Department of Immunology and Microbiology, Rush University Medical Center, Cohn Research Building, Rm.414, 1735 W. Harrison Street, Chicago, IL, 60612, USA.
J Neurovirol. 2018 Feb;24(1):113-118. doi: 10.1007/s13365-017-0588-y. Epub 2017 Oct 31.
We assessed firing and voltage-gated Ca influx in medial prefrontal cortex (mPFC) pyramidal neurons from older (12 months old) HIV-1 transgenic (Tg) rats. We found that neurons from older Tg rats showed increased firing compared to non-Tg rats, but Ca spikes were unchanged. However, stronger excitatory stimulation was needed to evoke Ca spikes, which was associated with reduced mPFC Ca1.2 L-type Ca channel (L-channel) protein. In contrast, L-channel protein was unaltered in younger (6-7 weeks old) Tg rats, which we previously found had enhanced neuronal Ca influx. These studies demonstrate that aging alters HIV-induced Ca channel dysfunction that affects mPFC activity.
我们评估了来自老年（12 个月大）HIV-1 转基因（Tg）大鼠的前额皮质（mPFC）中间神经元的放电和电压门控 Ca 内流。我们发现，与非 Tg 大鼠相比，老年 Tg 大鼠的神经元放电增加，但 Ca spikes 不变。然而，需要更强的兴奋性刺激来引发 Ca spikes，这与 mPFC Ca1.2 L 型钙通道（L-通道）蛋白的减少有关。相比之下，我们之前发现年轻（6-7 周龄）Tg 大鼠的神经元 Ca 内流增强，但 L-通道蛋白没有改变。这些研究表明，衰老改变了 HIV 诱导的钙通道功能障碍，从而影响了 mPFC 的活动。
