshold for the free fatty acid, linoleic acid (LA). Surprisingly, the CT is unresponsive to lingual application of LA alone. LA may require a background of saliva to activate taste cells. This would explain, in part, the discrepancy between my behavioral data (in which saliva is present) and CT electrophysiological data (in which saliva is rinsed off). In support of this idea, CTX results in a secondary decrease in saliva production via denervation of the submaxillary and sublingual salivary glands, suggesting that impairment of LA taste discrimination may be attributable to removal of CT sensory information, a secondary decrease in saliva, or both. Moreover, electrophysiological studies of isolated taste receptors have shown that LA inhibits delayed rectifying potassium channels, presumably broadening action potentials, and augmenting responses to other taste stimuli. Thus, the contribution of the CT in this process may depend upon the presence of saliva and/or other taste stimuli. Accordingly, the present studies investigated the role of the CT in free fatty acid taste processing by measuring LA taste thresholds after removal of the submaxillary and sublingual salivary glands. I found that removal of these salivary glands raised LA discrimination thresholds (i.e. from ~ 11 μM to ~ 22 μM). However, this effect was not as pronounced as observed previously in CTX animals (i.e. from ~ 11 μM to ~ 44 μM), suggesting that CTX impairs LA taste discrimination both by removal of CT sensory input as well as decreased saliva. Moreover, I recorded electrophysiological activity of the CT in response to LA mixed in artificial saliva (AS), as well as in response to LA mixed with salivary sodium. The CT was unresponsive to lingual application of LA mixed in AS, but the addition of LA increased CT responses to salivary sodium. Finally, I recorded CT electrophysiological activity in response to LA‐taste mixtures (monosodium glutamate: MSG, sodium chloride: NaCl, sucrose: SUC, citric acid: CA, and quinine hydrochloride; QHCl) in anesthetized male rats. Co‐application of LA and both MSG and NaCl elicited greater CT responses than did either MSG or NaCl presented alone. However, the addition of LA did not alter CT responses to SUC, CA and QHCl. These results suggest that saliva is important in mediating behavioral responses to fat taste, but AS may lack components necessary for LA taste transduction. Moreover, free fatty acids (such as LA) modulate gustatory responses to taste stimuli (including MSG and NaCl), beginning with an initial interaction with salivary sodium.