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Postsynaptic IP3 receptor-mediated Ca2+ release modulates synaptic transmission in hippocampal neurons.
Brain Res Mol Brain Res 2005; 135(1-2):232-48BR

Abstract

Ca(2+)-dependent mechanisms are important in regulating synaptic transmission. The results herein indicate that whole-cell perfusion of inositol 1,4,5-trisphosphate receptor (IP(3)R) agonists greatly enhanced excitatory postsynaptic current (EPSC) amplitudes in postsynaptic hippocampal CA1 neurons. IP(3)R agonist-mediated increases in synaptic transmission changed during development and paralleled age-dependent increases in hippocampal type-1 IP(3)Rs. IP(3)R agonist-mediated increases in EPSC amplitudes were inhibited by postsynaptic perfusion of inhibitors of Ca(2+)/calmodulin, PKC and Ca(2+)/calmodulin-dependent protein kinase II. Postsynaptic perfusion of inhibitors of smooth endoplasmic reticulum (SER) Ca(2+)-ATPases, which deplete intracellular Ca(2+) stores, also enhanced EPSC amplitudes. Postsynaptic perfusion of the IP(3)R agonist adenophostin (AdA) during subthreshold stimulation appeared to convert silent to active synapses; synaptic transmission at these active synapses was completely blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Postsynaptic IP(3)R-mediated Ca(2+) release also produced a significant increase in spontaneous EPSC frequency. These results indicate that Ca(2+) release from intracellular stores play a key role in regulating the function of postsynaptic AMPARs.

Authors+Show Affiliations

Department of Molecular Biosciences, University of Kansas, Lawrence, KS 66045-2106, USA. ptkelly@ku.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15857686

Citation

Kelly, Paul T., et al. "Postsynaptic IP3 Receptor-mediated Ca2+ Release Modulates Synaptic Transmission in Hippocampal Neurons." Brain Research. Molecular Brain Research, vol. 135, no. 1-2, 2005, pp. 232-48.
Kelly PT, Mackinnon RL, Dietz RV, et al. Postsynaptic IP3 receptor-mediated Ca2+ release modulates synaptic transmission in hippocampal neurons. Brain Res Mol Brain Res. 2005;135(1-2):232-48.
Kelly, P. T., Mackinnon, R. L., Dietz, R. V., Maher, B. J., & Wang, J. (2005). Postsynaptic IP3 receptor-mediated Ca2+ release modulates synaptic transmission in hippocampal neurons. Brain Research. Molecular Brain Research, 135(1-2), pp. 232-48.
Kelly PT, et al. Postsynaptic IP3 Receptor-mediated Ca2+ Release Modulates Synaptic Transmission in Hippocampal Neurons. Brain Res Mol Brain Res. 2005 Apr 27;135(1-2):232-48. PubMed PMID: 15857686.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Postsynaptic IP3 receptor-mediated Ca2+ release modulates synaptic transmission in hippocampal neurons. AU - Kelly,Paul T, AU - Mackinnon,Roger L,2nd AU - Dietz,Roger V, AU - Maher,Brady J, AU - Wang,J, PY - 2004/06/27/received PY - 2004/12/15/revised PY - 2004/12/20/accepted PY - 2005/4/29/pubmed PY - 2005/7/26/medline PY - 2005/4/29/entrez SP - 232 EP - 48 JF - Brain research. Molecular brain research JO - Brain Res. Mol. Brain Res. VL - 135 IS - 1-2 N2 - Ca(2+)-dependent mechanisms are important in regulating synaptic transmission. The results herein indicate that whole-cell perfusion of inositol 1,4,5-trisphosphate receptor (IP(3)R) agonists greatly enhanced excitatory postsynaptic current (EPSC) amplitudes in postsynaptic hippocampal CA1 neurons. IP(3)R agonist-mediated increases in synaptic transmission changed during development and paralleled age-dependent increases in hippocampal type-1 IP(3)Rs. IP(3)R agonist-mediated increases in EPSC amplitudes were inhibited by postsynaptic perfusion of inhibitors of Ca(2+)/calmodulin, PKC and Ca(2+)/calmodulin-dependent protein kinase II. Postsynaptic perfusion of inhibitors of smooth endoplasmic reticulum (SER) Ca(2+)-ATPases, which deplete intracellular Ca(2+) stores, also enhanced EPSC amplitudes. Postsynaptic perfusion of the IP(3)R agonist adenophostin (AdA) during subthreshold stimulation appeared to convert silent to active synapses; synaptic transmission at these active synapses was completely blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Postsynaptic IP(3)R-mediated Ca(2+) release also produced a significant increase in spontaneous EPSC frequency. These results indicate that Ca(2+) release from intracellular stores play a key role in regulating the function of postsynaptic AMPARs. SN - 0169-328X UR - https://www.unboundmedicine.com/medline/citation/15857686/Postsynaptic_IP3_receptor_mediated_Ca2+_release_modulates_synaptic_transmission_in_hippocampal_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0169-328X(04)00637-0 DB - PRIME DP - Unbound Medicine ER -