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Titolo:
Time-dependent reversal of long-term potentiation by low-frequency stimulation at the hippocampal mossy fiber-CA3 synapses
Autore:
Chen, YL; Huang, CC; Hsu, KS;
Indirizzi:
Natl Cheng Kung Univ, Coll Med, Dept Pharmacol, Tainan 701, Taiwan Natl Cheng Kung Univ Tainan Taiwan 701 ept Pharmacol, Tainan 701, Taiwan
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 11, volume: 21, anno: 2001,
pagine: 3705 - 3714
SICI:
0270-6474(20010601)21:11<3705:TROLPB>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
METABOTROPIC GLUTAMATE RECEPTORS; SYNAPTIC PLASTICITY; RAT HIPPOCAMPUS; HETEROSYNAPTIC DEPRESSION; PROTEIN PHOSPHATASES; 2 FORMS; LTP; RESPONSES; DEPOTENTIATION; ANTAGONISTS;
Keywords:
long-term potentiation (LTP); long-term depression (LTD); depotentiation; metabotropic glutamate receptor (mGluR); mossy fiber pathway; hippocampus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Hsu, KS Natl Cheng Kung Univ, Coll Med, Dept Pharmacol, 1 Ta-Hsiue Rd, Tainan 701,Taiwan Natl Cheng Kung Univ 1 Ta-Hsiue Rd Tainan Taiwan 701 n 701,Taiwan
Citazione:
Y.L. Chen et al., "Time-dependent reversal of long-term potentiation by low-frequency stimulation at the hippocampal mossy fiber-CA3 synapses", J NEUROSC, 21(11), 2001, pp. 3705-3714

Abstract

Using mouse hippocampal slices, we studied the induction of depotentiationof long-term potentiation (LTP) at the mossy fiber synapses onto CA3 pyramidal neurons. A long train of low-frequency (1 Hz/900 pulses) stimulation (LFS) induced a long-term depression of baseline synaptic transmission or depotentiation of previously established LTP, which was reversible and was independent of NMDA receptor activation. This LFS-induced depotentiation was observed when the stimulus was delivered 1 or 10 min after LTP induction. However, when LFS was applied at 30 min after induction, significantly less depotentiation was found. The induction of depotentiation on one input was associated with a heterosynaptic reverse of the LTP induced previously on aseparate pathway. In addition, this LFS-induced depotentiation appeared tobe mediated by the activation of group 2 metabotropic glutamate receptors (mGluRs), because it was mimicked by the bath-applied group 2 agonist (2S, 2'R, 3'R)- 2-(2',3'-dicarboxycyclopropyl) glycine and was specifically inhibited by the group 2 antagonists (S) -alpha -methyl-4-carboxyphenylglycine and (alphaS)-alpha -amino-alpha- (1S,2S) 2-carboxycyclopropyl- 9H-xanthine-9-propanic acid. Moreover, the induction of depotentiation was entirely normal when synaptic transmission is blocked by glutamate receptor antagonist kynurenic acid and was associated with a reversal of paired-pulse facilitation attenuation during LTP expression. Pretreatment of the hippocampal slices with G(i/o)-protein inhibitor pertussis toxin (PTX) prevented the LFS-induced depotentiation. These results suggest that the activation of presynaptic group 2 mGluRs and in turn triggering a PTX-sensitive G(i/o)-protein-coupled signaling cascade may contribute to the LFS-induced depotentiation atthe mossy fiber-CA3 synapses.

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Documento generato il 02/04/20 alle ore 00:15:40