title: The effects of vestibular lesions on hippocampal function in rats.
abstract: Interest in interaction between the vestibular system and the hippocampus was stimulated by evidence that peripheral vestibular lesions could impair performance in learning and memory tasks requiring spatial information processing. By the 1990s, electrophysiological data were emerging that the brainstem vestibular nucleus complex (VNC) and the hippocampus were connected polysynaptically and that hippocampal place cells could respond to vestibular stimulation. The aim of this review is to summarise and critically evaluate research published in the last 5 years that has seen major progress in understanding the effects of vestibular damage on the hippocampus. In addition to new behavioural studies demonstrating that animals with vestibular lesions exhibit impairments in spatial memory tasks, electrophysiological studies have confirmed long-latency, polysynaptic pathways between the VNC and the hippocampus. Peripheral vestibular lesions have been shown to cause long-term changes in place cell function, hippocampal EEG activity and even CA1 field potentials in brain slices maintained in vitro. During the same period, neurochemical investigations have shown that some hippocampal subregions exhibit long-term changes in the expression of neuronal nitric oxide synthase, arginase I and II, and the NR1 and NR2A N-methyl-D-aspartate (NMDA) receptor subunits following peripheral vestibular damage. Despite the progress, a number of important issues remain to be resolved, such as the possible contribution of auditory damage associated with vestibular lesions, to the hippocampal effects observed. Furthermore, although these studies demonstrate that damage to the vestibular system does have a long-term impact on the electrophysiological and neurochemical function of the hippocampus, they do not indicate precisely how vestibular information might be used in hippocampal functions such as developing spatial representations of the environment. Understanding this will require detailed electrical stimulation and lesion studies to elucidate the way in which different kinds of vestibular information are transmitted to various hippocampal subregions.
authors.affiliation: Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago, Dunedin, New Zealand. paul.smith@stonebow.otago.ac.nz
authors.forename: Paul F
authors.initials: PF
authors.lastname: Smith
authors.forename: Arata
authors.initials: A
authors.lastname: Horii
authors.forename: Noah
authors.initials: N
authors.lastname: Russell
authors.forename: David K
authors.initials: DK
authors.lastname: Bilkey
authors.forename: Yiwen
authors.initials: Y
authors.lastname: Zheng
authors.forename: Ping
authors.initials: P
authors.lastname: Liu
authors.forename: D Steve
authors.initials: DS
authors.lastname: Kerr
authors.forename: Cynthia L
authors.initials: CL
authors.lastname: Darlington
mesh_terms: D000818:Animals; D006624:Hippocampus / Q000502:physiology* / Q000503:physiopathology; D008569:Memory Disorders / Q000209:etiology* / Q000503:physiopathology; D009434:Neural Pathways / Q000502:physiology*; D009949:Orientation / Q000502:physiology; D004856:Postural Balance / Q000502:physiology; D051381:Rats; D013028:Space Perception / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology; D015837:Vestibular Diseases / Q000150:complications* / Q000503:physiopathology; D014726:Vestibular Nuclei / Q000502:physiology*; D014722:Vestibule, Labyrinth / Q000293:injuries / Q000503:physiopathology