Dorsal cochlear nucleus

Federal government websites often end in. The site is secure. Tinnitus, the perception of a phantom sound, is a common consequence of damage to the auditory periphery.

The dorsal cochlear nucleus DCN integrates auditory and multisensory signals at the earliest levels of auditory processing. Proposed roles for this region include sound localization in the vertical plane, head orientation to sounds of interest, and suppression of sensitivity to expected sounds. Auditory and non-auditory information streams to the DCN are refined by a remarkably complex array of inhibitory and excitatory interneurons, and the role of each cell type is gaining increasing attention. One inhibitory neuron that has been poorly appreciated to date is the superficial stellate cell. Here we review previous studies and describe new results that reveal the surprisingly rich interactions that this tiny interneuron has with its neighbors, interactions which enable it to respond to both multisensory and auditory afferents. The dorsal cochlear nucleus DCN is an auditory structure unique to mammals, with anatomical, physiological and molecular similarities to the cerebellar cortex and the electrosensory lobe of mormyrid electric fish ELL; Oertel and Young, ; Bell et al. Fusiform principal cells receive auditory input onto their basal dendrites and multisensory input onto their apical dendrites Figure 1.

Dorsal cochlear nucleus

The dorsal cochlear nucleus DCN , also known as the " tuberculum acusticum " is a cortex-like structure on the dorso-lateral surface of the brainstem. Along with the ventral cochlear nucleus VCN , it forms the cochlear nucleus CN , where all auditory nerve fibers from the cochlea form their first synapses. The DCN differs from the ventral portion of the CN as it not only projects to the central nucleus a subdivision of the inferior colliculus CIC , but also receives efferent innervation from the auditory cortex , superior olivary complex and the inferior colliculus. The cytoarchitecture and neurochemistry of the DCN is similar to that of the cerebellum , an important concept in theories of DCN function. The pyramidal cells or giant cells are a major cell grouping of the DCN. These cells are the target of two different input systems. The first system arises from the auditory nerve, and carries acoustic information. The second set of inputs is relayed through a set of small granule cells in the cochlear nucleus. There are also a great number of neighbouring cartwheel cells. This projection overlaps with that of the lateral superior olive LSO in a well-defined manner, [3] where they form the primary excitatory input for ICC type O units. Principal cells in the DCN have very complex frequency intensity tuning curves. Classified as cochlear nucleus type IV cells, [5] the firing rate may be very rapid in response to a low intensity sound at one frequency and then fall below the spontaneous rate with only a small increment in stimulus frequency or intensity. The firing rate may then increase with another increment in intensity or frequency. Type IV cells are excited by wide band noise, and particularly excited by a noise-notch stimulus directly below the cell's best frequency BF. While the VCN bushy cells aid in the location of a sound stimulus on the horizontal axis via their inputs to the superior olivary complex , type IV cells may participate in localization of the sound stimulus on the vertical axis.

Mice were anesthetized by isoflurane inhalation and then decapitated.

Metrics details. The dorsal cochlear nucleus DCN is a region known to integrate somatosensory and auditory inputs and is identified as a potential key structure in the generation of phantom sound perception, especially noise-induced tinnitus. Yet, how altered homeostatic plasticity of the DCN induces and maintains the sensation of tinnitus is not clear. Mice were exposed to loud noise 9—11kHz, 90dBSPL, 1h, followed by 2h of silence , and auditory brainstem responses ABRs and gap prepulse inhibition of acoustic startle GPIAS were recorded 2 days before and 2 weeks after noise exposure to identify animals with a significantly decreased inhibition of startle, indicating tinnitus but without permanent hearing loss. We found that lowering DCN activity in mice displaying tinnitus-related behavior reduces tinnitus, but lowering DCN activity during noise exposure does not prevent noise-induced tinnitus. The origin of tinnitus pathophysiology has been linked to the dorsal cochlear nucleus DCN of the auditory brainstem [ 5 — 9 ]; however, tinnitus generation and perception mechanisms are not well separated and far from completely understood. Noise overexposure is known to alter firing properties of DCN cells [ 10 — 14 ], even after brief sound exposure at loud intensities [ 15 ].

