PMID- 17234703
OWN - NLM
STAT- MEDLINE
DCOM- 20070529
LR  - 20240511
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 580
IP  - Pt 1
DP  - 2007 Apr 1
TI  - Reliable long-lasting depression interacts with variable short-term facilitation 
      to determine corticostriatal paired-pulse plasticity in young rats.
PG  - 225-40
AB  - 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.
FAU - Akopian, G
AU  - Akopian G
AD  - Andrus Gerontology Center and USC Program in Neuroscience, University of Southern 
      California, Los Angeles, CA 90089-0191, USA.
FAU - Walsh, J P
AU  - Walsh JP
LA  - eng
GR  - R01 AG021937/AG/NIA NIH HHS/United States
GR  - AG12679/AG/NIA NIH HHS/United States
GR  - AG21937/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20070118
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (GABA Agonists)
RN  - 0 (GABA Antagonists)
RN  - 0 (Neurotransmitter Agents)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, GABA-A)
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - SY7Q814VUP (Calcium)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Action Potentials/drug effects/physiology
MH  - Animals
MH  - Calcium/physiology
MH  - Cerebral Cortex/drug effects/*physiology
MH  - Dopamine/physiology
MH  - Electric Stimulation
MH  - Electrophysiology
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Female
MH  - GABA Agonists/pharmacology
MH  - GABA Antagonists/pharmacology
MH  - Neostriatum/drug effects/*physiology
MH  - Neuronal Plasticity/drug effects/*physiology
MH  - Neurons, Afferent/drug effects/physiology
MH  - Neurotransmitter Agents/physiology
MH  - Patch-Clamp Techniques
MH  - Pregnancy
MH  - Presynaptic Terminals/drug effects/physiology
MH  - Rats
MH  - Rats, Inbred F344
MH  - Receptors, AMPA/drug effects
MH  - Receptors, GABA-A/drug effects/physiology
MH  - Receptors, Metabotropic Glutamate/agonists/antagonists & inhibitors/physiology
PMC - PMC2075419
EDAT- 2007/01/20 09:00
MHDA- 2007/05/30 09:00
PMCR- 2008/04/01
CRDT- 2007/01/20 09:00
PHST- 2007/01/20 09:00 [pubmed]
PHST- 2007/05/30 09:00 [medline]
PHST- 2007/01/20 09:00 [entrez]
PHST- 2008/04/01 00:00 [pmc-release]
AID - jphysiol.2006.115790 [pii]
AID - 10.1113/jphysiol.2006.115790 [doi]
PST - ppublish
SO  - J Physiol. 2007 Apr 1;580(Pt 1):225-40. doi: 10.1113/jphysiol.2006.115790. Epub 
      2007 Jan 18.