Assessing the Role of GLUK5and GLUK6at Hippocampal Mossy Fiber Synapses

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Abstract
It has been suggested recently that presynaptic kainate receptors (KARs) are involved in short-term and long-term synaptic plasticity at hippocampal mossy fiber synapses. Using genetic deletion and pharmacology, we here assess the role of GLUK5and GLUK6in synaptic plasticity at hippocampal mossy fiber synapses. We found that the kainate-induced facilitation was completely abolished in theGLUK6-/-mice, whereas it was unaffected in theGLUK5-/-. Consistent with this finding, synaptic facilitation was reduced in theGLUK6-/-and was normal in theGLUK5-/-. In agreement with these results and ruling out any compensatory effects in the genetic deletion models, application of the GLUK5-specific antagonistLY382884[(3S,4aR,6S,8aR)-6-(4-carboxyphenyl)methyl-1,2,3,4,4a,5,6,7,8,8a-decahydroisoquinoline-3-carboxylic acid] did not affect short-term and long-term synaptic plasticity at the hippocampal mossy fiber synapses. We therefore conclude that the facilitatory effects of kainate on mossy fiber synaptic transmission are mediated by GLUK6-containing KARs.