Garcia-Munoz M, Young S J, Groves P M
University of California, School of Medicine, Department of Psychiatry, San Diego, La Jolla 92093.
Brain Res. 1991 Jun 14;551(1-2):207-15. doi: 10.1016/0006-8993(91)90934-n.
The influence of impulse activity and glutamate receptor stimulation on the electrical excitability of the corticostriatal terminal field was explored. Antidromic responses were recorded from prefrontal cortical neurons the electrical stimulation of their terminal field in the contralateral striatum. Terminal excitability was assessed by determining the percentage of subthreshold current stimulus presentations eliciting an antidromic response. Terminal excitability was found to be positively correlated with variations in spontaneous firing rate: increases and decreases in firing rate were accompanied by corresponding changes in the percentage of antidromic responses elicited by a subthreshold stimulus. Drugs were applied to the striatal stimulation site in a volume of 312 nl delivered over 5 min. Striatal administration of either the competitive NMDA antagonist D-alpha-aminoadipate (DAA) or D-2-amino-7-phosphonoheptanoate (AP-7) or the competitive non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3 dione (CNQX) blocked the correlation between excitability and firing rate. Further examination revealed that the terminal field was rendered more excitable for a period of 20-80 ms following the arrival of an action potential. This post-impulse facilitation of terminal excitability was attenuated after local application of AP-7 (10 microM) or CNQX (20 microM). At half these doses, AP-7 or CNQX produced a non-significant effect, however when administered simultaneously a significant attenuation was observed. The participation of interneurons in these excitability effects was ruled out since they were still seen following kainic acid lesions. We propose that this impulse-dependent enhancement in terminal excitability results from the release of glutamate induced by the action potential in the terminal field and the subsequent stimulation of glutamate autoreceptors on the terminals.
研究了冲动活动和谷氨酸受体刺激对皮质纹状体终末场电兴奋性的影响。通过对前额叶皮质神经元进行电刺激，记录其在对侧纹状体终末场的逆向反应。通过确定引发逆向反应的阈下电流刺激呈现的百分比来评估终末兴奋性。发现终末兴奋性与自发放电率的变化呈正相关：放电率的增加和减少伴随着阈下刺激引发的逆向反应百分比的相应变化。将药物以312 nl的体积在5分钟内施用于纹状体刺激部位。纹状体内注射竞争性NMDA拮抗剂D-α-氨基己二酸（DAA）或D-2-氨基-7-磷酸庚酸（AP-7）或竞争性非NMDA拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）可阻断兴奋性与放电率之间的相关性。进一步研究表明，在动作电位到达后20 - 80毫秒内，终末场的兴奋性增强。局部应用AP-7（10 μM）或CNQX（20 μM）后，这种冲动后终末兴奋性的促进作用减弱。在这些剂量减半时，AP-7或CNQX产生的影响不显著，然而同时给药时则观察到显著的减弱。由于在 kainic 酸损伤后仍能观察到这些兴奋性效应，因此排除了中间神经元参与其中的可能性。我们认为，这种依赖于冲动的终末兴奋性增强是由终末场动作电位诱导的谷氨酸释放以及随后对终末上谷氨酸自身受体的刺激所致。
