Mammalian taste buds are comprised of specialized neuroepithelial cells that act as sensors for molecules that provide nutrition (e.g., carbohydrates, amino acids, and salts) and those that are potentially harmful (e.g., certain plant compounds and strong acids). Type II and III taste bud cells (TBCs) detect molecules described by humans as "sweet," "bitter," "umami," and "sour." TBCs that detect metallic ions, described by humans as "salty," are undefined. Historically, type I glial-like TBCs have been thought to play a supportive role in the taste bud, but little research has been done to explore their role in taste transduction. Some evidence implies that type I cells may detect sodium (Na 1 ) via an amiloride-sensitive mechanism, suggesting they play a role in Na 1 taste transduction. We used an optogenetic approach to study type I TBCs by driving the expression of the light-sensitive channelrhodopsin-2 (ChR2) in type I GAD65 1 TBCs of male and female mice. Optogenetic stimulation of GAD65 1 TBCs increased chorda tympani nerve activity and activated gustatory neurons in the rostral nucleus tractus solitarius. "N neurons," whose NaCl responses were blocked by the amiloride analog benzamil, responded robustly to light stimulation of GAD65 1 TBCs on the anterior tongue. Two-bottle preference tests were conducted under Na 1 -replete and Na 1 -deplete conditions to assess the behavioral impact of optogenetic stimulation of GAD65 1 TBCs. Under Na 1 -deplete conditions GAD65-ChR2-EYFP mice displayed a robust preference for H 2 O illuminated with 470 nm light versus nonilluminated H 2 O, suggesting that type I glial-like TBCs are sufficient for driving a behavior that resembles Na 1 appetite.