Loss of vestibular function is known to cause spatial memory deficits and hippocampal dysfunction, in terms of impaired place cell firing and abnormal theta rhythm. Based on these results, it has been of interest to determine whether vestibular loss also affects the development and maintenance of long-term potentiation (LTP) in the hippocampus. This article summarizes and critically reviews the studies of hippocampal LTP following a vestibular loss and its relationship to NMDA receptor expression, that have been published to date. Although the available in vitro studies indicate that unilateral vestibular loss (UVL) results in reduced hippocampal field potentials in CA1 and the dentate gyrus (DG), the in vivo studies involving bilateral vestibular loss (BVL) do not. This may be due to the differences between UVL and BVL or it could be a result of in vitro/in vivo differences. One in vitro study reported a decrease in LTP in hippocampal slices following UVL; however, the two available in vivo studies have reported different results: either no effect or an increase in EPSP/Population Spike (ES) potentiation. This discrepancy may be due to the different high-frequency stimulation (HFS) paradigms used to induce LTP. The increased ES potentiation following BVL may be related to an increase in synaptic NMDA receptors, possibly increasing the flow of vestibular input coming into CA1, with a loss of selectivity. This might cause increased excitability and synaptic noise, which might lead to a degradation of spatial learning and memory.

已知前庭功能丧失会导致空间记忆缺陷和海马功能障碍，即位置细胞放电受损和θ节律异常。基于这些结果，确定前庭丧失是否也会影响海马长时程增强（LTP）的发育和维持一直很有意义。本文总结并批判性地回顾了迄今为止已发表的前庭丧失后海马 LTP 及其与 NMDA 受体表达关系的研究。虽然可用的体外研究表明，单侧前庭功能丧失 (UVL) 会导致 CA1 和齿状回 (DG) 的海马场电位降低，体内涉及双侧前庭丧失（BVL）的研究则不然。这可能是由于 UVL 和 BVL 之间的差异，或者可能是由于体外/体内差异。一体外研究报告 UVL 后海马切片中的 LTP 降低；然而，这两个可用体内研究报告了不同的结果：要么没有影响，要么 EPSP/群体尖峰 (ES) 增强作用有所增加。这种差异可能是由于用于诱导 LTP 的高频刺激 (HFS) 范例不同所致。BVL 后 ES 增强的增加可能与突触 NMDA 受体的增加有关，可能增加进入 CA1 的前庭输入流量，但选择性丧失。这可能会导致兴奋性和突触噪音增加，从而可能导致空间学习和记忆力下降。