Optogenetic Stimulation of Type I GAD65+ Cells in Taste Buds Activates Gustatory Neurons and Drives Appetitive Licking Behavior in Sodium-Depleted Mice
Optogenetic Stimulation of Type I GAD65+ Cells in Taste Buds Activates Gustatory Neurons and Drives Appetitive Licking Behavior in Sodium-Depleted Mice
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DOI：
10.1523/jneurosci.0597-20.2020
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发表时间：
2020-10-07
影响因子：
5.3
通讯作者：
Breza, Joseph M.
中科院分区：
文献类型：
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作者：
Baumer-Harrison, Caitlin;Raymond, Martin A.;Breza, Joseph M.
哺乳动物的味蕾由专门的神经上皮细胞组成，这些细胞充当提供营养分子（例如碳水化合物、氨基酸和盐）和潜在有害分子（例如某些植物化合物和强酸）的传感器。II型和III型味蕾细胞（tbc）检测被人类描述为“甜”、“苦”、“鲜味”和“酸”的分子。探测金属离子的tbc，被人类描述为“咸的”，是未定义的。从历史上看，I型胶质样tbc被认为在味蕾中起支持作用，但很少有研究探索它们在味觉转导中的作用。一些证据表明，I型细胞可能通过阿米洛利敏感机制检测钠（Na+），这表明它们在Na（+）味觉传导中发挥作用。我们利用光遗传学方法，通过驱动光敏感通道视紫红质-2 （ChR2）在雄性和雌性小鼠I型GAD65(+) tbc中的表达来研究I型tbc。光遗传刺激GAD65(+) TBCs增加了鼓室索神经的活性，激活了吻侧孤束核的味觉神经元。“N神经元”的NaCl反应被amiloride类似物benzamil阻断，对前舌上GAD65(+) tbc的光刺激反应强烈。在NA（+）充满和NA（+）耗尽条件下进行两瓶偏好试验，以评估光遗传刺激GAD65(+) tbc对行为的影响。在NA（+）缺乏的条件下，GAD65-ChR2-EYFP小鼠对470 nm光照射的H2O比未照射的H2O表现出强烈的偏好，这表明I型胶质样tbc足以驱动类似NA（+）食欲的行为。
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+) via an amiloride-sensitive mechanism, suggesting they play a role in NA(+) 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(+) TBCs of male and female mice. Optogenetic stimulation of GAD65(+) 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(+) TBCs on the anterior tongue. Two-bottle preference tests were conducted under NA(+)-replete and NA(+)-deplete conditions to assess the behavioral impact of optogenetic stimulation of GAD65(+) TBCs. Under NA(+)-deplete conditions GAD65-ChR2-EYFP mice displayed a robust preference for H2O illuminated with 470 nm light versus nonilluminated H2O, suggesting that type I glial-like TBCs are sufficient for driving a behavior that resembles NA(+) appetite.