响度听觉过敏在自闭症儿童和成人中很常见。响度听觉过敏的症状被认为是由中枢听觉增益的病理性增加引起的。然而，自闭症患者听觉皮层中声音诱发活动增加的原因尚不清楚。众所周知，谷氨酸能丘脑皮质投射神经元中血清素转运蛋白的瞬时早期表达调节小鼠桶状皮层中的感觉图制作。此外，在丘脑神经元特异性血清素转运蛋白敲除小鼠中，血清素水平过高会导致表达生长抑素的 GABA 能神经元减少。
5-羟色胺转运蛋白也在大鼠大脑中从 E12 到 P10 的内侧膝状体中表达，这一时期与膝状皮质投射相吻合。此外，发育中的大脑中的高血清素状况在自闭症中也很常见。综上所述，我们提出以下假设；(1) 发育中的大脑中的高血清素状况经常发生在自闭症患者身上。(2) 这些高血清素条件诱导听觉皮层中 GABA 神经元的减少。(3) 听觉皮层中抑制性神经元的减少导致自闭症患者的听觉过敏。
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.
