Cognitive impairment of obstructive sleep apnea syndrome (OSAS) patients is related to the basal forebrain (BF) cholinergic neurons. To further investigate the effect of the excitation or inhibition of BF cholinergic neurons on cognitive ability, we employed a chronic intermittent hypoxia (CIH) mice model and implanted microinjection cannulas in the BFs for targeted intervention, finally performed the behavioral experiments and examined immunohistochemistry and biochemical changes in the BFs. The results showed that (1) CIH induced cognitive decline in mice. (2) The excitation of BF cholinergic neurons attenuated cognitive decline, while the inhibition of these neurons aggravated cognitive impairment. (3) Microinjection of adenosine into the BF aggravated cognitive decline, while caffeine improved cognitive ability. (4) CIH induced BF cholinergic neuron injury in mice. (5) The excitation of BF cholinergic neurons alleviated cholinergic neuron injury, while the inhibition of these neurons aggravated this injury. (6) Microinjection of adenosine into the BF aggravated cholinergic neuron injury, while caffeine alleviated this injury. (7) CIH induced endoplasmic reticulum stress, oxidative stress and inflammatory responses in the BFs of mice. (8) The excitation of BF cholinergic neurons mitigated endoplasmic reticulum stress, oxidative stress and inflammatory responses in the BF in mice, while the inhibition of BF cholinergic neurons worsened these responses in the BF. (9) Microinjection of adenosine into the BF aggravated endoplasmic reticulum stress, oxidative stress and the inflammatory response, while caffeine alleviated these responses. This work indicates that CIH induces BF cholinergic neuron injury through multiple pathways, including endoplasmic reticulum stress, oxidative stress and the inflammatory response, thereby leading to cognitive dysfunction in mice. BF cholinergic neurons play a vital role in these pathways, thus reducing cholinergic neuron injury and restoring cognitive function in mice. Adenosine, which is an upstream modifier of acetylcholine, also plays an important role in altering cognitive ability.

阻塞性睡眠呼吸暂停综合征 (OSAS) 患者的认知障碍与基底前脑 (BF) 胆碱能神经元有关。为了进一步研究BF胆碱能神经元的兴奋或抑制对认知能力的影响，我们采用慢性间歇性缺氧（CIH）小鼠模型并在BFs中植入显微注射管进行靶向干预，最后进行行为实验并检查免疫组织化学和生化BF 的变化。结果表明(1)CIH诱导小鼠认知能力下降。(2)BF胆碱能神经元的兴奋减弱了认知衰退，而这些神经元的抑制则加重了认知障碍。(3) BF 显微注射腺苷加重认知能力下降，而咖啡因改善认知能力。(4)CIH诱导小鼠BF胆碱能神经元损伤。(5)BF胆碱能神经元的兴奋减轻了胆碱能神经元的损伤，而这些神经元的抑制则加重了这种损伤。(6) BF 微量注射腺苷加重了胆碱能神经元损伤，而咖啡因减轻了这种损伤。(7)CIH诱导小鼠BFs内质网应激、氧化应激和炎症反应。(8) BF胆碱能神经元的兴奋减轻了小鼠BF中的内质网应激、氧化应激和炎症反应，而BF胆碱能神经元的抑制使BF中的这些反应恶化。(9) 将腺苷微量注射到 BF 中加剧了内质网应激、氧化应激和炎症反应，而咖啡因则减轻了这些反应。这项工作表明CIH通过多种途径诱导BF胆碱能神经元损伤，包括内质网应激、氧化应激和炎症反应，从而导致小鼠认知功能障碍。BF 胆碱能神经元在这些通路中起着至关重要的作用，从而减少胆碱能神经元损伤并恢复小鼠的认知功能。腺苷是乙酰胆碱的上游调节剂，在改变认知能力方面也起着重要作用。