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Increase in AMPA receptor-mediated miniature EPSC amplitude after chronic NMDA receptor blockade in cultured hippocampal neurons.
Neurosci Lett. 2007 May 11; 418(1):4-8.NL

Abstract

Synaptic scaling has been reported as scaling up of AMPA receptors (AMPAR)-mediated miniature excitatory postsynaptic currents (mEPSCs) induced by blockade of action potentials or AMPAR. Here, we show a novel type of synaptic scaling induced by N-methyl-D-aspartate receptors (NMDAR) blockade. In the present study, we analyzed AMPAR-mediated mEPSCs of D-(-)-2-amino-5-phosphonopentanoic acid (AP5)-treated hippocampal neurons (16 days in vitro) for 48 h in low-density cultures, using a whole-cell patch-clamp technique. The mEPSC amplitudes recorded from chronic AP5-treated neurons (25.5+/-0.3 pA; n=30 neurons) were significantly larger than that recorded from control neurons (21.6+/-0.2 pA; n=30 neurons, p<0.05), whereas the frequency of mEPSCs was not changed. Immunocytochemistry showed that the number of synapsin I clusters of AP5-treated neurons was not different from that of control neurons. Cumulative amplitude histograms revealed that the amplitude of mEPSCs was scaled multiplicatively after AP5 treatment. GluR2-lacking AMPAR were not involved in the scaling observed here. Together, our data indicate that NMDAR activity, as well as AMPAR activity, is involved in the negative feedback plasticity of AMPAR-mediated synaptic activity.

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Authors+Show Affiliations

Kato K
Department of Neurobiology and Behavior, Gunma University Graduate School of Medicine, Maebashi, Japan.
Sekino Y
No affiliation info available
Takahashi H
No affiliation info available
Yasuda H
No affiliation info available
Shirao T
No affiliation info available

MeSH

AnimalsCells, CulturedExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsHippocampusImmunohistochemistryNeuronal PlasticityNeuronsPatch-Clamp TechniquesRatsRats, WistarReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17395372

Citation

Kato, Kenichi, et al. "Increase in AMPA Receptor-mediated Miniature EPSC Amplitude After Chronic NMDA Receptor Blockade in Cultured Hippocampal Neurons." Neuroscience Letters, vol. 418, no. 1, 2007, pp. 4-8.
Kato K, Sekino Y, Takahashi H, et al. Increase in AMPA receptor-mediated miniature EPSC amplitude after chronic NMDA receptor blockade in cultured hippocampal neurons. Neurosci Lett. 2007;418(1):4-8.
Kato, K., Sekino, Y., Takahashi, H., Yasuda, H., & Shirao, T. (2007). Increase in AMPA receptor-mediated miniature EPSC amplitude after chronic NMDA receptor blockade in cultured hippocampal neurons. Neuroscience Letters, 418(1), 4-8.
Kato K, et al. Increase in AMPA Receptor-mediated Miniature EPSC Amplitude After Chronic NMDA Receptor Blockade in Cultured Hippocampal Neurons. Neurosci Lett. 2007 May 11;418(1):4-8. PubMed PMID: 17395372.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increase in AMPA receptor-mediated miniature EPSC amplitude after chronic NMDA receptor blockade in cultured hippocampal neurons. AU - Kato,Kenichi, AU - Sekino,Yuko, AU - Takahashi,Hideto, AU - Yasuda,Hiroki, AU - Shirao,Tomoaki, Y1 - 2007/03/01/ PY - 2007/01/10/received PY - 2007/02/23/revised PY - 2007/02/23/accepted PY - 2007/3/31/pubmed PY - 2007/7/13/medline PY - 2007/3/31/entrez SP - 4 EP - 8 JF - Neuroscience letters JO - Neurosci Lett VL - 418 IS - 1 N2 - Synaptic scaling has been reported as scaling up of AMPA receptors (AMPAR)-mediated miniature excitatory postsynaptic currents (mEPSCs) induced by blockade of action potentials or AMPAR. Here, we show a novel type of synaptic scaling induced by N-methyl-D-aspartate receptors (NMDAR) blockade. In the present study, we analyzed AMPAR-mediated mEPSCs of D-(-)-2-amino-5-phosphonopentanoic acid (AP5)-treated hippocampal neurons (16 days in vitro) for 48 h in low-density cultures, using a whole-cell patch-clamp technique. The mEPSC amplitudes recorded from chronic AP5-treated neurons (25.5+/-0.3 pA; n=30 neurons) were significantly larger than that recorded from control neurons (21.6+/-0.2 pA; n=30 neurons, p<0.05), whereas the frequency of mEPSCs was not changed. Immunocytochemistry showed that the number of synapsin I clusters of AP5-treated neurons was not different from that of control neurons. Cumulative amplitude histograms revealed that the amplitude of mEPSCs was scaled multiplicatively after AP5 treatment. GluR2-lacking AMPAR were not involved in the scaling observed here. Together, our data indicate that NMDAR activity, as well as AMPAR activity, is involved in the negative feedback plasticity of AMPAR-mediated synaptic activity. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/17395372/Increase_in_AMPA_receptor_mediated_miniature_EPSC_amplitude_after_chronic_NMDA_receptor_blockade_in_cultured_hippocampal_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(07)00251-0 DB - PRIME DP - Unbound Medicine ER -