Information travels from the receptors in the organ of Corti of the inner ear cochlear hair cells to the central nervous system, carried by the vestibulocochlear nerve CN VIII. This pathway ultimately reaches the primary auditory cortex for conscious perception. In addition, unconscious processing of auditory information occurs in parallel. In this article, we will discuss the anatomy of the auditory pathway — its components, anatomical course, and relevant anatomical landmarks. The auditory pathway is complex in that divergence and convergence of information happens at different stages. The spiral ganglion houses the cell bodies of the first order neurons ganglion refers to a collection of cell bodies outside the central nervous system.

Dorsal cochlear nucleus

Purpose: Eight lines of evidence implicating the dorsal cochlear nucleus DCN as a tinnitus contributing site are reviewed. We now expand the presentation of this model, elaborate on its essential details, and provide answers to commonly asked questions regarding its validity. Conclusions: Over the past decade, numerous studies have converged to support the hypothesis that the DCN may be an important brain center in the generation and modulation of tinnitus. Although other auditory centers have been similarly implicated, the DCN deserves special emphasis because, as a primary acoustic nucleus, it occupies a potentially pivotal position in the hierarchy of functional processes leading to the emergence of tinnitus percepts. Moreover, because a great deal is known about the underlying cellular categories and the details of synaptic circuitry within the DCN, this brain center offers a potentially powerful model for probing mechanisms underlying tinnitus. Abstract Purpose: Eight lines of evidence implicating the dorsal cochlear nucleus DCN as a tinnitus contributing site are reviewed. Publication types Review.

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Spinal cord injury induces serotonin supersensitivity without increasing intrinsic excitability of mouse V2a interneurons. Tympanic tympanic plexus lesser petrosal otic ganglion Stylopharyngeal branch Pharyngeal branches Tonsillar branches Lingual branches Carotid sinus. In the second, groups of fusiform cells were activated following light exposure in slices taken from mice expressing channelrhodopsin2 ChR2 specifically in fusiform cells, which in turn drove action potentials in SSCs. If so, then the AHP communicated by the fusiform cells might serve to upset such synchronous firing, as shown for AHPs in cerebellar Golgi cells Vervaeke et al. However, in marked contrast to this dense labeling, trigeminal ganglion fibers in the cochlear nucleus were undetectable Figures 4B,D. However, it was clear that these same synapses also released glycine, because an antagonist of GABA A receptors, SR, did not fully eliminate inhibitory transmission, but transmission was blocked by a mixture of SR and strychnine. Cisplatin ototoxicity. Moore et al. Nuclei anterior olfactory nucleus Course olfactory bulb olfactory tract. The other possibility is that the DCX-ir UBCs are mature neurons that have retained the capacity for synaptic plasticity, and that DCX expression is a reflection of that plastic capability. Localization of monoamines in the lower brain stem.

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Prog Brain Res. Although the average response showed a significant decrease in firing frequency upon CNO administration, the modulation appeared bidirectional with 54 unit decreasing and 31 units increasing firing rate Fig. Only somata are represented. Summary of evidence pointing to a role of the dorsal cochlear nucleus in the etiology of tinnitus. The cytoarchitecture and neurochemistry of the DCN is similar to that of the cerebellum , an important concept in theories of DCN function. To test this possibility, we examined the effects of inhibitors and activators of the cAMP pathway on the 5-HT current. Effect of repetitive transcranial magnetic stimulation on auditory function following acoustic trauma. Second, there are somatosensory inputs to the DCN that can modulate spontaneous activity and might mediate the somatic-auditory interactions seen in tinnitus patients. Middleton, J. Auditory system. Nahir, B. Several observations confirmed that labeling with this approach was sufficient to label nearly all ganglionic inputs. Mice were returned to their home cage and left approximately 1 month Fig.