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期刊论文

Research report Interleukin-2 modulates N-methyl-D-aspartate receptors of native mesolimbic neurons

陶亮Jiang Hong Ye ab* Liang Tao a Steven S. Zalcman c

Brain Research 894(2001)241-248,-0001,():

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摘要/描述

Interleukin (IL)-2 is a brain-derived cytokine that influences mesocorticolimbic dopamine release, and is associated with pathological outcomes that are mediated, at least in part, by aberrations in mesolimbic neurotransmission. The mechanisms by which IL-2 modulates mesolimbic transmission, however, are not known. The NMDA receptor/channel (NMDAR) plays an essential role in neuronal excitability of mesolimbic neurons; we thus examined in neonatal rats the effects of IL-2 on NMDA-activated current (I) in NMDA voltage-clamped neurons freshly isolated from the ventral tegmental area (VTA), the site of origin of the mesolimbic system. IL-2 (0.01-500ng/ml) alone had no effect on membrane conductance. When co-applied with NMDA, IL-2 (50-500ng/ml) significantly potentiated I. In contrast, doses as low as 0.01ng/ml markedly decreased the NMDA response. Dose–response analysis showed that NMDA IL-2 (.50 ng/ml) increased the maximal I, without changing the EC, indicating that IL-2 potentiates I by increasing the NMDA 50 NMDA efficacy of the NMDAR. Moreover, current-voltage analysis revealed that IL-2 potentiation of I was voltage-dependent, being NMDA greater at negative potentials. In contrast, IL-2 inhibition of I was voltage-independent, and IL-2 did not alter the reversal potential. NMDA Additionally, IL-2 (1ng/ml) shifted the NMDA concentration-response curve to the right, significantly increasing the EC for NMDA 50 without changing the maximal I, suggesting that IL-2 inhibits the NMDAR by a competitive mechanism. IL-2 thus acts as a potent NMDA modulator of the NMDAR. IL-2-induced alterations of responses to NMDAR activation may contribute to synaptic plasticity in the mesolimbic system and to pathological outcomes associated with this system.

版权说明:以下全部内容由陶亮上传于   2009年04月20日 09时16分32秒,版权归本人所有。

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