PMID- 17035530
OWN - NLM
STAT- MEDLINE
DCOM- 20061108
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 26
IP  - 41
DP  - 2006 Oct 11
TI  - Different mechanisms exist for the plasticity of glutamate reuptake during early 
      long-term potentiation (LTP) and late LTP.
PG  - 10461-71
AB  - Regulation of glutamate reuptake occurs along with several forms of synaptic 
      plasticity. These associations led to the hypothesis that regulation of glutamate 
      uptake is a general component of plasticity at glutamatergic synapses. We tested 
      this hypothesis by determining whether glutamate uptake is regulated during both 
      the early phases (E-LTP) and late phases (L-LTP) of long-term potentiation (LTP). 
      We found that glutamate uptake was rapidly increased within minutes after 
      induction of LTP and that the increase in glutamate uptake persisted for at least 
      3 h in CA1 of the hippocampus. NMDA receptor activation and Na+-dependent 
      high-affinity glutamate transporters were responsible for the regulation of 
      glutamate uptake during all phases of LTP. However, different mechanisms appear 
      to be responsible for the increase in glutamate uptake during E-LTP and L-LTP. 
      The increase in glutamate uptake observed during E-LTP did not require new 
      protein synthesis, was mediated by PKC but not cAMP, and as previously shown was 
      attributable to EAAC1 (excitatory amino acid carrier-1), a neuronal glutamate 
      transporter. On the other hand, the increase in glutamate uptake during L-LTP 
      required new protein synthesis and was mediated by the cAMP-PKA (protein kinase 
      A) pathway, and it involved a different glutamate transporter, GLT1a (glutamate 
      transporter subtype 1a). The switch in mechanisms regulating glutamate uptake 
      between E-LTP and L-LTP paralleled the differences in the mechanisms responsible 
      for the induction of E-LTP and L-LTP. Moreover, the differences in signaling 
      pathways and transporters involved in regulating glutamate uptake during E-LTP 
      and L-LTP indicate that different functions and/or sites may exist for the 
      changes in glutamate uptake during E-LTP and L-LTP.
FAU - Pita-Almenar, Juan D
AU  - Pita-Almenar JD
AD  - Department of Biology and Biochemistry, University of Houston, Houston, Texas 
      77204-5001, USA.
FAU - Collado, Maria Sol
AU  - Collado MS
FAU - Colbert, Costa M
AU  - Colbert CM
FAU - Eskin, Arnold
AU  - Eskin A
LA  - eng
GR  - R01 NS042156/NS/NINDS NIH HHS/United States
GR  - NS42156/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 3KX376GY7L (Glutamic Acid)
SB  - IM
MH  - Animals
MH  - Glutamic Acid/*metabolism
MH  - Hippocampus/metabolism
MH  - In Vitro Techniques
MH  - Long-Term Potentiation/*physiology
MH  - Male
MH  - Neuronal Plasticity/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Time Factors
PMC - PMC6674676
EDAT- 2006/10/13 09:00
MHDA- 2006/11/10 09:00
PMCR- 2007/04/11
CRDT- 2006/10/13 09:00
PHST- 2006/10/13 09:00 [pubmed]
PHST- 2006/11/10 09:00 [medline]
PHST- 2006/10/13 09:00 [entrez]
PHST- 2007/04/11 00:00 [pmc-release]
AID - 26/41/10461 [pii]
AID - 3152583 [pii]
AID - 10.1523/JNEUROSCI.2579-06.2006 [doi]
PST - ppublish
SO  - J Neurosci. 2006 Oct 11;26(41):10461-71. doi: 10.1523/JNEUROSCI.2579-06.2006.