Heynen A J, Bilkey D K
Department of Psychology, University of Otago, Dunedin, New Zealand.
Hippocampus. 1994 Dec;4(6):683-95. doi: 10.1002/hipo.450040606.
Previous research has suggested that the entorhinal cortex plays a major role in the production of type 1 rhythmical slow-wave activity (RSA) recorded in the hippocampus of the freely moving preparation. In the present experiment we investigated the contribution of the entorhinal cortex to the type 2 fields recorded under urethane anesthesia. Rats had stimulating electrodes and cannulae filled with procaine positioned in the perforant pathway of one or both hemispheres. Recording electrodes were positioned in the dorsal hippocampus of each hemisphere to record perforant path and commissural/associational evoked potentials and RSA fields. Following unilateral procaine blockade, a decrease in RSA amplitude was observed in the stratum oriens and fissure regions of both hemispheres. Concomitant with this change in RSA, there was a loss of perforant path evoked responses, although commissural/associational control potentials remained unaltered. A greater reduction in RSA amplitude was observed following bilateral procaine microinfusion. RSA phase reversal also occurred more dorsally in microelectrode depth profiles conducted through the hippocampus during perforant path inactivation. In current source density analyses performed under baseline conditions, large rhythmic sinks were observed in stratum oriens, in stratum radiatum, and in strata adjacent to the hippocampal fissure. A rhythmic source was often observed in stratum pyramidale. Following perforant path inactivation decreases in the magnitude of the phasic sinks located near the fissure and stratum radiatum were observed. In contrast to the reduction in RSA amplitude observed in the stratum oriens region, the sink in this region and the source in stratum pyramidale remained relatively unaltered. These results demonstrate that the entorhinal region contributes to the production of RSA observed under urethane anesthesia. Furthermore, the CSD and amplitude changes following perforant path inactivation suggest that a substantial portion of RSA recorded in stratum oriens may result from ventrally located RSA dipoles.
先前的研究表明，内嗅皮层在自由活动动物海马体中记录到的1型节律性慢波活动（RSA）的产生中起主要作用。在本实验中，我们研究了内嗅皮层对在乌拉坦麻醉下记录到的2型场的贡献。将刺激电极和充满普鲁卡因的套管置于一侧或双侧半球的穿通通路中。记录电极置于每个半球的背侧海马体中，以记录穿通通路和连合/联合诱发电位以及RSA场。单侧普鲁卡因阻断后，在两侧半球的海马下托层和海马裂区域观察到RSA振幅降低。与RSA的这种变化同时发生的是，穿通通路诱发反应消失，尽管连合/联合控制电位保持不变。双侧微量注射普鲁卡因后，观察到RSA振幅有更大程度的降低。在穿通通路失活期间，通过海马体进行的微电极深度剖面分析中，RSA相位反转也更多地发生在背侧。在基线条件下进行的电流源密度分析中，在海马下托层、辐射层以及与海马裂相邻的层中观察到较大的节律性汇。在锥体细胞层中经常观察到节律性源。穿通通路失活后，观察到靠近海马裂和辐射层的相位性汇的幅度减小。与海马下托层区域观察到的RSA振幅降低相反，该区域的汇和锥体细胞层中的源保持相对不变。这些结果表明，内嗅区域对乌拉坦麻醉下观察到的RSA的产生有贡献。此外，穿通通路失活后的CSD和振幅变化表明，在海马下托层记录到的RSA的很大一部分可能来自位于腹侧的RSA偶极子。
