Document Detail


Local protein synthesis and GABAB receptors regulate the reversibility of long-term potentiation at murine hippocampal mossy fibre-CA3 synapses.
MedLine Citation:
PMID:  15345751     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reversal of long-term potentiation (LTP) by long trains of low-frequency stimulation is generally referred to as depotentiation. One of the intriguing aspects of depotentiation is that the magnitude of depotentiation is inversely proportional to the time lag of depotentiation stimulation following LTP induction. Although the mechanisms underlying depotentiation have been widely explored, the factors that regulate the susceptibility of LTP to depotentiation stimulation remain largely unclear. We now report that multiple trains of high-frequency stimulation provide immediate synaptic resistance to depotentiation stimulation at the mossy fibre-CA3 synapses. The synaptic resistance to depotentiation stimulation depends on the amount of synaptic stimulation used to induce LTP; it is prevented by protein synthesis inhibitors and is input specific. In contrast, neither the transection of mossy fibre axons near granule cell somata nor the application of RNA synthesis inhibitors influences synaptic resistance to depotentiation stimulation. We also provide evidence that the induction of depotentiation is regulated by GABA(B) receptors. Application of a GABA(B) receptor antagonist significantly promoted the synaptic resistance to depotentiation stimulation, whereas inhibition of GABA transport delayed the onset of this synaptic resistance. These results suggest that local protein synthesis is required for the development of synaptic resistance to depotentiation stimulation, whereas the activation of GABA(B) receptors promotes the susceptibility to depotentiation stimulation. These two factors may crucially regulate the reversal and stability of long-term information storage.
Authors:
Chiung-Chun Huang; Kuei-Sen Hsu
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-09-02
Journal Detail:
Title:  The Journal of physiology     Volume:  561     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-19     Completed Date:  2005-04-06     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  91-108     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, College of Medicine, National Cheng Kung University, No. 1, Ta-Hsiue Road, Tainan 701, Taiwan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Baclofen / pharmacology
Electric Stimulation
Excitatory Postsynaptic Potentials / drug effects,  physiology
GABA Agonists / pharmacology
GABA Antagonists / pharmacology
Long-Term Potentiation / physiology*
Mice
Mice, Inbred C57BL
Morpholines / pharmacology
Mossy Fibers, Hippocampal / physiology*
Neuronal Plasticity / physiology
Patch-Clamp Techniques
Presynaptic Terminals / physiology*
Receptors, GABA-B / physiology*
gamma-Aminobutyric Acid / physiology
Chemical
Reg. No./Substance:
0/(+)-(S)-5,5-dimethylmorpholinyl-2-acetic acid; 0/GABA Agonists; 0/GABA Antagonists; 0/Morpholines; 0/Receptors, GABA-B; 1134-47-0/Baclofen; 56-12-2/gamma-Aminobutyric Acid
Comments/Corrections

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