听觉部分丧失同时会伴随听觉过敏，即对较大的、甚或中等程度的声音灵敏度增强。这是有点儿矛盾的现象，其机制尚不清楚，而这种现象的确是由声音造成的痛苦，就像创伤性声音对听觉正常的人所造成的痛苦一样。
现在，在分离出的大鼠耳蜗中用千兆欧姆封接光纤内记录及燃料标记方法所做实验，确定长期很神秘的II型耳蜗传入神经元为指示创伤性声音的一个潜在通道。这些神经元从耳蜗外毛细胞接收突触输入，并以与体细胞C-纤维相似的方式被ATP激发（ATP已知在组织损伤期间会被释放出来）。在音量很高的创伤性声音下，毛细胞活动与所释放的ATP相结合，可能会为这些在解剖学上比较独特的II型耳蜗传入神经元提供充分“刺激”。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 461, 1126-1129 (22 October 2009) | doi:10.1038/nature08487
The postsynaptic function of type II cochlear afferents
Catherine Weisz1, Elisabeth Glowatzki1,2 & Paul Fuchs1,2
1 The Department of Neuroscience,
2 The Department of Otolaryngology-Head and Neck Surgery, The Center for Hearing and Balance and the Center for Sensory Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
4 Correspondence to: Paul Fuchs1,2 Correspondence and requests for materials should be addressed to P.F.
The mammalian cochlea is innervated by two classes of sensory neurons. Type I neurons make up 90–95% of the cochlear nerve and contact single inner hair cells to provide acoustic analysis as we know it. In contrast, the far less numerous type II neurons arborize extensively among outer hair cells (OHCs)1, 2 and supporting cells3, 4. Their scarcity and smaller calibre axons have made them the subject of much speculation, but little experimental progress for the past 50 years. Here we record from type II fibres near their terminal arbors under OHCs to show that they receive excitatory glutamatergic synaptic input. The type II peripheral arbor conducts action potentials, but the small and infrequent glutamatergic excitation indicates a requirement for strong acoustic stimulation. Furthermore, we show that type II neurons are excited by ATP. Exogenous ATP depolarized type II neurons, both directly and by evoking glutamatergic synaptic input5. These results prove that type II neurons function as cochlear afferents, and can be modulated by ATP. The lesser magnitude of synaptic drive dictates a fundamentally different role in auditory signalling from that of type I afferents.
