Exposure to loud sound (acoustic overexposure; AOE) induces hearing loss and damages cellular structures at multiple locations in the auditory pathway. Whether AOE can also induce changes in myelin sheaths of the auditory nerve (AN) is an important issue particularly because these changes can be responsible for impaired action potential propagation along the AN. Here we investigate the effects of AOE on morphological and electrophysiological features of the centrally directed part of the rat AN projecting from the cochlear spiral ganglion to brainstem cochlear nuclei. Using electron microscopy and immunocytochemistry, we show that AOE elongates the AN nodes of Ranvier and triggers notable perinodal morphological changes. Compound action potential recordings of the AN coupled to biophysical modeling demonstrated that these nodal and perinodal structural changes were associated with decreased conduction velocity and conduction block. Furthermore, AOE decreased the number of release sites in the cochlear nuclei associated with the reduced amplitudes of EPSCs evoked by AN stimulation. In conclusion, AN dysmyelination may be of fundamental importance in auditory impairment following exposure to loud sound.

The dorsal cochlear nucleus (DCN) is a first relay of the central auditory system as well as a site for integration of multimodal information. Vesicular glutamate transporters VGLUT-1 and VGLUT-2 selectively package glutamate into synaptic vesicles and are found to have different patterns of organization in the DCN. Whereas auditory nerve fibers predominantly co-label with VGLUT-1, somatosensory inputs predominantly co-label with VGLUT-2. Here, we used retrograde and anterograde transport of fluorescent conjugated dextran amine (DA) to demonstrate that the lateral vestibular nucleus (LVN) exhibits ipsilateral projections to both fusiform and deep layers of the rat DCN. Stimulating the LVN induced glutamatergic synaptic currents in fusiform cells and granule cell interneurones. We combined the dextran amine neuronal tracing method with immunohistochemistry and showed that labeled projections from the LVN are co-labeled with VGLUT-2 by contrast to VGLUT-1. Wistar rats were exposed to a loud single tone (15 kHz, 110 dB SPL) for 6 hours. Five days after acoustic overexposure, the level of expression of VGLUT-1 in the DCN was decreased whereas the level of expression of VGLUT-2 in the DCN was increased including terminals originating from the LVN. VGLUT-2 mediated projections from the LVN to the DCN are likely to play a role in the head position in response to sound. Amplification of VGLUT-2 expression after acoustic overexposure could be a compensatory mechanism from vestibular inputs in response to hearing loss and to a decrease of VGLUT-1 expression from auditory nerve fibers.

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Animal models have demonstrated that tinnitus is a pathology of dysfunctional excitability in the central auditory system, in particular in the dorsal cochlear nucleus (DCN) of the brainstem. We used a murine model and studied whether acoustic over-exposure leading to hearing loss and tinnitus, affects long-term potentiation (LTP) at DCN multisensory synapses. Whole cell and field potential recordings were used to study the effects on release probability and synaptic plasticity, respectively in brainstem slices. Shifts in hearing threshold were quantified by auditory brainstem recordings, and gap-induced prepulse inhibition of the acoustic startle reflex was used as an index for tinnitus. An increased release probability that saturated LTP and thereby induced metaplasticity at DCN multisensory synapses, was observed 4–5 days following acoustic over-exposure. Perfusion of an NMDA receptor antagonist or decreasing extracellular calcium concentration, decreased the release probability and restored LTP following acoustic over-exposure. In vivo administration of magnesium-threonate following acoustic over-exposure restored LTP at DCN multisensory synapses, and reduced gap detection deficits observed four months following acoustic over-exposure. These observations suggest that consequences of noise-induced metaplasticity could underlie the gap detection deficits that follow acoustic over-exposure, and that early therapeutic intervention could target metaplasticity and alleviate tinnitus.

This study sets out to evaluate the effectiveness of transcutaneous electrical nerve stimulation (TENS) in the management of calf muscle spasticity in children with cerebral palsy. The study follows a one group pre-test–post-test design involving fifteen children with spastic cerebral palsy, presenting with calf muscle spasticity. Spasticity was assessed before and after a 30 min application of TENS to the bilateral calf muscles. The H-reflex (electromyography) of the calf muscles and Modified Ashworth Scale (MAS) served as a measure of spasticity. A goniometer was used to measure the range of motion (ROM) angles for ankle dorsiflexion. We report here no significant difference (p > 0.05) between the left and right H-reflex responses, MAS scores, and ROM scores recorded at baseline (pre-test). Correlation analysis show no correlation (p > 0.05) between the pre-test HA Max (maximum H-reflex amplitude)/MA Max (maximum M-Wave Amplitude) ratio and MAS scores of both the left and right calf muscles. However, TENS significantly reduced (p < 0.05) the HA of the left calf muscle and MAS scores of the left and right calf muscles. Additionally, TENS significantly increased the ROM scores of the left and right calf muscles. Our findings lend support to existing evidence that TENS is effective in reducing spasticity. The potential mechanism underlying this effect is a reduction in neuron excitability.