Irvine D R, Rajan R
Department of Psychology, Monash University, Clayton, Vic., Australia.
Acta Otolaryngol Suppl. 1997;532:39-45. doi: 10.3109/00016489709126143.
Restricted cochlear lesions in adult animals, causing partial deafness, result in a reorganization of primary auditory cortex (AI) such that the region deprived of its normal input by the lesion is occupied by an expanded representation of peri-lesion cochlear regions, and hence of peri-lesion frequencies. One possible mechanism underlying the change in frequency responsiveness involved in such reorganization is that inputs to the cortical neurons at frequencies at and near their "new" post-lesion characteristic frequencies (CFs) are normally present but suppressed by inhibition, and are "unmasked" by the effects of the lesion. Evidence in support of this explanation is provided by two-tone forward-masking experiments which reveal that many AI neurons receive surround inhibitory input. When input to such neurons at their CF is reduced by an intense temporary-threshold-shift (TTS)-inducing stimulus, the response areas of some neurons expand into the region of their inhibitory surrounds, the effect that would be expected if unmasking were involved in cortical reorganization. In other neurons, however, response areas contracted after the TTS-inducing stimulation. Although unmasking of normally-inhibited inputs is likely to contribute to auditory cortical reorganization, the immediate unmasking that is seen in visual and somatosensory systems is unlikely to play a major role in auditory cortical reorganization, as no evidence of immediate unmasking was seen following acute cochlear lesions in guinea pigs.
成年动物中导致部分失聪的局限性耳蜗损伤会引起初级听觉皮层(AI)的重组,使得因损伤而失去正常输入的区域被损伤周围耳蜗区域(以及损伤周围频率)的扩大表征所占据。这种重组所涉及的频率反应性变化的一种可能机制是,皮层神经元在其“新的”损伤后特征频率(CF)及附近频率的输入通常存在,但被抑制所压制,并且因损伤的影响而“去抑制”。支持这一解释的证据来自双音前掩蔽实验,该实验表明许多AI神经元接受周围抑制性输入。当通过强烈的诱发暂时性阈移(TTS)的刺激降低此类神经元在其CF的输入时,一些神经元的反应区域会扩展到其抑制性周围区域,这是如果去抑制参与皮层重组所预期的效果。然而,在其他神经元中,诱发TTS的刺激后反应区域缩小。虽然对正常被抑制输入的去抑制可能有助于听觉皮层重组,但在视觉和体感系统中所见的即时去抑制不太可能在听觉皮层重组中起主要作用,因为在豚鼠急性耳蜗损伤后未见到即时去抑制的证据。