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Reliable long‐lasting depression interacts with variable short‐term facilitation to determine corticostriatal paired‐pulse plasticity in young rats
Author(s) -
Akopian G.,
Walsh J. P.
Publication year - 2007
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.115790
Subject(s) - neural facilitation , ampa receptor , neuroscience , chemistry , glutamate receptor , nmda receptor , psychology , excitatory postsynaptic potential , receptor , inhibitory postsynaptic potential , biochemistry
Synaptic plasticity at corticostraital synapses is proposed to fine tune movment and improve motor skills. We found paired‐pulse plasticity at corticostriatal synapses reflected variably expressed short‐term facilitation blended with a consistent background of longer‐lasting depression. Presynaptic modulation via neuotransmitter receptor activation was ruled out as a mechanism for long‐lasting paired‐pulse depression by examining the effect of selective receptor antagonists. EPSC amplitude and paired‐pulse plasticity, however, was influenced by block of D2 dopamine receptors. Block of glutamate transport with l ‐transdicarboxylic acid (PDC) reduced EPSCs, possibly through a mechanism of AMPA receptor desensitization. Removal of AMPA receptor desensitization with cyclothiazide reduced the paired‐pulse depression at long‐duration interstimulus intervals (ISIs), indicating that AMPA receptor desensitization participates in corticostriatal paired‐pulse plasticity. The low‐affinity glutamate receptor antagonist cis ‐2,3‐piperidine dicarboxylic acid (PDA) increased paired‐pulse depression, suggesting that a presynaptic component also exists for long‐lasting paired‐pulse depression. Low Ca 2+ –high Mg 2+ or BAPTA‐AM dramatically reduced the amplitude of corticostriatal EPSCs and both manipulations increased the expression of facilitation and, to a lesser extent, they reduced long‐lasting paired‐pulse depression. EGTA‐AM produced a smaller reduction in EPSC amplitude and it did not alter paired‐pulse facilitation, but in contrast to low Ca 2+ and BAPTA‐AM, EGTA‐AM increased long‐lasting paired‐pulse depression. These experiments suggest that facilitation and depression are sensitive to vesicle depletion, which is dependent upon changes in peak Ca 2+ (i.e. low Ca 2+ –high Mg 2+ or BAPTA‐AM). In addition, the action of EGTA‐AM suggests that basal Ca 2+ regulates the recovery from long‐lasting paired‐pulse depression, possibly thourgh a Ca 2+ ‐sensitive process of vesicle delivery.