鸣唱行为是鸣禽特有的一类复杂行为，必须经后天学习而获得，并且高度依赖于听觉经验。对鸣禽鸣唱行为的研究将为人类语言，以及人类复杂认知行为的神经机制的研究提供有价值的参考。临界型鸣禽斑胸草雀（Taeniopygia guttata）和白腰文鸟（Lonchura domestica）在成年后仍需要听觉反馈来维持其正常的鸣唱，致聋将会导致其正常鸣声发生退化。目前，对于成年鸣禽致聋后鸣唱退化的神经机制的研究还非常匮乏，通过研究致聋对神经系统的影响将深化我们对听觉与发声的整合机制的理解。GABA是脊椎动物脑中存在最广泛的抑制性神经递质，参与到鸣禽发声的感觉和运动过程中，在经验依赖的可塑性中发挥重要作用。GABA(A)受体是GABA的一类重要受体，在鸣唱的产生和学习过程中发挥重要的调节作用。GAD67（谷氨酸脱羧酶），是合成GABA的一种关键的限速酶，它是GABA能神经元的一种特异标志物。为了更深入地从分子生物学水平研究致聋对鸣唱行为和神经系统的影响，本实验选择了这几种广泛参与到鸣唱过程中的分子GABA、GABA(A)受体以及GAD67，研究致聋对这三者在成年雄性白腰文鸟听觉发声相关核团中表达的影响，以期为揭示听觉反馈与鸣唱控制之间的内在机制提供线索。原位杂交实验检测了GAD67mRNA在听觉发声控制核团中的表达情况，免疫组织化学方法检测了GABA、GABA(A)受体和GAD67在上述核团中的蛋白水平表达变化。结果表明：1、耳蜗摘除对成年雄性白腰文鸟耳蜗核（NM）影响显著，使核团体积减小、神经元密度升高和神经元直径变小；2、GAD67蛋白和mRNA的表达基本一致；3、GABA、GABA(A)受体和GAD67的表达存在相似的空间特征；4、致聋后白腰文鸟听觉核团（MLd、Ov）中GABA和GABA(A)受体的阳性标记细胞密度增加，而在发声运动核团（HVC、RA）中GABA和GABAAR的阳性标记细胞密度减少。致聋引起的GABA、GABA(A)受体和GAD67在白腰文鸟听觉发声系统中的表达变化说明了GABA确实参与了致聋引起的发声可塑性调节。

Birdsong is an intricate and learned behavior, relying on auditory experience in development. The studies of birdsong behavior provide us a valuable reference in developing general principles that contribute to human speech and human complex cognitive behavior. Auditory feedback is necessary to maintain the stability of adult songs in zebra finches (Taeniopygia guttata) and Bengalese finches (Lonchura domestica). Removal of auditory feedback by deafening can make the singing behavior degrade dramatically. This suggests that the mature auditory and vocal system keep exchanging information actively. However, few data are available concerning the neural mechanism of the deterioration of the songs of adult songbird. We attempt to reveal the neural mechanisms behind this behavior changes. We focused on three molecules: GABA (γ-aminobutyric acid), GABA(A)receptor and GAD67(Glutamic acid decarboxylase). GABA is the main inhibitory neurotransmitter in the vertebrate brain. It is believed to play a role in experience-dependent plasticity. GABA(A)receptor is the member of the ligand-gated ion channel superfamily; GABA(A)receptor-mediated inhibition has been implicated in both sensory and motor aspects of vocalizations in songbird. GAD67, which is the rate-limiting enzyme that synthesize transmitter GABA, is a specific GABAergic marker. GAD67 mRNA is quantified in the auditory and vocal system using in situ hybridization; GABA, GABAAR and GAD67 protein were detected by immunohistochemistry methods. Our data showed that deafening induced the reduction in the volume and cell size of NM and the increment in the positive cell density in NM. There were similar expression patterns of GABA, GABAAR and GAD67 within auditory and vocal system of adult Bengalese finch brain. After surgical Cochlea ablation, there was an increase of GABA and GABAAR expression in the auditory nuclei (MLd and Ov), while their expression decreased strongly in the vocal motor pathway (HVC and RA). On the whole, the GAD67 mRNA expression was consistent with the protein. Thus, the changes of GABA, GABAAR and GAD67 expression induced by deafening suggested that GABA played a critical role in vocal plasticity by deafness.