Brain and behavior · 2025
Modulation of Auditory Cortex Activity in Salicylate-Induced Tinnitus Rats via Deep Brain Stimulation of the Inferior Colliculus.
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Akbarnejad Zeinab, Bagherian Kasra, Noorbakhsh Seyed Ali, Jouzdani Ali Fathi, Mahmoudian Saeid, Mirsalehi Marjan, Jafarian Maryam, Mohammadi Ronak, Asghari Alimohamad, Asadpour Abdoreza
Аннотация
BACKGROUND: Tinnitus, a self-reported perceptual disorder, is currently believed to arise from maladaptive plasticity due to reduced sensory input. While deep brain stimulation (DBS) has shown promise in alleviating tinnitus-related behaviors, its effects on neuronal activity remain unclear. This study aimed to evaluate the spontaneous firing rates (SFRs) of the primary auditory cortex (A1) before and after DBS of the external cortex of the inferior colliculus (ECIC) in a rat model of tinnitus.
METHODS: Tinnitus was induced in rats through sodium salicylate injections for 14 consecutive days, while the control group received normal saline injections over the same period. We conducted tinnitus and hearing assessments using the gap pre-pulse inhibition of the acoustic startle (GPIAS) and pre-pulse inhibition (PPI) tests. From day 14, both groups underwent DBS of the ECIC and single unit recordings from the A1.
RESULTS: Before ECIC stimulation, A1 neurons in rats with potential tinnitus exhibited significantly higher spontaneous activity compared to controls. Following ECIC stimulation, the SFRs in the group displaying abnormal GPIAS responses significantly decreased, and the difference between the tinnitus and control groups was no longer significant. Additionally, inter-spike interval (ISI) analysis revealed a higher frequency of short ISIs (<5 ms) in rats with potential tinnitus, which decreased after DBS, aligning with values observed in the control group.
CONCLUSION: ECIC stimulation effectively modulates A1 hyperactivity, highlighting its role in tinnitus pathophysiology. These findings warrant further research into ECIC's role in tinnitus regulation, which could inform future therapeutic interventions and enhance mathematical models of tinnitus mechanisms.
METHODS: Tinnitus was induced in rats through sodium salicylate injections for 14 consecutive days, while the control group received normal saline injections over the same period. We conducted tinnitus and hearing assessments using the gap pre-pulse inhibition of the acoustic startle (GPIAS) and pre-pulse inhibition (PPI) tests. From day 14, both groups underwent DBS of the ECIC and single unit recordings from the A1.
RESULTS: Before ECIC stimulation, A1 neurons in rats with potential tinnitus exhibited significantly higher spontaneous activity compared to controls. Following ECIC stimulation, the SFRs in the group displaying abnormal GPIAS responses significantly decreased, and the difference between the tinnitus and control groups was no longer significant. Additionally, inter-spike interval (ISI) analysis revealed a higher frequency of short ISIs (<5 ms) in rats with potential tinnitus, which decreased after DBS, aligning with values observed in the control group.
CONCLUSION: ECIC stimulation effectively modulates A1 hyperactivity, highlighting its role in tinnitus pathophysiology. These findings warrant further research into ECIC's role in tinnitus regulation, which could inform future therapeutic interventions and enhance mathematical models of tinnitus mechanisms.