Department of Neurosurgery, Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, the Netherlands; European Graduate School of Neuroscience (EURON), Maastricht University, Maastricht, the Netherlands.
Department of Neurosurgery, Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, the Netherlands.
J Chem Neuroanat. 2019 Mar;96:34-40. doi: 10.1016/j.jchemneu.2018.12.001. Epub 2018 Dec 5.
Fornix deep brain stimulation (DBS) has the ability to refurbish memory functions in animal models with experimental dementia. One of the possible underlying mechanisms is the acute increase of acetylcholine in the hippocampus. Another suggested hypothesis is neuroplasticity. Recent work in rats has shown that acute fornix DBS can modulate neurotrophic factors as well as synaptic plasticity markers on the short-term. Here, we want to test the hypothesis that acute fornix DBS can also lead to long-term effects on neuroplasticity. Rats received DBS at 100 Hz, 100 μA and 100 μs pulse width for 4 h with electrodes placed bilaterally in the fornix. Seven weeks after stimulation, rats were sacrificed. BDNF, p-CREB, SV2 and synaptophysin immunohistochemistry was performed for their brains. No differences were found in the number of BDNF, p-CREB or SV2 positive cells for fornix DBS rats when compared to sham. Surprisingly, the density of synaptophysin immunoreactive presynaptic boutons was significantly decreased in the CA1 and CA3 subregion of the hippocampus for DBS rats. Therefore, fornix DBS might induce long-term depression related mechanisms.
穹窿脑深部刺激（DBS）有能力修复实验性痴呆动物模型中的记忆功能。可能的潜在机制之一是海马体内乙酰胆碱的急性增加。另一种假设是神经可塑性。最近在大鼠中的研究表明，急性穹窿 DBS 可以在短期内调节神经营养因子和突触可塑性标志物。在这里，我们想测试急性穹窿 DBS 也可以导致神经可塑性的长期影响的假设。大鼠接受了 100Hz、100μA 和 100μs 脉冲宽度的 DBS，持续 4 小时，电极双侧放置在穹窿内。刺激 7 周后，处死大鼠。对其大脑进行 BDNF、p-CREB、SV2 和突触素免疫组织化学检测。与假手术组相比，穹窿 DBS 大鼠的 BDNF、p-CREB 或 SV2 阳性细胞数量没有差异。令人惊讶的是，DBS 大鼠海马 CA1 和 CA3 区的突触素免疫反应性突触前末梢密度显著降低。因此，穹窿 DBS 可能诱导长期抑郁相关机制。
