Lenn N J
J Comp Neurol. 1978 Sep 1;181(1):93-115. doi: 10.1002/cne.901810106.
Changes in the normal synaptogenetic pattern of the interpeduncular nucleus (IPN) were induced by destruction of one or both habenular nuclei in neonatal rats. The S synapses, the principal habenulointerpeduncular (H-IPN) afferents, were reduced in number and delayed in time of appearance by unilateral lesions. They were eliminated by bilateral lesions. The crest synapses, also of habenular origin, appeared at ten days of age and were apparently normal in structure after unilateral lesions. However, this actually represented a change in connectivity, since normal crest synapses are of bilateral origin. Following bilateral habenular lesions abnormal crest synapses appeared at 28 days of age. These had normal postsynaptic structure, but presynaptically were formed by non-habenular axons, usually of two different types of each crest synapse. Lesions induced an early appearance of F synapses, at three days, instead of the normal time after six days of age. Apparently similar processes containing flattened vesicles formed somatic contacts only in lesioned animals beginning at 21 days of age. The axosomatic synapses which were only occassional in the adult appeared at the normal time in lesioned animals. At 28 days of age in both unilaterally and bilaterally lesioned animals there was an increase in the number of somatic synapses. This increase was due to an increase of the normal somatic endings plus the appearance of somatic synapses containing flattened vesicles. Both types of somatic contacts were found in similar numbers at subsequent ages up to three months. The changes in S synapses represent Wallerian degeneration. The formation of unilaterally derived crest synapses in unilaterally lesioned animals is interpreted as evidence for a specific recognition mechanism. A postsynaptic control mechanism is proposed to explain the formation of heterologous crest synapses, with the usual distinctive geometry but involving abnormal, non-habenular presynaptic elements four weeks following neonatal bilateral lesions. The increase in axosomatic synapses is unusual since the dendrites of IPN neurons were deafferented, not their somata. The factors leading to the changes in somatic synapses are discussed. The findings reveal new examples of the complexity of neuronal adaptation to CNS lesions in early life.
新生大鼠一侧或双侧缰核损毁可诱导脚间核（IPN）正常突触发生模式的改变。S突触是主要的缰核 - 脚间核（H - IPN）传入纤维，单侧损伤使其数量减少且出现时间延迟。双侧损伤则使其消失。同样起源于缰核的嵴突触在10日龄时出现，单侧损伤后其结构看似正常。然而，这实际上代表了连接性的改变，因为正常的嵴突触是双侧起源的。双侧缰核损伤后，异常的嵴突触在28日龄时出现。这些突触具有正常的突触后结构，但突触前是由非缰核轴突形成的，每个嵴突触通常有两种不同类型。损伤导致F突触在3日龄时提前出现，而不是正常的6日龄之后。明显类似的含有扁平囊泡的结构仅在21日龄开始的损伤动物中形成体细胞接触。成年时偶尔出现的轴体突触在损伤动物中正常时间出现。在28日龄时，单侧和双侧损伤的动物中体细胞突触数量均增加。这种增加是由于正常体细胞末梢数量增加以及含有扁平囊泡的体细胞突触出现。在随后直至三个月的年龄中，两种类型的体细胞接触数量相似。S突触的变化代表华勒氏变性。单侧损伤动物中单侧起源的嵴突触的形成被解释为存在特定识别机制的证据。提出了一种突触后控制机制来解释异源嵴突触的形成，其具有通常独特的几何形状，但在新生双侧损伤四周后涉及异常的、非缰核的突触前成分。轴体突触的增加并不寻常，因为IPN神经元的树突去传入了，而不是它们的胞体。讨论了导致体细胞突触变化的因素。这些发现揭示了神经元在生命早期对中枢神经系统损伤适应复杂性的新例子。
