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We show that up\u2010regulation of the glutamate transporter GLT\u20101 by ceftriaxone severely impaired mGluR\u2010dependent long\u2010term depression (LTD), induced at rat mossy fibre (MF)\u2013CA3 synapses by repetitive stimulation of afferent fibres. This effect involved GLT\u20101, since LTD was rescued by the selective GLT\u20101 antagonist dihydrokainate (DHK). DHK <jats:italic>per se<\/jats:italic> produced a modest decrease in fEPSP amplitude that rapidly regained control levels after DHK wash out. Moreover, the degree of fEPSP inhibition induced by the low\u2010affinity glutamate receptor antagonist \u03b3\u2010DGG was similar during basal synaptic transmission but not during LTD, indicating that in ceftriaxone\u2010treated rats LTD induction did not alter synaptic glutamate transient concentration. Furthermore, ceftriaxone\u2010induced GLT\u20101 up\u2010regulation significantly reduced the magnitude of LTP at MF\u2013CA3 synapses but not at Schaffer collateral\u2013CA1 synapses. Postembedding immunogold studies in rats showed an increased density of gold particles coding for GLT\u20101a in astrocytic processes and in mossy fibre terminals; in the latter, gold particles were located near and within the active zones. In both CEF\u2010treated and untreated GLT\u20101 KO mice used for verifying the specificity of immunostaining, the density of gold particles in MF terminals was comparable to background levels. The enhanced expression of GLT\u20101 at release sites may prevent activation of presynaptic receptors, thus revealing a novel mechanism by which GLT\u20101 regulates synaptic plasticity in the hippocampus.<\/jats:p>","DOI":"10.1113\/jphysiol.2009.177881","type":"journal-article","created":{"date-parts":[[2009,8,4]],"date-time":"2009-08-04T01:27:45Z","timestamp":1249349265000},"page":"4575-4588","source":"Crossref","is-referenced-by-count":86,"title":["Up\u2010regulation of GLT\u20101 severely impairs LTD at mossy fibre\u2013CA3 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