Department of Life Sciences, Texas A&M University - Corpus Christi, Corpus Christi, Texas 78412, USA; Department of Biological Sciences, University of Cincinnati, Cincinnati, Ohio 45221, USA.
Department of Life Sciences, Texas A&M University - Corpus Christi, Corpus Christi, Texas 78412, USA; Department of Cell Systems and Anatomy, University of Texas Health San Antonio, San Antonio, Texas 78229, USA.
Behav Brain Res. 2020 Apr 6;383:112504. doi: 10.1016/j.bbr.2020.112504. Epub 2020 Jan 22.
This study investigated the signaling cascades involved in the long-term storage of the balance between defensive and appetitive behaviors observed when the mollusk Aplysia is exposed to aversive experience. In Aplysia, repeated trials of aversive stimuli induce concurrent sensitization of defensive withdrawal reflexes and suppression of feeding for at least 24 h. This long-term storage of the balance between withdrawal reflexes and feeding is sustained, at least in part, by increased excitability of the tail sensory neurons (SNs) controlling the withdrawal reflexes, and by decreased excitability of feeding decision-making neuron B51. Nitric oxide (NO) is required for the induction of both long-term sensitization and feeding suppression. At the cellular level, NO is also required for long-term decreased B51 excitability but not for long-term increased SN excitability. Here, we characterized the signaling cascade downstream of NO contributing to the long-term storage of the balance between withdrawal reflexes and feeding. We found protein kinase G (PKG) necessary for both long-term sensitization and feeding suppression, indicating that a NO-PKG cascade governs the long-term storage of the balance between defensive and appetitive responses in Aplysia. The role of PKG on feeding suppression was paralleled at the cellular level where a cGMP-PKG pathway was required for long-term decreased B51 excitability. In the defensive circuit, the cGMP-PKG pathway was not necessary for long-term increased SN excitability, suggesting that other cellular correlates of long-term sensitization might depend on the GMP-PKG cascade to sustain the behavioral change.
本研究探讨了在 mollusk Aplysia 暴露于厌恶刺激时观察到的防御和食欲行为之间的平衡的长期存储中涉及的信号级联。在 Aplysia 中，重复的厌恶刺激试验会导致防御性撤退反射同时敏化，并至少持续 24 小时抑制进食。这种撤退反射和进食之间的平衡的长期存储至少部分是通过控制撤退反射的尾部感觉神经元 (SN) 的兴奋性增加和进食决策神经元 B51 的兴奋性降低来维持的。一氧化氮 (NO) 是长时程敏化和进食抑制的诱导所必需的。在细胞水平上，NO 也需要长期降低 B51 的兴奋性，但不需要长期增加 SN 的兴奋性。在这里，我们描述了 NO 下游的信号级联，该级联有助于撤退反射和进食之间平衡的长期存储。我们发现蛋白激酶 G (PKG) 对于长期敏化和进食抑制都是必需的，这表明 NO-PKG 级联控制了 Aplysia 中防御和食欲反应之间平衡的长期存储。PKG 在进食抑制中的作用在细胞水平上是平行的，其中 cGMP-PKG 途径是长期降低 B51 兴奋性所必需的。在防御回路中，cGMP-PKG 途径对于长期增加的 SN 兴奋性不是必需的，这表明长期敏化的其他细胞相关性可能依赖于 cGMP-PKG 级联来维持行为变化。
