首页> 外文期刊>Journal of Neurophysiology >Augmentation of Plasticity of the Central Auditory System by the Basal Forebrain and/or Somatosensory Cortex.
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Augmentation of Plasticity of the Central Auditory System by the Basal Forebrain and/or Somatosensory Cortex.

机译:基底前脑和/或体感皮层增强中央听觉系统的可塑性。

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Auditory conditioning (associative learning) or focal electric stimulation of the primary auditory cortex (AC) evokes reorganization (plasticity) of the cochleotopic (frequency) map of the inferior colliculus (IC) as well as that of the AC. The reorganization results from shifts in the best frequencies (BFs) and frequency-tuning curves of single neurons. Since the importance of the cholinergic basal forebrain for cortical plasticity and the importance of the somatosensory cortex and the corticofugal auditory system for collicular and cortical plasticity have been demonstrated, Gao and Suga proposed a hypothesis that states that the AC and corticofugal system play an important role in evoking auditory collicular and cortical plasticity and that auditory and somatosensory signals from the cerebral cortex to the basal forebrain play an important role in augmenting collicular and cortical plasticity. To test their hypothesis, we studied whether the amount and the duration of plasticity of both collicular and cortical neurons evoked by electric stimulation of the AC or by acoustic stimulation were increased by electric stimulation of the basal forebrain and/or the somatosensory cortex. In adult big brown bats (Eptesicus fuscus), we made the following major findings. 1) Collicular and cortical plasticity evoked by electric stimulation of the AC is augmented by electric stimulation of the basal forebrain. The amount of augmentation is larger for cortical plasticity than for collicular plasticity. 2) Collicular and cortical plasticity evoked by AC stimulation is augmented by somatosensory cortical stimulation mimicking fear conditioning. The amount of augmentation is larger for cortical plasticity than for collicular plasticity. 3) Collicular and cortical plasticity evoked by both AC and basal forebrain stimulations is further augmented by somatosensory cortical stimulation. 4) A lesion of the basal forebrain tends to reduce collicular and cortical plasticity evoked by AC stimulation. The reduction is small and statistically insignificant for collicular plasticity but significant for cortical plasticity. 5) The lesion of the basal forebrain eliminates the augmentation of collicular and cortical plasticity that otherwise would be evoked by somatosensory cortical stimulation. 6) Collicular and cortical plasticity evoked by repetitive acoustic stimuli is augmented by basal forebrain and/or somatosensory cortical stimulation. However, the lesion of the basal forebrain eliminates the augmentation of collicular and cortical plasticity that otherwise would be evoked by somatosensory cortical stimulation. These findings support the hypothesis proposed by Gao and Suga.
机译:初级听觉皮层(AC)的听觉条件(联想学习)或局灶性电刺激引起下丘脑(IC)和AC的耳蜗(频率)图的重组(可塑性)。重组是由单个神经元的最佳频率(BFs)和频率调谐曲线的移动引起的。由于已经证明了胆碱能基底前脑对皮质可塑性的重要性以及体感皮质和皮质ugul听觉系统对胶质和皮质可塑性的重要性,Gao和Suga提出了一个假设,该假设指出AC和皮质ugugal系统起着重要作用。在诱发听觉胶体和皮质可塑性方面,从大脑皮层到基底前脑的听觉和体感信号在增强胶体和皮质可塑性中起重要作用。为了检验他们的假设,我们研究了通过电刺激基底前脑和/或体感皮层,是否增加了通过交流电刺激或声刺激诱发的神经元和皮质神经元的数量和持续时间。在成年大棕蝙蝠(Eptesicus fuscus)中,我们取得了以下主要发现。 1)交流电刺激诱发的皮质和皮质可塑性通过基底前脑电刺激增强。皮质可塑性的增强量大于胶体可塑性的增强量。 2)模仿恐惧条件的体感皮质刺激增强了AC刺激引起的胶质和皮质可塑性。皮质可塑性的增强量大于胶体可塑性的增强量。 3)体感皮层刺激进一步增强了AC和基底前脑刺激引起的胶质和皮层可塑性。 4)基底前脑病变往往会降低AC刺激引起的胶质和皮质可塑性。减少量很小,在统计上对胶束可塑性不明显,但对皮层可塑性却显着。 5)基底前脑病变消除了胶体和皮质可塑性的增强,否则这种增强会由体感皮质刺激引起。 6)重复性听觉刺激引起的胶体和皮质可塑性通过基础前脑和/或体感皮质刺激来增强。但是,基底前脑的病变消除了胶体和皮质可塑性的增强,否则胶体和皮质可塑性会因体感皮质刺激而引起。这些发现支持了高和苏加提出的假设。

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