Neuromodulation : journal of the International Neuromodulation Society · 2026
Auditory Cortex Photobiomodulation Ameliorates Tinnitus-like Behavior by Reversing Synaptic Excitation/Inhibition Imbalance in Mice.
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Zhang Zhixin, Wu Zongyi, He Dongdong, Zhang Chi, Xue Xinmiao, Liu Peng, Jiang Yvke, Lv Shuhan, Yang Shuzhi, Diao Mingfang, Zhao Danheng, Zhao Pengjv, Zhu Li, Shen Weidong, Yang Shiming, Wang Fangyuan
Аннотация
OBJECTIVES: To investigate whether transcranial photobiomodulation (PBM) targeting the auditory cortex can ameliorate noise-induced tinnitus-like behavior in mice by reversing synaptic excitation/inhibition (E/I) imbalance.
MATERIALS AND METHODS: A noise-induced tinnitus mouse model was established (116 dB SPL, 1 h). Tinnitus-like behavior was assessed using gap prepulse inhibition (PPI) of acoustic startle (Gap-PPI), with PPI as a control for sensorimotor gating. Auditory brainstem responses (ABR) were recorded to evaluate peripheral hearing. Immunohistochemistry was performed to quantify c-Fos, GluN1, and GABAA R-α1 expression in the auditory cortex, including colocalization analysis within activated neurons. Transcranial PBM (830 nm, 40 mW/cm2) was delivered to the auditory cortex. The nonthermal nature of PBM was confirmed by intracerebral temperature monitoring and optical transmission measurements.
RESULTS: PBM at 40 mW/cm2 penetrated the skull with negligible optical drift and induced <0.5 °C brain temperature rise, confirming nonthermal neuromodulation. Noise exposure selectively reduced Gap-PPI ratio without affecting PPI, indicating tinnitus-like behavior. ABR thresholds showed mid-to-high frequency hearing loss that was not reversed by PBM. In tinnitus mice, auditory cortex exhibited increased c-Fos+ cells, upregulation of GluN1 and downregulation of GABAA R-α1 specifically within c-Fos+ neurons, reflecting E/I imbalance and hyperexcitability. A single session of PBM rapidly (from day four) and sustainably (≥28 days) alleviated tinnitus-like behavior, reversed the molecular alterations, and restored coexpression ratios of GluN1 and GABAA R-α1 in activated neurons. Sham-PBM had no effect. Linear regression confirmed significant correlations between receptor coexpression and Gap-PPI (GluN1: negative; GABAA R-α1: positive).
CONCLUSIONS: Auditory cortex E/I imbalance driven by neuron-subtype-specific changes in GluN1 and GABAA R-α1 underlies noise-induced tinnitus-like behavior. Targeted transcranial PBM reverses these molecular alterations, restores local circuit balance, and provides rapid, sustained behavioral improvement without affecting peripheral hearing or sensorimotor gating. PBM represents a promising noninvasive neuromodulation strategy for tinnitus.
MATERIALS AND METHODS: A noise-induced tinnitus mouse model was established (116 dB SPL, 1 h). Tinnitus-like behavior was assessed using gap prepulse inhibition (PPI) of acoustic startle (Gap-PPI), with PPI as a control for sensorimotor gating. Auditory brainstem responses (ABR) were recorded to evaluate peripheral hearing. Immunohistochemistry was performed to quantify c-Fos, GluN1, and GABAA R-α1 expression in the auditory cortex, including colocalization analysis within activated neurons. Transcranial PBM (830 nm, 40 mW/cm2) was delivered to the auditory cortex. The nonthermal nature of PBM was confirmed by intracerebral temperature monitoring and optical transmission measurements.
RESULTS: PBM at 40 mW/cm2 penetrated the skull with negligible optical drift and induced <0.5 °C brain temperature rise, confirming nonthermal neuromodulation. Noise exposure selectively reduced Gap-PPI ratio without affecting PPI, indicating tinnitus-like behavior. ABR thresholds showed mid-to-high frequency hearing loss that was not reversed by PBM. In tinnitus mice, auditory cortex exhibited increased c-Fos+ cells, upregulation of GluN1 and downregulation of GABAA R-α1 specifically within c-Fos+ neurons, reflecting E/I imbalance and hyperexcitability. A single session of PBM rapidly (from day four) and sustainably (≥28 days) alleviated tinnitus-like behavior, reversed the molecular alterations, and restored coexpression ratios of GluN1 and GABAA R-α1 in activated neurons. Sham-PBM had no effect. Linear regression confirmed significant correlations between receptor coexpression and Gap-PPI (GluN1: negative; GABAA R-α1: positive).
CONCLUSIONS: Auditory cortex E/I imbalance driven by neuron-subtype-specific changes in GluN1 and GABAA R-α1 underlies noise-induced tinnitus-like behavior. Targeted transcranial PBM reverses these molecular alterations, restores local circuit balance, and provides rapid, sustained behavioral improvement without affecting peripheral hearing or sensorimotor gating. PBM represents a promising noninvasive neuromodulation strategy for tinnitus.