NEURAL BASIS OF AUDIO-VOCAL INTEGRATION

这些研究的长期目标是了解感官 有关环境的信息被转换为运动命令， 引导适应行为。在这种情况下，神经机制 听觉反馈对发声控制的影响 将对哺乳动物的中枢神经系统进行研究。焦点放在 脑内某些神经元(VOC抑制神经元)的意义 听觉反馈控制的中脑半球旁被盖 清醒的马蹄蝙蝠发出的声音。这些蝙蝠准确地 通过听觉控制其回声定位呼叫的频率 蝙蝠休息时(休息频率)和休息时的反馈 频移回波信号的飞行和补偿(多普勒频移 补偿行为)。以往的研究表明，VOC抑制 丘脑旁被盖中的神经元在大脑中起重要作用 通过抑制性听觉控制发声频率 反馈机制。这一假设将通过使用 在以前的研究中被证明是成功的实验方法 另一种脊椎动物行为的感觉-运动控制 电鱼的回避反应。具体地说：(1)将进行测试 丘脑旁VOC抑制神经元是否积极参与 静止频率和多普勒频移补偿的控制 行为。为此，包含这些神经元的区域将是 从立体定位学和电生理学的角度确定，然后是VOC- 抑制神经元将被GABA激动剂可逆灭活 麝香酚(GABA-A，R(+))百氯芬(GABA-B)和反式-4-氨基甲酸 (GABAC)，而静息频率和多普勒频移 薪酬行为受到监控。(2)将确定是否 VOC抑制神经元通过抑制的方式提供听觉反馈 或者是兴奋机制。这将通过刺激VOC来实现- 谷氨酸激动剂NMDA、AMPA和Kainic对神经元的抑制作用 酸，同时监测谷氨酸激动剂的作用 在发声频率上进行注射。如果音频-声音反馈是 抑制，刺激，从而增加神经元的活性应该 降低静息和多普勒频移时发出的发声频率 如果反馈是激励性的，他们应该增加薪酬。 这些研究的结果将提供对神经的新见解。 听觉-发声控制机制在清醒、行为中的实现 动物，还可以提供一种更好地理解各种 人声基本参数的故障，如语音信号的变化 聋人说话时的基频。

The long-term goal of these studies is to understand how sensory information about the environment is transformed into motor commands that guide adaptive behavior. In this context, the neural mechanisms underlying the control of vocalization in response to auditory feedback in the mammalian central nervous system will be investigated. Focus is on the significance of certain neurons (VOC-inhibition neurons) situated in the midbrain paralemniscal tegmentum for auditory feedback control of vocalizations in awake, behaving horseshoe bats. These bats accurately control the frequency of their echolocation calls through auditory feedback both when the bat is at rest (resting frequency) and when it is flying and compensating for frequency-shifted echo signals (Doppler-shift compensation behavior). Previous studies suggest that VOC-inhibition neurons in the paralemniscal tegmentum play an important role in the control of vocalization frequencies through an inhibitory auditory feedback mechanism. This hypothesis will be verified by employing an experimental approach that proved to be successful in previous studies on the sensory-motor control of another vertebrate behavior, the "Jamming Avoidance Response" in electric fish. Specifically: (1) It will be tested whether paralemniscal VOC-inhibition neurons are actively involved in the control of the resting frequency and of Doppler-shift compensation behavior. For that purpose, the region containing these neurons will be identified stereotaxically and electrophysiologically and then VOC- inhibition neurons will be reversibly inactivated with the GABA agonists Muscimol (GABA-A, R(+)Baclofen (GABA-B), and trans-4-aminocrotonic acid (GABAC), respectively, while the resting frequency and the Doppler-shift compensation behavior are monitored. (2) It will be determined whether VOC-inhibition neurons provide auditory feedback by means of an inhibitory or excitatory mechanism. This will be achieved by stimulating VOC- inhibition neurons with the Glutamate agonists NMDA, AMPA, and Kainic acid, respectively, while monitoring the effects of glutamate agonist injections on the vocalization frequency. If audio-vocal feedback is inhibitory, stimulation and thus increasing neuronal activity should decrease vocalization frequencies emitted at rest and during Doppler-shift compensation while they should increase if the feedback is excitatory. The results of these studies will provide new insights into the neural implementation of audio-vocal control mechanisms in awake, behaving animals and could also provide an approach to better understand various malfunctions of basic parameters of human voice, such as changes in the fundamental frequency that occur in speaking deaf humans.