Bracci E, Ballerini L, Nistri A
Biophysics Sector and Istituto Nazionale di Fisica della Materia Unit, International School for Advanced Studies (SISSA), 34013 Trieste, Italy.
J Neurosci. 1996 Nov 1;16(21):7063-76. doi: 10.1523/JNEUROSCI.16-21-07063.1996.
Spontaneous rhythmic bursting induced by coapplication of strychnine (1 microM) and bicuculline (20 microM) was observed with electrophysiological recording from pairs of lumbar ventral roots (usually L5) in an isolated preparation of the neonatal rat spinal cord. Bursting was insensitive to exogenously applied GABA or glycine, confirming that it was attributable to block of glycine and GABAA receptor-mediated inhibition. NMDA accelerated bursting in a dose-dependent manner. Complete coronal spinal transection at L3 or L6 level did not block bursting recorded from L5 or L2 roots, respectively. Gradual cutting of the cord along the midline through a sagittal plane preserved bursting activity in both disconnected sides but led to loss of synchronicity. Once the spinal cord was fully separated into left and right halves, regular bursting persisted on each side with no phase-coupling between the two preparations. Section along a frontal plane to remove dorsal horns and much of the central canal area did not affect burst frequency or left-to-right synchronicity, whereas it reduced burst duration. A quadrant preparation containing mainly a single ventral horn displayed enhanced burst frequency while bursts became very short events. Bath application of 5-hydroxytryptamine (30 microM) or NMDA (5 microM) increased burst frequency and decreased burst duration in all types of preparation except the isolated quadrants, in which brief bursts were accelerated but not shortened by these chemical agents. These results suggest that bursting induced by strychnine and bicuculline apparently relied on distinct mechanisms for burst triggering and intraburst structure. The first required a relatively smaller neuronal network that was confined to a ventral quadrant. Intraburst structure was dependent on a larger circuitry comprising either both ventral horns or one side of the spinal cord including more than two segments.
在新生大鼠脊髓的离体标本中，通过对成对的腰腹根（通常为L5）进行电生理记录，观察到同时应用士的宁（1微摩尔）和荷包牡丹碱（20微摩尔）诱导的自发性节律性爆发。爆发对外源性应用的GABA或甘氨酸不敏感，证实其归因于甘氨酸和GABAA受体介导的抑制作用的阻断。NMDA以剂量依赖性方式加速爆发。在L3或L6水平进行完全冠状脊髓横断术，分别不会阻断从L5或L2根记录到的爆发。沿矢状面通过中线逐渐切断脊髓，在两侧分离的情况下均保留了爆发活动，但导致同步性丧失。一旦脊髓完全分离为左右两半，每一侧都持续有规律的爆发，两个标本之间没有相位耦合。沿额面切开以去除背角和大部分中央管区域，不影响爆发频率或左右同步性，但会缩短爆发持续时间。主要包含单个腹角的象限标本显示爆发频率增加，而爆发变为非常短暂的事件。除了分离的象限标本外，在所有类型的标本中，浴用5-羟色胺（30微摩尔）或NMDA（5微摩尔）均可增加爆发频率并缩短爆发持续时间，在分离的象限标本中，这些化学试剂可加速短暂爆发，但不会使其缩短。这些结果表明，士的宁和荷包牡丹碱诱导的爆发显然依赖于不同的爆发触发机制和爆发内结构机制。第一种机制需要一个相对较小的神经元网络，该网络局限于腹侧象限。爆发内结构依赖于一个更大的神经回路，该回路包括两个腹角或脊髓的一侧，包括两个以上节段。
