Brain changes in response to nerve damage or cochlear trauma can generate pathological neural activity that is believed to be responsible for many types of chronic pain and tinnitus1–3. Several studies have reported that the severity of chronic pain and tinnitus is correlated with the degree of map reorganization in somatosensory and auditory cortex, respectively1,4. Direct electrical or transcranial magnetic stimulation of sensory cortex can temporarily disrupt these phantom sensations5. However, there is as yet no direct evidence for a causal role of plasticity in the generation of pain or tinnitus. Here we report evidence that reversing the brain changes responsible can eliminate the perceptual impairment in an animal model of noise-induced tinnitus. Exposure to intense noise degrades the frequency tuning of auditory cortex neurons and increases cortical synchronization. Repeatedly pairing tones with brief pulses of vagus nerve stimulation completely eliminated the physiological and behavioural correlates of tinnitus in noise-exposed rats. These improvements persisted for weeks after the end of therapy. This method for restoring neural activity to normal may be applicable to a variety of neurological disorders.
Background Individuals with communication disorders, such as aphasia, exhibit weak auditory cortex responses to speech sounds and language impairments. Previous studies have demonstrated that pairing vagus nerve stimulation (VNS) with tones or tone trains can enhance both the spectral and temporal processing of sounds in auditory cortex, and can be used to reverse pathological primary auditory cortex (A1) plasticity in a rodent model of chronic tinnitus. Objective/Hypothesis We predicted that pairing VNS with speech sounds would strengthen the A1 response to the paired speech sounds. Methods The speech sounds ‘rad’ and ‘lad’ were paired with VNS three hundred times per day for twenty days. A1 responses to both paired and novel speech sounds were recorded twenty four hours after the last VNS pairing session in anesthetized rats. Response strength, latency and neurometric decoding were compared between VNS speech paired and control rats. Results Our results show that VNS paired with speech sounds strengthened the auditory cortex response to the paired sounds, but did not strengthen the amplitude of the response to novel speech sounds. Responses to the paired sounds were faster and less variable in VNS speech paired rats compared to control rats. Neural plasticity that was specific to the frequency, intensity, and temporal characteristics of the paired speech sounds resulted in enhanced neural detection. Conclusion VNS speech sound pairing provides a novel method to enhance speech sound processing in the central auditory system. Delivery of VNS during speech therapy could improve outcomes in individuals with receptive language deficits.
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