Synaptic zinc plasticity shapes adaptive and maladaptive cortical plasticity following cochlear injury.

Summary

Noise-induced cochlear damage triggers bidirectional synaptic zinc signaling plasticity in the primary auditory cortex, potentiating excitatory neurons and parvalbumin (PV) interneurons while suppressing somatostatin interneurons. This same zinc-driven plasticity underlies both the beneficial restoration of sound-detection thresholds and the harmful cortical hyperactivity linked to tinnitus and hyperacusis, identifying synaptic zinc signaling as a candidate drug target.

Key findings

• Cochlear injury triggers bidirectional synaptic zinc plasticity in auditory cortex.
• Zinc plasticity potentiates excitatory and PV-interneuron activity while suppressing somatostatin-interneuron activity.
• The same mechanism both restores sound-detection thresholds (adaptive) and drives the hyperactivity linked to tinnitus/hyperacusis (maladaptive).
• Identifies synaptic zinc signaling as a candidate therapeutic target.