Sanguino-Gómez Jeniffer, Buurstede Jacobus C, Abiega Oihane, Fitzsimons Carlos P, Lucassen Paul J, Eggen Bart J L, Lesuis Sylvie L, Meijer Onno C, Krugers Harm J
Brain Plasticity Group, SILS-CNS, University of Amsterdam, Amsterdam, The Netherlands.
Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands.
Eur J Neurosci. 2022 May;55(9-10):2491-2518. doi: 10.1111/ejn.15188. Epub 2021 May 4.
Stressful experiences evoke, among others, a rapid increase in brain (nor)epinephrine (NE) levels and a slower increase in glucocorticoid hormones (GCs) in the brain. Microglia are key regulators of neuronal function and contain receptors for NE and GCs. These brain cells may therefore potentially be involved in modulating stress effects on neuronal function and learning and memory. In this review, we discuss that stress induces (1) an increase in microglial numbers as well as (2) a shift toward a pro-inflammatory profile. These microglia have (3) impaired crosstalk with neurons and (4) disrupted glutamate signaling. Moreover, microglial immune responses after stress (5) alter the kynurenine pathway through metabolites that impair glutamatergic transmission. All these effects could be involved in the impairments in memory and in synaptic plasticity caused by (prolonged) stress, implicating microglia as a potential novel target in stress-related memory impairments.
压力性经历尤其会引起大脑中（去甲）肾上腺素（NE）水平迅速升高，以及大脑中糖皮质激素（GCs）水平缓慢升高。小胶质细胞是神经元功能的关键调节因子，且含有NE和GCs的受体。因此，这些脑细胞可能潜在地参与调节压力对神经元功能以及学习和记忆的影响。在本综述中，我们讨论了压力会诱导：（1）小胶质细胞数量增加，以及（2）向促炎状态转变。这些小胶质细胞存在：（3）与神经元的串扰受损，以及（4）谷氨酸信号传导中断。此外，压力后的小胶质细胞免疫反应（5）通过损害谷氨酸能传递的代谢物改变犬尿氨酸途径。所有这些效应可能都与（长期）压力导致的记忆和突触可塑性损伤有关，这意味着小胶质细胞可能是压力相关记忆损伤的一个潜在新靶点。
