Ackermann R F, Finch D M, Babb T L, Engel J
J Neurosci. 1984 Jan;4(1):251-64. doi: 10.1523/JNEUROSCI.04-01-00251.1984.
The locally subnormal brain metabolism observed in some experiments utilizing the Sokoloff 2-deoxyglucose (2-DG) method has often been attributed to postsynaptic inhibition despite the fact that inhibitory postsynaptic potentials are themselves caused by energy-requiring mechanisms. To explore this issue, neurophysiologically confirmed long-duration recurrent inhibition of hippocampal pyramidal unit firing was induced by low frequency (2 to 4 Hz) stimulation of the fornix for 60 min following intravenous infusion of [14C]-2-DG. The resulting autoradiograms showed that long-duration suppression of pyramidal cell firing was accompanied by distinctly increased hippocampal 2-DG uptake, particularly in the stratum pyramidale, which contains a dense plexus of inhibitory interneuronal terminals upon pyramidal cells. Both the pyramidal inhibition and the increased 2-DG uptake were confined to the ipsilateral hippocampus in animals with previously severed fornices and hippocampal commissures. In a second series of rats, the excitatory entorhinohippocampal "perforant path" (PP) was stimulated at low frequency (2 to 9 Hz) following 2-DG administration. At 2 to 4 Hz, each PP stimulation resulted in a brief burst of pyramidal unit firing followed by short-duration firing suppression; this result was associated with paradoxically decreased 2-DG uptake in the ipsilateral stratum molecular. By contrast, 7 to 9 Hz entorhinal stimulation induced PP-mediated excitation immediately followed by powerful intrinsic hippocampal inhibition, evidenced by prolonged pyramidal unit suppression after each stimulation. This suppression was accompanied by increased 2-DG uptake in the dentate stratum molecular and hippocampal stratum pyramidale. Thus it appeared that even with entorhinal stimulation, hippocampal 2-DG uptake was more closely associated with long-duration recurrent inhibition than with transient pyramidal excitation. Therefore, although it still remains possible that regions of hypometabolism observed in some previous 2-DG studies may actually reflect mild inhibition, other mechanisms such as disfacilitation are more likely mechanisms for this metabolic pattern.
在一些采用索科洛夫2-脱氧葡萄糖（2-DG）方法的实验中观察到的局部脑代谢低于正常水平，尽管抑制性突触后电位本身是由需要能量的机制引起的，但这种情况常常被归因于突触后抑制。为了探究这个问题，在静脉注射[14C]-2-DG后，通过低频（2至4赫兹）刺激穹窿60分钟，诱导出经神经生理学证实的海马锥体单元放电的长时间反复抑制。所得的放射自显影片显示，锥体细胞放电的长时间抑制伴随着海马2-DG摄取明显增加，特别是在锥体层，该层含有密集的抑制性中间神经元终末丛，作用于锥体细胞。在先前切断穹窿和海马连合的动物中，锥体抑制和2-DG摄取增加都局限于同侧海马。在第二组大鼠中，在给予2-DG后，以低频（2至9赫兹）刺激兴奋性内嗅-海马“穿通通路”（PP）。在2至4赫兹时，每次PP刺激都会导致锥体单元放电短暂爆发，随后是短时间的放电抑制；这一结果与同侧分子层中2-DG摄取反常减少有关。相比之下，7至9赫兹的内嗅刺激立即诱导PP介导的兴奋，随后是强大的海马内在抑制，每次刺激后锥体单元长时间抑制证明了这一点。这种抑制伴随着齿状分子层和海马锥体层中2-DG摄取增加。因此，似乎即使在内嗅刺激下，海马2-DG摄取与长时间反复抑制的关系比与短暂的锥体兴奋更密切。因此，尽管在一些先前的2-DG研究中观察到的代谢减低区域实际上可能反映轻度抑制，但其他机制如去易化更可能是这种代谢模式的机制。
