The effects of electrical stimulation of the peripheral vestibular system on neurochemical release in the rat striatum.

For over a century, it has been speculated that the vestibular system transmits information about self-motion to the striatum. There have been inconsistent reports of such a connection, and interest in the subject has been increased by the experimental use of galvanic vestibular stimulation in the treatment of Parkinson's Disease patients. Nonetheless, there are few data available on the effects of vestibular stimulation on neurochemical changes in the striatum.

Single neuron activity and c-Fos expression in the rat striatum following electrical stimulation of the peripheral vestibular system.

Connections between the vestibular system and the basal ganglia have been postulated since the early 20th century. However, the results of electrophysiological studies investigating neuronal responses to electrical stimulation of the vestibular system have been inconsistent. The aim of this study was to investigate the effects of electrical stimulation of the vestibular labyrinth on single neuron activity and c-Fos expression in the rat striatum.

Effects of acute altered gravity during parabolic flight and/or vestibular loss on cell proliferation in the rat dentate gyrus.

Both parabolic flight, i.e. a condition of altered gravity, and loss of vestibular function, have been suggested to affect spatial learning and memory, which is known to be influenced by neurogenesis in the hippocampus.

The vestibular-basal ganglia connection: balancing motor control.

Connections between the vestibular system and the basal ganglia have been sporadically studied over the last century. Electrophysiological studies of field potentials in animals have shown that most areas of the striatum respond to electrical vestibular stimulation while human studies isolated responses to vestibular stimulation to the putamen of the striatum. Protein studies have shown inconsistent results regarding changes in receptor levels of a number of receptor types.

The effects of acute stress-induced sleep disturbance on acoustic trauma-induced tinnitus in rats.

Chronic tinnitus is a debilitating condition and often accompanied by anxiety, depression, and sleep disturbance. It has been suggested that sleep disturbance, such as insomnia, may be a risk factor/predictor for tinnitus-related distress and the two conditions may share common neurobiological mechanisms. This study investigated whether acute stress-induced sleep disturbance could increase the susceptibility to acoustic trauma-induced tinnitus in rats.

Galvanic vestibular stimulation impairs cell proliferation and neurogenesis in the rat hippocampus but not spatial memory.

Galvanic vestibular stimulation (GVS) is a method of activating the peripheral vestibular system using direct current that is widely employed in clinical neurological testing. Since movement is recognized to stimulate hippocampal neurogenesis and movement is impossible without activation of the vestibular system, we speculated that activating the vestibular system in rats while minimizing movement, by delivering GVS under anesthesia, would affect hippocampal cell proliferation and neurogenesis, and spatial memory. Compared with the sham control group, the number of cells incorporating the DNA replication marker, bromodeoxyuridine (BrdU), was significantly reduced in the bilateral hippocampi in both the cathode left-anode right and cathode right-anode left stimulation groups (P ≤ 0.

Glutamate receptor subunit and calmodulin kinase II expression, with and without T maze training, in the rat hippocampus following bilateral vestibular deafferentation.

Unlabelled: Many previous studies have shown that lesions of the peripheral vestibular system result in spatial memory deficits and electrophysiological dysfunction in the hippocampus. Given the importance of glutamate as a neurotransmitter in the hippocampus, it was predicted that bilateral vestibular deafferentation (BVD) would alter the expression of NMDA and AMPA receptors in this area of the brain.

Methods: The expression of the NR1, NR2A, NR2B, GluR1, GluR2, GluR3 and GluR 4 glutamate receptor subunits, as well as calmodulin kinase IIα (CaMKIIα) and phosphorylated CaMKIIα (pCaMKIIα), was measured in the rat CA1, CA2/3 and dentate gyrus (DG) subregions of the hippocampus, at 24 h, 72 h, 1 week, 1 month and 6 months following BVD, using western blotting.

Evidence that Memantine Reduces Chronic Tinnitus Caused by Acoustic Trauma in Rats.

Subjective tinnitus is a chronic neurological disorder in which phantom sounds are perceived. Increasing evidence suggests that tinnitus is caused by neuronal hyperactivity in auditory brain regions, either due to a decrease in synaptic inhibition or an increase in synaptic excitation. One drug investigated for the treatment of tinnitus has been the uncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist, memantine, although the evidence relating to it has been unconvincing to date.

The D₂ dopamine receptor and locomotor hyperactivity following bilateral vestibular deafferentation in the rat.

Rats and mice with bilateral vestibular loss exhibit dramatic locomotor hyperactivity and circling behaviours, which to date cannot be explained. Dysfunction of the striatal dopaminergic system is responsible for a number of known movement disorders and the D(2) dopamine receptor is known to be implicated. Therefore, it is possible that changes in striatal function are responsible for locomotor hyperactivity and circling following bilateral vestibular lesions.

The effects of the D2 dopamine receptor antagonist, eticlopride, on attention following bilateral vestibular deafferentation in the rat.

Loss of vestibular function has been associated with cognitive impairment, including attentional problems. The aim of this study was to investigate the effects of the D(2) dopamine receptor antagonist, eticlopride (0.02, 0.

The effects of the synthetic cannabinoid receptor agonists, WIN55,212-2 and CP55,940, on salicylate-induced tinnitus in rats.

Previous studies in animals and humans have shown that, in some cases at least, anti-epileptic drugs can reduce the severity of tinnitus. Given that cannabinoid receptor agonists have been shown to exert anti-epileptic effects in some circumstances, we investigated whether two synthetic CB(1)/CB(2) receptor agonists, WIN55,212-2, and CP55,940, could inhibit the behavioural manifestations of salicylate-induced tinnitus in rats in a conditioned suppression task. We found that neither WIN55,212-2 (3.