Effects of acetylcholine and atropine on plasticity of central auditory neurons caused by conditioning in bats
Effects of acetylcholine and atropine on plasticity of central auditory neurons caused by conditioning in bats
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DOI：
10.1152/jn.2001.86.1.211
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发表时间：
2001-07-01
影响因子：
2.5
通讯作者：
Suga, NB
中科院分区：
文献类型：
--
作者：
Ji, WQ;Gao, EQ;Suga, NB
在大褐蝠（Eptesicus fuscus）中，先用声刺激进行条件反射，然后再进行腿部电刺激，会导致丘和皮层神经元的频率调谐曲线和最佳频率（以下简称BF移位）发生变化，即下丘（IC）和听觉皮层（AC）的耳蜗异位（频率）图发生重组。在调理后180 min，胶原蛋白移位恢复，但皮质蛋白移位持续时间超过26 h。胶原蛋白移位不是由调理引起的，因为在调理过程中AC被灭活。综上所述，脑枕部移位是由皮质听觉系统引起的。由于体感觉皮层在条件反射过程中失活，因此，枕状和皮层的BF移位都不是由条件反射引起的。因此，我们假设皮层的BF移位主要是由皮层下（如丘脑）BF移位和非听觉系统的活动引起的，如无条件的腿部刺激和胆碱能基底前脑激发的体感皮层。我们目前研究的主要目的是检验乙酰胆碱（ACh）是否能增强由条件反射引起的脑皮层和脑皮层的BF位移，以及阿托品是否能消除脑皮层的BF位移，但不能消除脑皮层的BF位移，这与之前的假设是一样的。在清醒的蝙蝠中，我们有以下发现。乙酰胆碱不仅通过皮质系统增强皮层脑区脑区移位，而且还增强了脑区的脑区移位。阿托品应用于AC可减少胶原蛋白移位，消除皮质蛋白移位。应用于IC的ACh显著增加了collcollal BF移位，但对皮质BF移位的影响很小。乙酰胆碱可使皮质BF位移持续4 h以上，但不能使collcollal BF位移持续3 h以上。它减少了皮质BF移位，但没有消除它。我们的研究结果支持这样的假设：脑皮层系统引起的脑皮层移位，以及基底前脑引起的交流电中乙酰胆碱水平的增加，都是脑皮层持久脑皮层移位的必要条件。
In the big brown bat (Eptesicus fuscus), conditioning with acoustic stimuli followed by electric leg-stimulation causes shifts in frequency-tuning curves and best frequencies (hereafter BF shifts) of collicular and cortical neurons, i.e., reorganization of the cochleotopic (frequency) maps in the inferior colliculus (IC) and auditory cortex (AC). The collicular BF shift recovers 180 min after the conditioning, but the cortical BF shift lasts longer than 26 h. The collicular BF shift is not caused by conditioning, as the AC is inactivated during conditioning. Therefore it has been concluded that the collicular BF shift is caused by the corticofugal auditory system. The collicular and cortical BF shifts both are not caused by conditioning as the somatosensory cortex is inactivated during conditioning. Therefore it has been hypothesized that the cortical BF shift is mostly caused by both the subcortical (e.g., collicular) BF shift and the activity of nonauditory systems such as the somatosensory cortex excited by an unconditioned leg-stimulation and the cholinergic basal forebrain. The main aims of our present studies are to examine whether acetylcholine (ACh) applied to the AC augments the collicular and cortical BF shifts caused by the conditioning and whether atropine applied to the AC abolishes the cortical BF shift but not the collicular BF shift, as expected from the preceding hypothesis. In the awake bat, we made the following findings. ACh applied to the AC augments not only the cortical BF shift but also the collicular BF shift through the corticofugal system. Atropine applied to the AC reduces the collicular BF shift and abolishes the cortical BF shift which otherwise would be caused. ACh applied to the IC significantly augments the collicular BF shift but affects the cortical BF shift only slightly. ACh makes the cortical BF shift long-lasting beyond 4 h, but it cannot make the collicular BF shift long-lasting beyond 3 h. Atropine applied to the IC abolishes the collicular BF shift. It reduces the cortical BF shift but does not abolish it. Our findings favor the hypothesis that the BF shifts evoked by the corticofugal system, and an increased ACh level in the AC evoked by the basal forebrain are both necessary to evoke a long-lasting cortical BF shift.