Reliable long-lasting depression interacts with variable short-term facilitation to determine corticostriatal paired-pulse plasticity in young rats.
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.
Akopian
G
G
Andrus Gerontology Center and USC Program in Neuroscience, University of Southern California, Los Angeles, CA 90089-0191, USA.
Walsh
J P
JP
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D004298:Dopamine / Q000502:physiology; D004558:Electric Stimulation; D004594:Electrophysiology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005260:Female; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D017072:Neostriatum / Q000187:drug effects / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D018408:Patch-Clamp Techniques; D011247:Pregnancy; D017729:Presynaptic Terminals / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011916:Rats, Inbred F344; D018091:Receptors, AMPA / Q000187:drug effects; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology; D018094:Receptors, Metabotropic Glutamate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology
D018755:GABA Agonists; D018756:GABA Antagonists; D018377:Neurotransmitter Agents; D018091:Receptors, AMPA; D011963:Receptors, GABA-A; D018094:Receptors, Metabotropic Glutamate; D002118:Calcium; D004298:Dopamine