Watzinger Ginger, Bennett Heather L
Department of Biology, Trinity College, Hartford, Connecticut, United States.
MicroPubl Biol. 2024 May 29;2024. doi: 10.17912/micropub.biology.001024. eCollection 2024.
Oxygen is vital for neuron development and function, and low oxygen (hypoxia) or 0% oxygen available (anoxia) conditions lead to neuronal dysfunction and death. Nonlethal forms of stress, prior to hypoxic or anoxic (preconditioning) environments protects neurons and increases survival to oxygen deprivation. Hyperpolarization of neurons prior to anoxia (neural preconditioning) increases survival, but the cellular and molecular pathways that confer survival are unclear. Here we report that loss in ceramide synthase gene, suppresses increased survival to anoxia in neural preconditioned animals, suggesting that HYL-2 functions upstream of the circuit that regulates neural preconditioning.
氧气对神经元的发育和功能至关重要,低氧(缺氧)或无氧气供应(无氧)条件会导致神经元功能障碍和死亡。在缺氧或无氧(预处理)环境之前的非致死性应激形式可保护神经元并提高其对缺氧的存活率。缺氧前神经元的超极化(神经预处理)可提高存活率,但赋予存活能力的细胞和分子途径尚不清楚。在此,我们报告神经酰胺合酶基因的缺失会抑制神经预处理动物对缺氧的存活率提高,这表明HYL-2在调节神经预处理的回路上游发挥作用。