Webber T J, Green E J, Winters R W, Schneiderman N, McCabe P M
Department of Psychology, University of Miami, Coral Gables, FL 33124, USA.
Exp Brain Res. 1999 Feb;124(3):295-303. doi: 10.1007/s002210050626.
Previous work from this laboratory has demonstrated that monosynaptic inputs from the brachium of the inferior colliculus (BIC) to the medial subdivision of the medial geniculate nucleus (mMG) strengthen as a result of associative conditioning with an acoustic conditioned stimulus (i.e., fear conditioning). One model that has been proposed to underlie certain types of neuronal plasticity involves the recruitment of N-methyl-D-aspartic acid (NMDA)-type glutamate receptors. The purpose of the present study was to examine the relative contributions of glutamatergic NMDA and non-NMDA receptors to synaptic transmission within this pathway. Individual contributions of the specific receptor types were assessed through the use of 2-amino-5-phosphonovaleric acid (AP5), a selective NMDA receptor antagonist, and 6-cyano-5-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA receptor antagonist. Bipolar stimulating electrodes were stereotaxically implanted in BIC and recording electrodes (attached to dual 32-gauge cannulae for delivery of drug) were positioned in mMG of New Zealand albino rabbits. Single pulses (150 micros, 100-350 microA) delivered to BIC resulted in short-latency (<4 ms) responses in mMG. BIC-evoked single-unit activity was recorded from mMG before, during, and at several intervals after injection of AP5, CNQX, and/or artificial cerebrospinal fluid (ACSF). Injection of either AP5 or CNQX, but not ACSF, significantly attenuated the short-latency BIC-evoked responses in the vast majority of cells tested. These findings suggest that the monosynaptic pathway from BIC to mMG is glutamatergic and that this pathway frequently employs NMDA-type receptors during electrically stimulated synaptic transmission. Due to the NMDA receptors' proposed role in plasticity (e.g., long-term potentiation), these results may have implications for understanding the mechanisms of synaptic plasticity observed at this synapse during associative learning.
该实验室先前的研究表明，在下丘臂（BIC）至内侧膝状核内侧亚区（mMG）的单突触输入，会因与听觉条件刺激（即恐惧条件反射）的联合条件反射而增强。为解释特定类型神经元可塑性所提出的一种模型涉及N-甲基-D-天冬氨酸（NMDA）型谷氨酸受体的募集。本研究的目的是检验谷氨酸能NMDA和非NMDA受体对该通路内突触传递的相对贡献。通过使用选择性NMDA受体拮抗剂2-氨基-5-磷酸基戊酸（AP5）和非NMDA受体拮抗剂6-氰基-5-硝基喹喔啉-2,3-二酮（CNQX）来评估特定受体类型的个体贡献。将双极刺激电极立体定位植入新西兰白化兔的BIC中，并将记录电极（连接到用于给药的双32号套管）置于mMG中。向BIC施加单脉冲（150微秒，100 - 350微安）会在mMG中产生短潜伏期（<4毫秒）的反应。在注射AP5、CNQX和/或人工脑脊液（ACSF）之前、期间以及注射后的几个时间间隔，记录mMG中由BIC诱发的单单位活动。注射AP5或CNQX，但不注射ACSF，在绝大多数测试细胞中显著减弱了由BIC诱发的短潜伏期反应。这些发现表明，从BIC到mMG的单突触通路是谷氨酸能的，并且在电刺激突触传递过程中该通路经常使用NMDA型受体。由于NMDA受体在可塑性（例如长时程增强）中所起的作用，这些结果可能对理解在联合学习期间在该突触观察到的突触可塑性机制具有启示意义。
