Virginia Merrill Bloedel Hearing Research Center, Department of Otolaryngology-Head and Neck Surgery, University of Washington School of Medicine, Seattle, Washington 98195, USA.
J Neurosci. 2012 Aug 15;32(33):11495-504. doi: 10.1523/JNEUROSCI.1737-12.2012.
Afferent input regulates neuronal dendritic patterning locally and globally through distinct mechanisms. To begin to understand these mechanisms, we differentially manipulate afferent input in vivo and assess effects on dendritic patterning of individual neurons in chicken nucleus laminaris (NL). Dendrites of NL neurons segregate into dorsal and ventral domains, receiving excitatory input from the ipsilateral and contralateral ears, respectively, via nucleus magnocellularis (NM). Blocking action potentials from one ear, by either cochlea removal or temporary treatment with tetrodotoxin (TTX), leads to rapid and significant retraction of affected NL dendrites (dorsal ipsilaterally and ventral contralaterally) within 8 h compared with the other dendrites of the same neurons. The degree of retraction is comparable with that induced by direct deafferentation resulting from transection of NM axons. Importantly, when inner ear activity is allowed to recover from TTX treatments, retracted NL dendrites regrow to their normal length within 48 h. The retraction and growth involve elimination of terminal branches and addition of new branches, respectively. Examination of changes in NL dendrites at 96 h after unilateral cochlea removal, a manipulation that induces cell loss in NM and persistent blockage of afferent excitatory action potentials, reveals a significant correlation between cell death in the ipsilateral NM and the degree of dendritic retraction in NL. These results demonstrate that presynaptic action potentials rapidly and reversibly regulate dendritic patterning of postsynaptic neurons in a compartment specific manner, whereas long-term dendritic maintenance may be regulated in a way that is correlated with the presence of silent presynaptic appositions.
传入输入通过不同的机制局部和全局地调节神经元树突模式。为了开始理解这些机制,我们在体内差异地操纵传入输入,并评估其对鸡核层(NL)中单个神经元树突模式的影响。NL 神经元的树突分为背侧和腹侧域,分别通过大细胞核(NM)接收来自同侧和对侧耳朵的兴奋性输入。通过耳蜗切除或用河豚毒素(TTX)进行临时处理阻断一只耳朵的动作电位,与同一神经元的其他树突相比,受影响的 NL 树突(同侧背侧和对侧腹侧)在 8 小时内迅速且显著回缩。回缩的程度与 NM 轴突横断导致的直接去传入引起的回缩相当。重要的是,当内耳活动从 TTX 处理中恢复时,回缩的 NL 树突在 48 小时内恢复到正常长度。回缩和生长分别涉及末端分支的消除和新分支的添加。在单侧耳蜗切除后 96 小时检查 NL 树突的变化,这种操作会导致 NM 中的细胞丢失和传入兴奋性动作电位的持续阻断,揭示了同侧 NM 中的细胞死亡与 NL 中树突回缩的程度之间存在显著相关性。这些结果表明,突触前动作电位以特定于隔室的方式快速且可逆地调节突触后神经元的树突模式,而长期树突维持可能以与沉默突触前毗邻相关的方式进行调节。