Abstract
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.
Highlights
Numerous studies over the last two decades have shown that damage to the peripheral vestibular system, especially bilateral lesions, results in spatial memory impairment in both animals and humans
unilateral vestibular loss (UVL) appears to cause a decrease in hippocampal field potentials following UVL in in vitro hippocampal slices (Zheng et al, 2003; Lee et al, 2017), this has not been demonstrated following bilateral vestibular loss (BVL) in vivo (Zheng et al, 2010; Truchet et al, 2019) and no UVL in vivo investigation has been conducted
UVL causes a massive asymmetry between the two vestibular nuclei (VN) in the brainstem, which is transmitted to higher brain regions, whereas BVL removes all vestibular input simultaneously but does not cause such an asymmetry
Summary
Numerous studies over the last two decades have shown that damage to the peripheral vestibular system, especially bilateral lesions, results in spatial memory impairment in both animals and humans (for reviews see Besnard et al, 2016; Smith, 2017; Agrawal et al, 2020). This memory impairment has been attributed to the effects of vestibular loss on the hippocampus, many other areas of the medial temporal lobe and cortex are likely to be involved as well. There is ample reason to think that the loss of vestibular function impairs normal hippocampal function and its role in spatial memory
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