Wilson C J, Chang H T, Kitai S T
Exp Brain Res. 1983;51(2):217-26. doi: 10.1007/BF00237197.
Stimulation of thalamic intralaminar nuclei or structures along the intrathalamic trajectory of thalamostriatal axons evoked complex EPSPs and subsequent hyperpolarizations in rat neostriatal spiny neurons identified by intracellular injection of horseradish peroxidase and/or antidromic activation from substantia nigra. In intact urethane-anesthetized rats, the initial EPSP portion of the response consisted of several components and lasted up to 75 ms. Short (1-10 ms) latency components exhibiting latency variations suggestive of a polysynaptic origin were often observed, and sometimes were the earliest components of the response. However, individual components of the excitatory response could not be clearly distinguished in most neurons and the earliest excitatory component usually appeared to be monosynaptic. After large acute aspiration lesions of ipsilateral cerebral cortex, the early polysynaptic EPSP components of thalamic-evoked EPSPs were absent or greatly attenuated. This suggested that most or all of the short latency polysynaptic EPSP components arose via a thalamo-cortico-striatal route. A short latency (1.6-4.0 ms) monosynaptic EPSP and a second excitatory component with a longer and more variable latency (8-28 ms) remained intact after acute decortication. These were not dependent upon intact corticothalamic or corticostriatal axons, since they were both still present in experiments performed as long as 4 days following ipsilateral hemidecortication. The longer latency excitatory response was shown to be polysynaptic by its latency variation with changes in stimulus intensity and frequency. This component of the response was abolished after acute thalamic hemitransections separating thalamostriatal neurons from their axons. In these experiments, stimulation of thalamostriatal axons rostral to the transection continued to evoke monosynaptic EPSPs in neostriatal spiny neurons. These EPSPs ranged from 1.8 to 3.0 ms in latency, had peak amplitudes up to 11 mV and were 20-37 ms in duration.
刺激丘脑板内核或沿丘脑纹状体轴突的丘脑内轨迹的结构,可在通过细胞内注射辣根过氧化物酶和/或来自黑质的逆向激活鉴定的大鼠新纹状体棘状神经元中诱发复合兴奋性突触后电位(EPSP)及随后的超极化。在完整的乌拉坦麻醉大鼠中,反应的初始EPSP部分由几个成分组成,持续长达75毫秒。经常观察到潜伏期短(1 - 10毫秒)的成分,其潜伏期变化提示多突触起源,有时是反应的最早成分。然而,在大多数神经元中,兴奋性反应的各个成分无法清晰区分,最早的兴奋性成分通常似乎是单突触的。在同侧大脑皮层进行大面积急性抽吸损伤后,丘脑诱发的EPSP的早期多突触EPSP成分缺失或大大减弱。这表明大多数或所有短潜伏期多突触EPSP成分是通过丘脑 - 皮质 - 纹状体途径产生的。急性去皮质后,短潜伏期(1.6 - 4.0毫秒)的单突触EPSP和潜伏期更长且更可变(8 - 28毫秒)的第二个兴奋性成分保持完整。这些不依赖于完整的皮质丘脑或皮质纹状体轴突,因为在同侧半去皮质后长达4天进行的实验中它们仍然存在。较长潜伏期的兴奋性反应通过其潜伏期随刺激强度和频率的变化而变化,表明是多突触的。在将丘脑纹状体神经元与其轴突分离的急性丘脑半横断后,反应的这一成分被消除。在这些实验中,在横断上方刺激丘脑纹状体轴突继续在新纹状体棘状神经元中诱发单突触EPSP。这些EPSP的潜伏期为1.8至3.0毫秒,峰值幅度高达11毫伏,持续时间为20 - 37毫秒。