NEURAL BASIS OF AUDIO-VOCAL INTEGRATION

这些研究的长期目标是了解感官 关于环境的信息被转换成运动指令， 引导适应行为。 在这种情况下，神经机制 作为对听觉反馈的发声控制的基础， 将研究哺乳动物的中枢神经系统。 重点是 某些神经元（VOC抑制神经元）位于 中脑听觉系被盖对听觉反馈的控制 清醒的马蹄蝙蝠发出的声音 这些蝙蝠准确地 通过听觉控制回声定位的频率 反馈时，蝙蝠是在休息（休息频率），当它是 飞行和补偿频移回波信号（多普勒频移 补偿行为）。 以前的研究表明，VOC抑制 中脑系被盖区的神经元在神经元的活动中起着重要的作用。 通过抑制性听觉控制发声频率 反馈机制 这一假设将通过采用 实验方法，证明是成功的，在以前的研究， 另一种脊椎动物行为的感觉运动控制， 电鱼中的“回避反应”。 具体而言：（1）将进行测试 中脑系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被 确定立体定位和电生理，然后VOC- 抑制神经元将被GABA激动剂可逆地失活 蝇蕈醇（GABA-A，R（+）巴氯芬（GABA-B）和反式-4-氨基巴豆酸 （GABAC），分别，而静息频率和多普勒频移 补偿行为受到监控。 (2)将决定是否 VOC抑制神经元通过抑制性的听觉反馈提供听觉反馈。 或兴奋机制。 这将通过刺激VOC来实现- 抑制神经元与谷氨酸激动剂NMDA，AMPA，和红藻氨酸 酸，同时监测谷氨酸受体激动剂的作用， 对发声频率进行注射如果声音反馈是 抑制、刺激并因此增加神经元活性， 减少在休息时和多普勒频移期间发出的发声频率 如果反馈是兴奋性的，则它们应该增加。 这些研究的结果将提供新的见解神经 在清醒、行为、 动物，也可以提供一种方法，以更好地了解各种 人的声音的基本参数的故障，如在 基本频率，发生在说话的聋人身上。

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.