<br>轻度应激源对大鼠衰老过程中杏仁核中央（CeA）和内侧（MeA）含有白细胞介素-1β的神经元的影响。,Acta Neurobiologiae Experimentalis

当前位置： X-MOL 学术 › › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

轻度应激源对大鼠衰老过程中杏仁核中央（CeA）和内侧（MeA）含有白细胞介素-1β的神经元的影响。
Acta Neurobiologiae Experimentalis Pub Date : 2015-01-01
Ewa Badowska-Szalewska ₁ , Beata Ludkiewicz ₂ , Jan H Spodnik ₂ , Rafał Krawczyk ₂ , Janusz Moryś ₂

Affiliation

促炎细胞因子——白细胞介素1β（IL-1β）在边缘系统结构的应激反应中发挥重要作用。应激对 IL-1β 的影响可能取决于个体发育年龄。该研究考察了急性和慢性暴露于强迫游泳 (FS) 或高光开放场 (HL-OF) 应激源对含有 IL-1β 的神经元的影响。使用双重免疫荧光染色来揭示 IL-1β/NeuN（NeuN - 神经元核标记物）的密度 - 杏仁核中央 (CeA) 和内侧 (MeA) 核中的免疫反应性 (ir) 细胞，这些细胞与调节密切相关情绪压力源和下丘脑-垂体-肾上腺轴（HPA）激活。这些实验中使用了成年（P90；P-出生后天）、中年（P360）和老年（P720）雄性Wistar Han大鼠。我们观察到 P90 与 P360 以及 P360 与 P720 大鼠中 CeA 和 MeA 中 IL-1β/NeuN-ir 细胞基础密度随年龄的增加。与非应激组相比，P90、P360 和 P720 大鼠的任何研究细胞核中的 IL-1β-ir 神经元密度均未引起急性或慢性 FS 的显着变化。然而，慢性而非急性 HL-OF 导致 P360 大鼠的 CeA 和 MeA 以及 P720 动物的 MeA 中 IL-1β/NeuN-ir 细胞密度显着增加。此外，与急性 HL-OF 相比，慢性 HL-OF 导致 P360 和 P720 大鼠的 CeA 和 MeA 中 IL-1β-ir 神经元密度增加。我们的结果可能表明 IL-1β 神经元参与 CeA 和 MeA 衰老过程的发展。此外，我们的结果指出，慢性HL-OF是诱发中老年大鼠MeA和/或CeA中IL-1β/NeuN-ir细胞密度增加的加重因素。这种增加可能是由于与退化衰老过程相关的 HPA 轴控制不足，并且似乎是衰老过程和压力的共同点。

"点击查看英文标题和摘要"

The influence of mild stressors on neurons containing interleukin-1β in the central (CeA) and medial (MeA) amygdala in the ageing process of rats.

Proinflammatory cytokine - interleukin 1β (IL-1β) plays an important role in stress reactions in the structures of limbic system. The impact of stress on IL-1β may depend on the ontogenetic age. The study examined the influence of acute and chronic exposure to forced swim (FS) or high-light open-field (HL-OF) stressors on neurons containing IL-1β. Double immunofluorescence staining was used to reveal the density of IL-1β/NeuN (NeuN - a neuronal nuclear marker) - immunoreactive (ir) cells in the amygdaloid central (CeA) and medial (MeA) nuclei, which are closely involved in the regulation of emotional stressors and hypothalamic-pituitary-adrenal axis (HPA) activation. Adult (P90; P - postnatal day), middle-aged (P360), and aged (P720) male Wistar Han rats were used in these experiments. We observed an age-dependent increase in the basal density of IL-1β/NeuN-ir cells in CeA and MeA in P90 vs. P360 and P360 vs. P720 rats. Neither acute nor chronic FS caused significant changes in the density of IL-1β-ir neurons in any of the investigated nuclei in P90, P360, and P720 rats as compared with the non-stressed groups. However, chronic but not acute HL-OF caused a marked increase in the density of IL-1β/NeuN-ir cells in the CeA and MeA of P360 rats and in MeA of the P720 animals. Moreover, chronic HL-OF led to an increase in the density of IL-1β-ir neurons in relation to acute HL-OF in the CeA and MeA of both P360 and P720 rats. Our results may indicate the involvement of IL-1β neurons in the development of ageing processes in CeA and MeA. Furthermore, our results point out that chronic HL-OF is an aggravating factor that induces an increase in the density of IL-1β/NeuN-ir cells in the MeA and/or CeA of middle-aged and aged rats. The increase is possibly due to insufficient control of the HPA axis associated with involutional ageing processes and seems to be a common denominator of the ageing process and stress.

更新日期：2019-11-01

点击分享

点击收藏