Johnson F, Bottjer S W
Department of Biological Sciences, University of Southern California, Los Angeles 90089-2520.
J Neurosci. 1993 Jun;13(6):2452-62. doi: 10.1523/JNEUROSCI.13-06-02452.1993.
A discrete network of forebrain nuclei underlies vocal learning and production in male zebra finches. Three nuclei within this network form a neural pathway that is particularly important for vocal learning in juveniles: area X of the avian striatum projects to the medial dorsolateral nucleus of the anterior thalamus (DLM), which in turn projects to the lateral magnocellular nucleus of the anterior neostriatum (IMAN). Lesions of any of these nuclei in juvenile birds disrupt normal vocal development, whereas the same lesions in adult birds have no effect on already-learned song. Because numerous studies have shown that neuronal survival in the developing nervous system depends on access to efferent targets, we have investigated the possibility that the survival of DLM neurons is similarly regulated over the course of vocal learning. Thus, the efferent target of DLM (IMAN) was lesioned electrolytically in male birds at various stages of vocal development (20, 40, 60 d of age and adult) and birds were killed either 2, 4, or 6 d postlesion. Electrolytic lesions of IMAN removed the single identified efferent target of DLM projection neurons and axotomized the terminal arborizations of these neurons. Although DLM does not normally lose neurons during vocal development, IMAN lesions in 20-d-old birds yielded numerous pyknotic cells throughout DLM by 4 d postlesion and a two-thirds reduction in DLM neuron density by 6 d postlesion. In contrast, IMAN lesions in adult birds had little or no effect on neuronal survival in DLM. Analysis of 40-d-old birds revealed significant but less substantial cell loss than in 20-d-old birds, whereas 60-d-old birds were not different from adults. The age-related decline in the vulnerability of DLM cells to IMAN lesion-induced death suggests that factors that regulate DLM neuron survival may also be involved in the acquisition of learned vocal behavior in songbirds.
雄性斑胸草雀的前脑核离散网络是发声学习和发声的基础。该网络中的三个核形成一条神经通路，对幼鸟的发声学习尤为重要：鸟类纹状体的X区投射到丘脑前内侧背外侧核（DLM），而DLM又投射到新纹状体前部的外侧大细胞核（IMAN）。幼鸟中这些核中的任何一个受损都会破坏正常的发声发育，而成年鸟中相同的损伤对已经学会的歌声没有影响。由于大量研究表明，发育中的神经系统中的神经元存活取决于能否接触到传出靶标，我们研究了DLM神经元的存活在发声学习过程中是否也受到类似调节的可能性。因此，在雄性鸟类发声发育的不同阶段（20、40、60日龄和成年），通过电解损伤DLM的传出靶标（IMAN），并在损伤后2、4或6天处死鸟类。IMAN的电解损伤消除了DLM投射神经元唯一确定的传出靶标，并切断了这些神经元的终末分支。虽然DLM在发声发育过程中通常不会丢失神经元，但20日龄鸟类的IMAN损伤在损伤后4天在整个DLM中产生了大量固缩细胞，到损伤后6天DLM神经元密度降低了三分之二。相比之下，成年鸟类的IMAN损伤对DLM中的神经元存活几乎没有影响。对40日龄鸟类的分析显示，细胞损失显著但不如20日龄鸟类严重，而60日龄鸟类与成年鸟类没有差异。DLM细胞对IMAN损伤诱导死亡的易感性随年龄下降，这表明调节DLM神经元存活的因素可能也参与了鸣禽习得性发声行为的获得。
