The tympanograms were type A, LY2835219 indicating normal function of the middle ear and Eustachian tube. Recruitment was revealed in the subjects by the lower dynamic range between hearing and stapedial acoustic reflex thresholds, which indicated that the lesions were in cochlea. The patients had absent distortion-product otoacoustic emissions at all frequencies, while auditory brainstem responses were present with normal inter-peak latencies. These results demonstrate that the nonlinear compression function of the cochlea was impaired and suggest that the lesion was near the outer hair cells. The TECTA gene encodes the a-tectorin protein in the striated sheet matrix, whereas the TM is an acellular gelatinous structure that contacts the hair cells in the organ of Corti; therefore, mutation of the TECTA gene leads to hearing loss. Worldwide, of the 33 reported DFNA8/12 mutations, only 4 have been observed in multiple unrelated families. It is difficult to research ADNSHL in depth because of the cost and time involved. In the past few years, NGS technologies have made great strides in both basic and clinical research, providing deeper insights into the complex genomic landscapes of many diseases. Due to the high genetic heterogeneity of hearing loss, targeted DNA capture and MPS appear to be ideal tools for investigating this disease. Dopamine is an important catecholamine neurotransmitter implicated in physiological functions. Abnormal neurotransmission of dopamine can lead to numerous neurological disorders, such as Parkinson’s disease. Studies on dopamine regulation have shown that PC12 cells, a rat pheochromocytoma cell line, synthesize, release, and reuptake dopamine in a manner similar to that of dopaminergic neurons. Compared to brain neuron cultures or tissue slices, PC12 cell culture consists of a homogeneous dopamine-containing population, which had been widely used in dopaminergic cell investigations, including those on cell differentiation, neural protection, drug screening, and cell implantation therapies. Conventional approaches for regulating dopamine release in PC12 cells are pharmaceutical or electrical stimulation techniques, which have critical limitation on controlling dopamine release. Pharmaceutical stimulation such as KCl solution has poor temporal resolution and untargetable regulation of dopamine release from PC12 cells. Few studies have used ES for dopamine release because crosstalk and imprecise stimulation site control might result in controversial outcomes. Among them, only some studies have demonstrated the inhibition effect of ES on dopamine release. These limitations restrict the application of dopamine release from PC12 cells as a precise cellular model for dopamine regulation. Optogenetic stimulation approach that uses channelrhodopsin-2 has been developed for providing more precise and targeted stimulation effect on cells.