Septal elicitation of hippocampal theta rhythm did not repair cognitive and emotional deficits resulting from vestibular lesions

Neo, Phoebe S.-H.; Carter, Donna; Zheng, Yiwen; Smith, Paul F.; Darlington, Cynthia L.; McNaughton, Neil

doi:10.1002/hipo.20963

Cited by 28 publications

(31 citation statements)

References 47 publications

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“…Although the BVD animals were hyperactive, theta rhythm was abnormal across the entire range of movement velocities. These results have recently been replicated by Neo et al (2012), who tried but failed to reverse the spatial memory and emotional deficits caused by BVD by electrically stimulating the septum in order to provide an artificial theta rhythm. Tai et al (2012) also recently showed that rats that are administered sodium arsanilate intratympanically exhibit a reduction in theta power.…”

Section: Effects Of Vestibular Lesions On Head Direction Cell and Plamentioning

confidence: 74%

From ear to uncertainty: vestibular contributions to cognitive function

Smith

Zheng

2013

Front. Integr. Neurosci.

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113

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In addition to the deficits in the vestibulo-ocular and vestibulo-spinal reflexes that occur following vestibular dysfunction, there is substantial evidence that vestibular loss also causes cognitive disorders, some of which may be due to the reflexive deficits and some of which are related to the role that ascending vestibular pathways to the limbic system and neocortex play in spatial orientation. In this review we summarize the evidence that vestibular loss causes cognitive disorders, especially spatial memory deficits, in animals and humans and critically evaluate the evidence that these deficits are not due to hearing loss, problems with motor control, oscillopsia or anxiety and depression. We review the evidence that vestibular lesions affect head direction and place cells as well as the emerging evidence that artificial activation of the vestibular system, using galvanic vestibular stimulation (GVS), can modulate cognitive function.

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Section: Effects Of Vestibular Lesions On Head Direction Cell and Plamentioning

confidence: 74%

From ear to uncertainty: vestibular contributions to cognitive function

Smith

Zheng

2013

Front. Integr. Neurosci.

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113

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“…In cats and dogs, passive translation does not increase the power but increases the peak frequency of theta (Arnolds et al, 1984). Moreover, vestibular lesions decrease the power and the frequency of theta (Russell et al, 2006; Neo et al, 2012; Tai et al, 2012). Nevertheless, restoration of theta in vestibular-deficient rats, by medial septum stimulation, is not sufficient to compensate for cognitive impairment induced by vestibular lesions (Neo et al, 2012).…”

Section: The Pathway From the Nucleus Reticularis Pontis Oralis To Tmentioning

confidence: 99%

Vestibular pathways involved in cognition

Hitier

Besnard

Smith

2014

Front. Integr. Neurosci.

264

215

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Recent discoveries have emphasized the role of the vestibular system in cognitive processes such as memory, spatial navigation and bodily self-consciousness. A precise understanding of the vestibular pathways involved is essential to understand the consequences of vestibular diseases for cognition, as well as develop therapeutic strategies to facilitate recovery. The knowledge of the “vestibular cortical projection areas”, defined as the cortical areas activated by vestibular stimulation, has dramatically increased over the last several years from both anatomical and functional points of view. Four major pathways have been hypothesized to transmit vestibular information to the vestibular cortex: (1) the vestibulo-thalamo-cortical pathway, which probably transmits spatial information about the environment via the parietal, entorhinal and perirhinal cortices to the hippocampus and is associated with spatial representation and self-versus object motion distinctions; (2) the pathway from the dorsal tegmental nucleus via the lateral mammillary nucleus, the anterodorsal nucleus of the thalamus to the entorhinal cortex, which transmits information for estimations of head direction; (3) the pathway via the nucleus reticularis pontis oralis, the supramammillary nucleus and the medial septum to the hippocampus, which transmits information supporting hippocampal theta rhythm and memory; and (4) a possible pathway via the cerebellum, and the ventral lateral nucleus of the thalamus (perhaps to the parietal cortex), which transmits information for spatial learning. Finally a new pathway is hypothesized via the basal ganglia, potentially involved in spatial learning and spatial memory. From these pathways, progressively emerges the anatomical network of vestibular cognition.

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“…This spatial memory impairment is likely to be related to hippocampal dysfunction, since both place cell responses (Stackman et al, 2002; Russell et al, 2003b) and theta rhythm have been reported to be abnormal (Russell et al, 2006; Neo et al, 2012; Tai et al, 2012; but see Stackman et al, 2002 for conflicting evidence regarding theta rhythm). On the other hand, CA1 and dentate gyrus (DG) field potentials and long-term potentiation (LTP) in vivo were not significantly affected by bilateral vestibular loss (Zheng et al, 2010a).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Bilateral Vestibular Loss on Hippocampal Volume, Neuronal Number, and Cell Proliferation in Rats

Zheng¹,

Balabhadrapatruni²,

Baek³

et al. 2012

Front. Neur.

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Previous studies in humans have shown that bilateral loss of vestibular function is associated with a significant bilateral atrophy of the hippocampus, which correlated with the patients’ spatial memory deficits. More recently, patients who had recovered from unilateral vestibular neuritis have been reported to exhibit a significant atrophy of the left posterior hippocampus. Therefore, we investigated whether bilateral vestibular deafferentation (BVD) would result in a decrease in neuronal number or volume in the rat hippocampus, using stereological methods. At 16 months post-BVD, we found no significant differences in hippocampal neuronal number or volume compared to sham controls, despite the fact that these animals exhibited severe spatial memory deficits. By contrast, using bromodeoxyuridine (BrdU) as a marker of cell proliferation, we found that the number of BrdU-labeled cells significantly increased in the dentate gyrus of the hippocampus between 48 h and 1 week following BVD. Although a substantial proportion of these cells survived for up to 1 month, the survival rate was significantly lower in BVD animals when compared with that in sham animals. These results suggest a dissociation between the effects of BVD on spatial memory and hippocampal structure in rats and humans, which cannot be explained by an injury-induced increase in cell proliferation.

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Septal elicitation of hippocampal theta rhythm did not repair cognitive and emotional deficits resulting from vestibular lesions

Cited by 28 publications

References 47 publications

From ear to uncertainty: vestibular contributions to cognitive function

From ear to uncertainty: vestibular contributions to cognitive function

Vestibular pathways involved in cognition

The Effects of Bilateral Vestibular Loss on Hippocampal Volume, Neuronal Number, and Cell Proliferation in Rats

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