Norton S, Culver B
Brain Res. 1977 Sep 2;132(3):455-65. doi: 10.1016/0006-8993(77)90194-9.
Interneurons of the caudate nucleus have been reported in the literature to respond to deafferentation by reduction in dendritic spines. In the studies reported here, caudate interneurons have been examined using the Golgi technique and increased numbers of spines were found in adult rats exposed to carbon monoxide as neonates. The development of spines on the caudate neurons was delayed for several days after an acute anoxic episode in 5-day-old rats exposed to carbon monoxide to the point of respiratory arrest. By the time the rats were 6 weeks old the caudate neurons had recovered to the point where they had essentially normal numbers of spines. At later ages (2- and 7-months old) the number of spines was greater in rats exposed perinatally to carbon monoxide than in control rats of the same age. The development of abnormal numbers of spines coincided with the time of recovery of rats from behavioral hyperactivity induced by carbon monoxide. The increased spines on the caudate neurons of the adult rats (7-months old) can be explained as a compensatory response to increased afferent flow to the caudate during the period of juvenile hyperactivity which reaches a peak at 6 weeks of age. It is proposed that the return to normal activity in the adult may be a consequence of increased activity of the caudate nucleus.
文献报道，尾状核中间神经元会因去传入作用而出现树突棘减少的情况。在本文所报道的研究中，运用高尔基技术对尾状核中间神经元进行了检查，结果发现，新生期暴露于一氧化碳的成年大鼠的树突棘数量增多。在5日龄暴露于一氧化碳直至呼吸停止的大鼠中，急性缺氧发作后，尾状核神经元上树突棘的发育延迟了数天。到大鼠6周龄时，尾状核神经元已恢复到基本具有正常数量树突棘的状态。在更大的年龄阶段（2月龄和7月龄），围产期暴露于一氧化碳的大鼠的树突棘数量比同年龄的对照大鼠更多。树突棘数量异常的发育与大鼠从一氧化碳诱导的行为多动中恢复的时间相吻合。成年大鼠（7月龄）尾状核神经元上树突棘增加可解释为在6周龄达到峰值的幼年多动期对尾状核传入流量增加的一种代偿反应。有人提出，成年期恢复到正常活动状态可能是尾状核活动增加的结果。
