Increase in Matrix Metalloproteinase-9 Levels in the Rat Medial Prefrontal Cortex After Cocaine Reinstatement of Conditioned Place Preference
Increase in Matrix Metalloproteinase-9 Levels in the Rat Medial Prefrontal Cortex After Cocaine Reinstatement of Conditioned Place Preference
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DOI：
10.1002/syn.20562
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发表时间：
2008-12-01
期刊：
影响因子：
2.3
通讯作者：
Sorg, Barbara A.
中科院分区：
文献类型：
--
作者：
Brown, Travis E.;Forquer, Melissa R.;Sorg, Barbara A.
最近，我们已经表明，抑制基质金属蛋白酶（MMP）活性抑制可卡因引发的条件性位置偏爱（CPP）大鼠的恢复。在这里，我们探讨了可卡因引发的恢复是否与内侧前额叶皮层（mPFC）或背侧海马中明胶酶MMP-2或MMP-9的活性增加有关。雄性Sprague-Dawley大鼠接受可卡因-CPP训练，然后进行消退训练，并注射盐水或可卡因引发。与生理盐水对照组相比，可卡因诱导的恢复在注射后1、3和24小时产生mPFC MMP-9活性的显著增加。MMP-9没有发生变化，在海马或MMP-2活性在任何一个脑区。此外，在没有灭绝期但在饲养笼中休息相同时间的动物中，在恢复后1小时未观察到mPFC MMP-9活性的变化。最后，在评估的三个时间点中的任何一个时间点，MMP-3蛋白水平在任何一个脑区都没有差异。这些结果表明，MMP-9的活性在mPFC的升高可能有助于突触重塑的可卡因记忆的重新激活，或者替代地，在恢复过程中的竞争性灭绝记忆的修改重要。Synapse 62：886-889，2008. (C)2008年威利-利斯。Inc.
Recently we have shown that inhibition of matrix metalloproteinase (MMP) activity suppresses the reinstatement of cocaine-primed conditioned place preference (CPP) in rats. Here we explored whether cocaine-primed reinstatement was associated with increased activity of the gelatinases, MMP-2 or MMP-9, in the medial prefrontal cortex (mPFC) or dorsal hippocampus. Male Sprague-Dawley rats underwent training for cocaine-CPP followed by extinction sessions and either saline- or cocaine-priming injections. Cocaine-induced reinstatement produced significant increases in mPFC MMP-9 activity at 1, 3 and 24 hr after injection compared with saline controls. No changes in MMP-9 occurred in the hippocampus or in MMP-2 activity in either brain region. Also, no changes in mPFC MMP-9 activity were observed 1 hr after reinstatement in animals given no extinction sessions but equivalent time off in the home cage. Finally, MMP-3 protein levels were not different in either brain region at any of the three time points assessed. These results suggest that an elevation in MMP-9 activity in the mPFC may contribute to synaptic remodeling important for the reactivation of a cocaine memory, or alternatively, for the modification of a competing extinction memory during reinstatement. Synapse 62:886-889, 2008. (C) 2008 Wiley-Liss. Inc.