Methamphetamine exacerbates neuroinflammatory response to lipopolysaccharide by activating dopamine D1-like receptors.
Methamphetamine exacerbates neuroinflammatory response to lipopolysaccharide by activating dopamine D1-like receptors.
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甲基苯丙胺通过激活多巴胺 D1 样受体，加剧对脂多糖的神经炎症反应。
DOI：
10.1016/j.intimp.2019.04.053
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发表时间：
2019-05
影响因子：
5.6
通讯作者：
Yanjiong Chen
中科院分区：
文献类型：
--
作者：
Biao Wang;Teng Chen;Li Xue;Jing Wang;Yuwei Jia;Guodong Li;Huixun Ren;Feng Wu;Min Wu;Yanjiong Chen
Methamphetamine (METH) is a highly addictive and widely abused drug worldwide. Although much research is on the drug's direct effects, METH may also alter host immunity. The mechanism by which METH influences immunity remains elusive. Here, C57BL6/J mice were intraperitoneally injected with 5 mg/kg METH four times at two-hour intervals. The microglial inhibitor minocycline or dopamine D1-like receptor antagonist SCH-23390 was also applied prior to METH injection. Twenty-four hours following the first METH injection, mice were challenged by lipopolysaccharide (LPS) at a dose of 330 μg/kg, and the hippocampus (Hip), caudate putamen (CPU), nucleus accumbens (NAc) and prefrontal cortex (PFC) were collected 4 h after LPS administration. IL-6 and TNF-α levels were detected by ELISA. The activation of D1-like receptors and microglial marker Iba1 were examined by immunohistochemical staining and Western blot. Finally, we examined the phosphorylation of ERK1/2 and CREB. We found that METH exposure increased LPS-induced IL-6 and TNF-α production in the Hip, CPU and NAc regions. METH also augmented microglia activation and D1/5DR expression in response to LPS. Moreover, administering SCH-23390 significantly reduced IL-6 and TNF-α production and Iba1 expression following LPS challenge. Similar inhibitory effects were also observed by minocycline administration. Moreover, phosphorylation of ERK1/2 and CREB was increased after METH and LPS exposure but decreased by SCH-23390. These data illustrate that METH exacerbates neuroinflammation response in LPS-stimulated mouse brains through dopamine D1-like receptors, microglia, and relevant signaling proteins, which may have therapeutic implications.
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影响因子：
3.6
作者：
Mizoguchi, H;Yamada, K;Nabeshima, T
通讯作者：
Nabeshima, T
影响因子：
4.4
作者：
Mikulak, Joanna;Bozzo, Luisa;Mavilio, Domenico
通讯作者：
Mavilio, Domenico
影响因子：
64.5
作者：
Brunet, A;Bonni, A;Greenberg, ME
通讯作者：
Greenberg, ME
影响因子：
3.4
作者：
Reza Arezoomandan;Esmail Riahi;A. Haghparast
通讯作者：
Reza Arezoomandan;Esmail Riahi;A. Haghparast
影响因子：
5.3
作者：
LaVoie, MJ;Card, JP;Hastings, TG
通讯作者：
Hastings, TG