The vestibular system is a sensory system that has evolved over millions of years to detect acceleration of the head, both rotational and translational, in three dimensions. One of its most important functions is to stabilize gaze during unexpected head movement; however, it is also important in the control of posture and autonomic reflexes. Theta rhythm is a 3- to 12-Hz oscillating EEG signal that is intimately linked to self-motion and is also known to be important in learning and memory. Many studies over the last two decades have shown that selective activation of the vestibular system, using either natural rotational or translational stimulation, or electrical stimulation of the peripheral vestibular system, can induce and modulate theta activity. Furthermore, inactivation of the vestibular system has been shown to significantly reduce theta in freely moving animals, which may be linked to its impairment of place cell function as well as spatial learning and memory. The pathways through which vestibular information modulate theta rhythm remain debatable. However, vestibular responses have been found in the pedunculopontine tegmental nucleus (PPTg) and activation of the vestibular system causes an increase in acetylcholine release into the hippocampus, probably from the medial septum. Therefore, a pathway from the vestibular nucleus complex and/or cerebellum to the PPTg, supramammillary nucleus, posterior hypothalamic nucleus, and septum to the hippocampus is likely. The modulation of theta by the vestibular system may have implications for vestibular effects on cognitive function and the contribution of vestibular impairment to the risk of dementia.
Vestibular dysfunction has been shown to cause spatial memory impairment. Neurophysiological studies indicate that bilateral vestibular loss (BVL), in particular, is associated with an impairment of the response of hippocampal place cells and theta rhythm. However, the specific neural pathways through which vestibular information reaches the hippocampus are yet to be fully elucidated. The aim of the present study was to further investigate the hypothesised 'theta-generating pathway' from the brainstem vestibular nucleus to the hippocampus. BVL, and in some cases, unilateral vestibular loss (UVL), induced by intratympanic sodium arsanilate injections in rats, were used to investigate the effects of vestibular loss on somatosensory-induced type 2 theta rhythm, acetylcholine (ACh) release in the hippocampus, and the number of cholinergic neurons in the pedunculopontine tegmental nucleus (PPTg), an important part of the theta-generating pathway. Under urethane anaesthesia, BVL was found to cause a significant increase in the maximum power of the type 2 theta (3-6 Hz) frequency band compared to UVL and sham animals. Rats with BVL generally exhibited a lower basal level of ACh release than sham rats; however, this difference was not statistically significant. The PPTg of BVL rats exhibited significantly more choline-acetyltransferase (ChAT)-positive neurons than that of sham animals, as did the contralateral PPTg of UVL animals; however, the number of ChAT-positive neurons on the ipsilateral side of UVL animals was not significantly different from sham animals. The results of these studies indicate that parts of the theta-generating pathway undergo a significant reorganisation following vestibular loss, which suggests that this pathway is important for the interaction between the vestibular system and the hippocampus.
Permanent vestibular loss has detrimental effects on the hippocampus, resulting in a disruption to spatial learning and memory, hippocampal theta rhythm and place cell field spatial coherence. Little is known about the vestibular system-related hippocampal cholinergic transmission. Since the pharmacological blockade of muscarinic acetylcholine (ACh) receptors within the hippocampus produces deficits in learning and memory, we hypothesized that ACh receptors may at least partly support the integration of vestibular input. Consequently, we examined the expression of M muscarinic ACh receptors in the hippocampus at 7 and 30 days following bilateral vestibular lesions (BVL) in rats using autoradiography. Animals were divided into sham (n = 12) and BVL (n = 11) groups. BVL animals received intratympanic injections of sodium arsanilate (30 mg/0.1 ml) under isoflurane anesthesia and sham animals received the same volume of saline. Analysis of the brain tissue revealed a significant reduction in the number of M receptors throughout the hippocampus and striatum at 30 days (P ≤ 0.0001), but not at 7 days following BVL. This suggests that the changes in learning and memory seen following vestibular damage may be in part due to the loss of M muscarinic receptors in the hippocampus and striatum. © 2016 Wiley Periodicals, Inc.
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