Aroniadou-Anderjaska V, Ennis M, Shipley M T
Department of Anatomy and Neurobiology and Program in Neuroscience, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
J Neurophysiol. 1999 Jul;82(1):489-94. doi: 10.1152/jn.1999.82.1.489.
Most neuronal interactions within the olfactory bulb network are mediated by dendrodendritic synapses. Dendritic transmitter release potentially could affect the parent dendrite as well as local neuronal elements that have receptors for the released transmitter. Here we report that under conditions that facilitate N-methyl-D-aspartate (NMDA) receptor activity (reduced GABAA inhibition and extracellular Mg2+), a single action potential evoked by brief intracellular current pulses in mitral cells is followed by a prolonged depolarization, which is blocked by an NMDA receptor antagonist. This depolarization also is evoked by a presumed calcium spike in the presence of tetrodotoxin. A similar NMDA-receptor-dependent prolonged depolarization is elicited by stimulation of the lateral olfactory tract at current intensities subthreshold for antidromic activation of the recorded neuron. These observations suggest that glutamate released from the dendrites of mitral cells excites the same and neighboring mitral cell dendrites. Further evidence suggests that both the apical and lateral dendrites of mitral cells participate in this recurrent excitation. These dendrodendritic interactions may play a role in the prolonged, NMDA-receptor-dependent depolarization of mitral/tufted cells evoked by olfactory nerve stimulation.
嗅球网络内的大多数神经元相互作用是由树突 - 树突突触介导的。树突递质释放可能会影响母树突以及对释放的递质具有受体的局部神经元成分。在此我们报告，在促进N - 甲基 - D - 天冬氨酸（NMDA）受体活性的条件下（降低GABAA抑制作用和细胞外Mg2 +浓度），在二尖瓣细胞中由短暂的细胞内电流脉冲诱发的单个动作电位之后会出现长时间的去极化，这被NMDA受体拮抗剂所阻断。在存在河豚毒素的情况下，假定的钙峰也会引发这种去极化。在低于记录神经元逆向激活阈值的电流强度下刺激外侧嗅束，也会引发类似的依赖NMDA受体的长时间去极化。这些观察结果表明，从二尖瓣细胞树突释放的谷氨酸会兴奋相同和相邻的二尖瓣细胞树突。进一步的证据表明，二尖瓣细胞的顶端和侧面树突都参与了这种反复性兴奋。这些树突 - 树突相互作用可能在嗅神经刺激诱发的二尖瓣/簇状细胞依赖NMDA受体的长时间去极化中起作用。
