Amzica F, Steriade M
Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Quebec, Canada.
J Neurosci. 1995 Jun;15(6):4658-77. doi: 10.1523/JNEUROSCI.15-06-04658.1995.
The intracortical synaptic linkages underlying the synchronization of a recently described slow (< 1 Hz) oscillation (Steriade et al., 1993b,c) were investigated in anesthetized cats by means of multisite extra- and intracellular recordings, including dual impalements, from rostral and caudal sites in the association cortical suprasylvian and marginal gyri, before and after reversible lidocaine inactivation or transections in the middle suprasylvian gyrus. Stimulus-evoked responses revealed that the rostral and caudal suprasylvian foci are reciprocally connected, with a preference for posterior-to-anterior responses. Lidocaine infusion between the stimulating and recording sites disrupted the intracortical synaptic linkage, while leaving unaffected the responses at the sites close to the stimulating electrodes. The high coherence between slowly oscillating field potentials and intracellular activities recorded from anterior and posterior suprasylvian foci was lost after reversible inactivation or transections in the middle suprasylvian gyrus, whereas the synchrony between adjacent foci within the anterior or posterior areas was preserved. Two to four hours after inactivation or transection the synchrony between all channels was totally or partially recovered. We introduced the synchrony coefficient (SyCo) and calculated the SyCo for closely located and distant sites. Lidocaine infusion or transection did not affect the SyCo between leads placed on the same site, but significantly (60%) decreased the SyCo between channels separated by the functionally inactivated or transected sector. Our results demonstrate that pathways within or beneath the suprasylvian gyrus sustain the synchronization of the slow oscillation between cortical sites. As the loss of long-range coherence was not permanent, intergyral paths and/or corticothalamocortical loops may exert compensatory functions after the disconnection of intrasuprasylvian synaptic linkages.
通过多部位细胞外和细胞内记录，包括双电极插入记录，在麻醉猫的上薛氏回和缘回联合皮质的嘴侧和尾侧部位，于上薛氏回中部进行可逆性利多卡因失活或横断前后，研究了最近描述的慢（<1Hz）振荡（Steriade等人，1993b，c）同步化的皮质内突触连接。刺激诱发反应显示，嘴侧和尾侧上薛氏回焦点相互连接，偏好后向前反应。在刺激和记录部位之间注入利多卡因破坏了皮质内突触连接，而不影响靠近刺激电极部位的反应。在上薛氏回嘴侧和尾侧焦点记录的慢振荡场电位与细胞内活动之间的高相干性，在上薛氏回中部进行可逆性失活或横断后丧失，而在前部或后部区域内相邻焦点之间的同步性得以保留。失活或横断后两到四小时，所有通道之间的同步性全部或部分恢复。我们引入了同步系数（SyCo），并计算了相邻和远距离部位的SyCo。注入利多卡因或横断不影响放置在同一部位的导联之间的SyCo，但显著（60%）降低了被功能失活或横断区域隔开的通道之间的SyCo。我们的结果表明，上薛氏回内或其下方的通路维持了皮质部位之间慢振荡的同步。由于远距离相干性的丧失并非永久性的，在上薛氏回内突触连接断开后，脑回间通路和/或皮质-丘脑-皮质环路可能发挥代偿功能。
