ArticleThe Journal of physiology2023
Increased pyramidal and VIP neuronal excitability in rat primary auditory cortex directly correlates with tinnitus behaviour.
Article in The Journal of physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Synaptic zinc plasticity shapes adaptive and maladaptive cortical plasticity following cochlear injury.Science advances · 2026Article
- A primary auditory cortex-anterior cingulate cortex circuit underlying cross-modal visceral pain modulation.Nature communications · 2026Article
- Application of neurodegenerative disease treatment strategies in tinnitus: mechanisms, translation, and prospects.Frontiers in aging neuroscience · 2026Review
- Case Report: Repeated courses of low-frequency rTMS for refractory tinnitus: an N-of-1 study.Frontiers in psychiatry · 2026Article
- Objective autonomic signatures of tinnitus and sound sensitivity disorders.Science translational medicine · 2025Article
- Association between obstructive sleep apnea and Tinnitus in the United States: NHANES 2005-2020.Sleep & breathing = Schlaf & Atmung · 2025Article
- Personalized Sound Therapy Combined with Low and High-Frequency Electromagnetic Stimulation for Chronic Tinnitus.Journal of personalized medicine · 2024Article
- Desensitizing nicotinic agents normalize tinnitus-related inhibitory dysfunction in the auditory cortex and ameliorate behavioral evidence of tinnitus.Frontiers in neuroscience · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Tinnitus affects roughly 15%-20% of the population while severely impacting 10% of those afflicted. Tinnitus pathology is multifactorial, generally initiated by damage to the auditory periphery, resulting in a cascade of maladaptive plastic changes at multiple levels of the central auditory neuraxis as well as limbic and non-auditory cortical centres. Using a well-established condition-suppression model of tinnitus, we measured tinnitus-related changes in the microcircuits of excitatory/inhibitory neurons onto layer 5 pyramidal neurons (PNs), as well as changes in the excitability of vasoactive intestinal peptide (VIP) neurons in primary auditory cortex (A1). Patch-clamp recordings from PNs in A1 slices showed tinnitus-related increases in spontaneous excitatory postsynaptic currents (sEPSCs) and decreases in spontaneous inhibitory postsynaptic currents (sIPSCs). Both measures could be correlated to the rat's behavioural evidence of tinnitus. Tinnitus-related changes in PN excitability were independent of changes in A1 excitatory or inhibitory cell numbers. VIP neurons, part of an A1 local circuit that can control the excitation of layer 5 PNs via disinhibitory mechanisms, showed significant tinnitus-related increases in excitability that directly correlated with the rat's behavioural tinnitus score. That PN and VIP changes directly correlated to tinnitus behaviour suggests an important role in A1 tinnitus pathology. Tinnitus-related A1 changes were similar to findings in studies of neuropathic pain in somatosensory cortex suggesting a common pathology of these troublesome perceptual impairments. Improved understanding between excitatory, inhibitory and disinhibitory sensory cortical circuits can serve as a model for testing therapeutic approaches to the treatment of tinnitus and chronic pain. KEY POINTS: We identified tinnitus-related changes in synaptic function of specific neuronal subtypes in a reliable animal model of tinnitus. The findings show direct and indirect tinnitus-related losses of normal inhibitory function at A1 layer 5 pyramidal cells, and increased VIP excitability. The findings are similar to what has been shown for neuropathic pain suggesting that restoring normal inhibitory function at synaptic inputs onto A1 pyramidal neurons (PNs) could conceptually reduce tinnitus discomfort.
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