Schaffer collateral and perforant path inputs activate different subtypes of NMDA receptors on the same CA1 pyramidal cell

Elda Arrigoni, Robert W. Greene

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

1. The two major inputs to CA1 pyramidal neurons, the perforant pathway (PP) that terminates on distal dendrites and the Schaffer collaterals (SCH) that terminate on proximal dendrites, activate both AMPA and N-methyl-D-aspartate (NMDA) receptors. 2. In an in vitro slice preparation, the pharmacologically isolated NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) (NMDA-EPSCs) of either pathway can be selectively activated onto a single CA1 pyramidal neuron. 3. Analysis of the decay phase of PP and SCH NMDA-EPSCs revealed no significant difference in their time constants, suggesting no apparent different distribution in NR2-subunit composition in the NMDA receptors (NMDAR) activated by the two synaptic inputs. 4. However, application of the NR2B-selective antagonist, ifenprodil, differently affected the NMDA-EPSCs activated by the PP and SCH inputs. The reduction of the PP responses was only 30% compared to 75% for the SCH responses. 5. In addition, for both pathways, the ifenprodil-insensitive component of the NMDA-EPSCs had significantly more rapid decay kinetics than those prior to application of ifenprodil. 6. Our results show a greater NR2B subunit contribution to the NMDA component of the SCH EPSC, compared to the NMDA component of the PP EPSC and that in single CA1 pyramidal neurons NMDA composition is anatomically specific to the afferent input.

Original languageEnglish (US)
Pages (from-to)317-322
Number of pages6
JournalBritish Journal of Pharmacology
Volume142
Issue number2
DOIs
StatePublished - May 2004

Fingerprint

Perforant Pathway
Pyramidal Cells
Excitatory Postsynaptic Potentials
N-Methylaspartate
N-Methyl-D-Aspartate Receptors
Hippocampus
Dendrites
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
ifenprodil

Keywords

  • EPSC decay kinetics
  • Ifenprodil
  • NMDA receptor-mediated EPSC
  • NR2B subunit
  • Perforant pathway
  • Schaffer collateral
  • Whole-cell patch-clamp

ASJC Scopus subject areas

  • Pharmacology

Cite this

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title = "Schaffer collateral and perforant path inputs activate different subtypes of NMDA receptors on the same CA1 pyramidal cell",
abstract = "1. The two major inputs to CA1 pyramidal neurons, the perforant pathway (PP) that terminates on distal dendrites and the Schaffer collaterals (SCH) that terminate on proximal dendrites, activate both AMPA and N-methyl-D-aspartate (NMDA) receptors. 2. In an in vitro slice preparation, the pharmacologically isolated NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) (NMDA-EPSCs) of either pathway can be selectively activated onto a single CA1 pyramidal neuron. 3. Analysis of the decay phase of PP and SCH NMDA-EPSCs revealed no significant difference in their time constants, suggesting no apparent different distribution in NR2-subunit composition in the NMDA receptors (NMDAR) activated by the two synaptic inputs. 4. However, application of the NR2B-selective antagonist, ifenprodil, differently affected the NMDA-EPSCs activated by the PP and SCH inputs. The reduction of the PP responses was only 30{\%} compared to 75{\%} for the SCH responses. 5. In addition, for both pathways, the ifenprodil-insensitive component of the NMDA-EPSCs had significantly more rapid decay kinetics than those prior to application of ifenprodil. 6. Our results show a greater NR2B subunit contribution to the NMDA component of the SCH EPSC, compared to the NMDA component of the PP EPSC and that in single CA1 pyramidal neurons NMDA composition is anatomically specific to the afferent input.",
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N2 - 1. The two major inputs to CA1 pyramidal neurons, the perforant pathway (PP) that terminates on distal dendrites and the Schaffer collaterals (SCH) that terminate on proximal dendrites, activate both AMPA and N-methyl-D-aspartate (NMDA) receptors. 2. In an in vitro slice preparation, the pharmacologically isolated NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) (NMDA-EPSCs) of either pathway can be selectively activated onto a single CA1 pyramidal neuron. 3. Analysis of the decay phase of PP and SCH NMDA-EPSCs revealed no significant difference in their time constants, suggesting no apparent different distribution in NR2-subunit composition in the NMDA receptors (NMDAR) activated by the two synaptic inputs. 4. However, application of the NR2B-selective antagonist, ifenprodil, differently affected the NMDA-EPSCs activated by the PP and SCH inputs. The reduction of the PP responses was only 30% compared to 75% for the SCH responses. 5. In addition, for both pathways, the ifenprodil-insensitive component of the NMDA-EPSCs had significantly more rapid decay kinetics than those prior to application of ifenprodil. 6. Our results show a greater NR2B subunit contribution to the NMDA component of the SCH EPSC, compared to the NMDA component of the PP EPSC and that in single CA1 pyramidal neurons NMDA composition is anatomically specific to the afferent input.

AB - 1. The two major inputs to CA1 pyramidal neurons, the perforant pathway (PP) that terminates on distal dendrites and the Schaffer collaterals (SCH) that terminate on proximal dendrites, activate both AMPA and N-methyl-D-aspartate (NMDA) receptors. 2. In an in vitro slice preparation, the pharmacologically isolated NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) (NMDA-EPSCs) of either pathway can be selectively activated onto a single CA1 pyramidal neuron. 3. Analysis of the decay phase of PP and SCH NMDA-EPSCs revealed no significant difference in their time constants, suggesting no apparent different distribution in NR2-subunit composition in the NMDA receptors (NMDAR) activated by the two synaptic inputs. 4. However, application of the NR2B-selective antagonist, ifenprodil, differently affected the NMDA-EPSCs activated by the PP and SCH inputs. The reduction of the PP responses was only 30% compared to 75% for the SCH responses. 5. In addition, for both pathways, the ifenprodil-insensitive component of the NMDA-EPSCs had significantly more rapid decay kinetics than those prior to application of ifenprodil. 6. Our results show a greater NR2B subunit contribution to the NMDA component of the SCH EPSC, compared to the NMDA component of the PP EPSC and that in single CA1 pyramidal neurons NMDA composition is anatomically specific to the afferent input.

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