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PMID: 17234703 Published · ppublish English Journal Article Research Support, N.I.H., Extramural

Reliable long-lasting depression interacts with variable short-term facilitation to determine corticostriatal paired-pulse plasticity in young rats.

The Journal of physiology ·Vol. 580 ·No. Pt 1 ·2007-04-01 ·Pages 225-40

Akopian G, Walsh JP

Abstract

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.

MeSH Terms
Action Potentials/drug effects,physiology Animals Calcium/physiology Cerebral Cortex/drug effects,physiology Dopamine/physiology Electric Stimulation Electrophysiology Excitatory Postsynaptic Potentials/drug effects,physiology Female GABA Agonists/pharmacology GABA Antagonists/pharmacology Neostriatum/drug effects,physiology Neuronal Plasticity/drug effects,physiology Neurons, Afferent/drug effects,physiology Neurotransmitter Agents/physiology Patch-Clamp Techniques Pregnancy Presynaptic Terminals/drug effects,physiology Rats Rats, Inbred F344 Receptors, AMPA/drug effects Receptors, GABA-A/drug effects,physiology Receptors, Metabotropic Glutamate/agonists,antagonists & inhibitors,physiology
Chemicals
GABA Agonists GABA Antagonists Neurotransmitter Agents Receptors, AMPA Receptors, GABA-A Receptors, Metabotropic Glutamate Calcium Dopamine
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Akopian G
Andrus Gerontology Center and USC Program in Neuroscience, University of Southern California, Los Angeles, CA 90089-0191, USA.
Walsh J P
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Article Info
Journal
The Journal of physiology
Abbr.
J Physiol
ISSN
0022-3751
Published
2007-04-01
Epub
2007-00-18
Pages
225-40
Language
English
Region
England
NLM ID
0266262
PMCID
PMC2075419
Subset
IM
Grants
NIA NIH HHS · R01 AG021937 · United States
NIA NIH HHS · AG12679 · United States
NIA NIH HHS · AG21937 · United States
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