【摘 要】
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Long term potentiation(LTP)and depression(LTD)are widely accepted as cellular mechanisms for learning and memory in the mammalian brain.But as both forms of long-term synaptic plasticity are considere
【机 构】
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Department of Pediatrics,Xijing Hospital,Xi'an,Shaanxi 710032,China
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
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Long term potentiation(LTP)and depression(LTD)are widely accepted as cellular mechanisms for learning and memory in the mammalian brain.But as both forms of long-term synaptic plasticity are considered likely to saturate,parallel investigations over the last two decades have sought compensatory mechanisms,such as homeostatic plasticity or synaptic scaling.One major problem is that LTP and LTD can be experimentally induced within a few minutes,whereas any observation of compensatory synaptic changes requires globally blocking neuronal activity for days using TTX.How these two very different forms of plasticity work in concert under physiological conditions remains a largely unanswered question.The present study takes advantage of the circuitry of the mormyrid fish cerebellum in which Purkinje cells(PCs)receive distinct excitatory parallel fiber(PF)and climbing fiber(CF)inputs and terminate locally on efferent cells(ECs)and other PCs.This arrangement has allowed us to use the dual whole-cell recording method in slice preparations to induce synaptic plasticity at a PCs PF synapses and monitor the same PCs inhibitory output onto its target cells.After identifying synaptically-connected cell pairs(PF-PC or PC-EC),LTD or LTP was induced at PF synapses in presynaptic PCs by pairing PF and CF inputs.Before and after the induction of each type of PF-PC plasticity,the inhibitory effects of the PCs on their target cells were carefully examined and compared.It was found that when LTD was induced at a PCs PF synapses,the same PCs inhibition in target cells was enhanced; whereas when LTP was induced,the PCs inhibition of its targets was suppressed.These results indicate that GABA release at PC axon terminals can be up-or downregulated by the synaptic strength of the same cells input synapses in an “online” fashion.Such rapid synaptic scaling may prevent a PCs output from saturating and thereby serve a homoeostatic purpose.
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