Loudness hyperacusis is common in autistic children and adults. The symptoms of loudness hyperacusis are thought to be generated by a pathological increase in central auditory gain. However, there remains unknown why increased sound-evoked activity in the auditory cortex occur in autism. It is well-known that transient early expression of serotonin transporter in glutamatergic thalamocortical projection neurons regulate sensory map elaboration in the barrel cortex in mice. In addition, in thalamic neuron-specific serotonin transporter knockout mice, hyperserotonin conditions cause the reduction of somatostatin-expressing GABAergic neurons.

Serotonin transporter is also expressed in the medial geniculate body from E12 to P10 in the rat brain, and this period coincides with geniculocortical projections. In addition, hyperserotonin conditions in the developing brain are frequently seen in autism. Taken together, we propose the following hypothesis; (1) Hyperserotonin conditions in the developing brain frequently occur in autism patients. (2) These hyperserotonin conditions induce the reduction of GABA neurons in auditory cortex. (3) This reduction of inhibitory neurons in auditory cortex causes hyperacusis in autism patients.