Dorsal Cochlear Nucleus Tinnitus Head Injury

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The Dorsal Cochlear Nucleus and Tinnitus

The dorsal cochlear nuleus (DCN) is a brainstem nucleus that receives direct input from the auditory nerve. During noise exposure, spontaneous firing rates in Fusiform cells, the principal output neurons of the DCN, increased. Increased activity is correlated with tinnitus generation. Noise exposure also triggers plastic readjustments in the DCN, which is linked to tinnitus generation.

axonal sprouting

Scientists are beginning to understand how the brain responds to a variety of sounds. Acoustic trauma disrupts the cochlear nucleus’ lateral inhibitory network, which extends across a wide range of frequencies. The increased excitability that results from the damage may result in alterations in transduction and neurotransmitter release. Furthermore, the changes in the brain may also alter the spontaneous activity of auditory nerve cells.

In animal models, the loss of surround inhibition after hearing damage could lead to gain enhancement at frequencies below the region where the cochlear damage occurred. These findings could lead to new ways to treat tinnitus, allowing the researchers to determine which brain pathways may be affected. However, further research is needed to identify which types of brain damage are most common.

evoked FA responses

We analyzed evoked FA responses in patients with tinnitus by comparing bushy cells and fusiform cells. In particular, we found that bushy cells show a higher firing rate and greater increases in RIF slope and peak. Furthermore, we found enhanced correlations between synchronous and spontaneous FA responses. This result confirms previous findings that bushy cells have a greater capacity for perceptual binding.

To further clarify the relation between bushy cell sound-evoked activity and tinnitus, we compared HI with TI. HI, bounded by the geometric BF of unit-pair relative to the TI carriers, did not show any correlation with the corresponding TI. However, HI and evoked synchrony were related to the percent change in non-prepulse startle amplitudes.

ablations of the dorsal cochlear nucleus

Ablations of the dorsal cochlea nucleus for tinnituses target the dorsal part of the DCN. These procedures disrupt major rostral outputs. They have been successfully used in animal models of tinnitus. MRI imaging studies have revealed abnormally elevated spontaneous neural activity in the DCN of animals with tinnitus.

An electrophysiological study showed that the DCN is regulated by activity in ipsilateral cranial nerves. This explains how tinnitus can be modulated by manipulations of the head or neck, and rarely affected by the contralateral side. Several types of neuronal plasticity have been found in the DCN, including increased bursting activity in the primary auditory cortex and the medial geniculate body.

Effect of blast exposure on spontaneous firing rates in the dorsal cochlear nucleus

An increasing body of evidence suggests that blast-induced tinnitus is related to an increase in auditory neural activity. However, the mechanism for the increased activity may not yet be fully understood. The brain regions that are most affected by blast exposure include the cochlea, primary auditory cortex, medial geniculate body, and cochlea.

High-pressure blast shock waves are known to cause tinnitus. The underlying mechanism of tinnitus may be related to damage to the structures of the ear or to direct brain impact. In addition, blast exposure may cause a cascade of neuroplastic changes in the auditory and nonauditory brain regions, and affect spontaneous firing rates in the dorsal cochlear nucleus (DCN). In the present study, we investigated the effect of a single blast on the SFR in rats with tinnitus. We assessed the rats’ behavioral evidence of tinnitus using a gap-detection startle-reflex paradigm. We also measured the SFRs of the rats’ ears three months after blast exposure.

Correlation between synaptophysin and PSD95

The expression of synaptophysin and PSD95 is correlated with the presence of damaged auditory pathways. Synaptophysin and PSD95 are pre and postsynaptic markers. After head injury, both proteins are up-regulated in the auditory cortex, a site of synaptogenesis. The present study also found that PSD95 and synaptophysin expression were elevated in the tinnitus group and decreased in the non-tinnitus group. However, the results were not statistically significant.

The early emergence of tinnitus may be due to a degeneration of cochlear fibers, which altered the structure of the central auditory system. Although the onset of tinnitus was not apparent in all rats at week one, the GPIAS recordings showed that the condition persisted for at least three weeks.

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