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Research ArticleNew Research, Neuronal Excitability

Presynaptic NR2A-Containing NMDARs Are Required for LTD between the Amygdala and the Perirhinal Cortex: A Potential Mechanism for the Emotional Modulation of Memory?

Michael D. Laing and Zafar I. Bashir
eNeuro 25 February 2015, 2 (1) ENEURO.0046-14.2015; https://doi.org/10.1523/ENEURO.0046-14.2015
Michael D. Laing
1Neuroscience and Mental Health Research Institute, Hadyn Ellis Building, Cathays, Cardiff, CF24 4HQ, United Kingdom
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Zafar I. Bashir
2School of Physiology and Pharmacology, Bristol University, Bristol, BS8 1TD, United Kingdom
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  • Figure 1
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    Figure 1

    LTD is NMDAR-dependent, but is not dependent on β-ADRs or VGCCs. A, Schematic diagram highlighting the recording and stimulating positions within the horizontal slice preparation with LA and PRh highlighted. L, Lateral; A, anterior; M, medial; P, posterior. B, Pooled data showing induction of LTD by LFS (200 pulses at 1 Hz, black circles) during application of a holding potential to −40 mV. Intercalated control experiments are presented as white circles. Inserts here and all graphs show response traces during baseline (black) and following manipulation (red). In all cases, the scale bar dimensions remain the same (150 pA by 15 ms). Dotted horizontal lines act as a visual aid to the 100% baseline and the gray vertical bars represent the period of LFS delivery. C, Pooled data highlighting that blockade of β-ADRs with propranolol did not prevent the induction of LTD. D, Pooled data showing that LTD induction was not dependent on VGCCs. E, Pooled data highlighting that bath application of D-AP5 prevented the induction of LTD. F, Pooled data to show that application of L-689,560 prevented the induction of LTD.

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    Figure 2

    Blockade of postsynaptic NMDARs did not prevent the induction of LTD. A, Application of the NMDAR pore-channel blocker MK-801 to the internal patch solution did not prevent LFS from inducing LTD. B, Control experiment demonstrating that NMDAR currents could not be evoked when MK-801 was present in the internal patch solution. B1, B2, Traces of an NMDAR EPSC at −40 mV and +40 mV in the absence (B1) and presence (B2) of internal MK-801. B3, Box plot demonstrating the peak amplitude of the NMDAR response in the presence and absence of MK-801 in the internal patch solution. C, Holding the cell at −90 mV during the delivery of LFS did not prevent the induction of LTD. D, Application of the calcium chelator BAPTA to the internal patch solution did not prevent the induction of LTD. **p ≤ 0.01, ***p ≤ 0.001.

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    Figure 3

    LTD induction relies on NR2A- but not NR2B-containing NMDARs. A, Bath application of the NR2B-selective antagonist RO 25-6981 did not prevent the induction of LTD. B, Bath application of the NR2A-selective antagonist NVP-AAM077 prevented the induction of LTD. C, Bath application of the NR2A-selective antagonist TCN-201 prevented the induction of LTD. D, Bath application of the CB1R antagonist AM 251 did not prevent the induction of LTD. E, Paired-pulse facilitation is observed at the LA−PRh input during baseline recording and 30 min post-LFS. However, the facilitation is reduced by the delivery of the LFS protocol. *p < 0.05.

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    Table 1:

    Statistical table

    Data structureType of testp value
    aNormal distributionPaired t test0.0045
    bNormal distributionPaired t test0.6
    cNormal distributionPaired T test0.01
    dNormal distributionPaired t test0.0089
    eNormal distributionPaired t test0.16
    fNormal distributionPaired t test0.41
    gNormal distributionPaired t test0.029
    hNormal distributionUnpaired t test0.92
    iNormal distributionUnpaired t test0.0015
    jNormal distributionUnpaired t test≤0.0001
    kNormal distributionPaired t test0.028
    lNormal distributionPaired t test≤0.0001
    mNormal distributionPaired t test0.012
    nNormal distributionPaired t test0.054
    oNormal distributionPaired t test0.22
    pNormal distributionPaired t test0.034
    qNormal distributionPaired t test0.044
    rNormal distributionUnpaired t test0.023
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eneuro: 2 (1)
eNeuro
Vol. 2, Issue 1
January/February 2015
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Presynaptic NR2A-Containing NMDARs Are Required for LTD between the Amygdala and the Perirhinal Cortex: A Potential Mechanism for the Emotional Modulation of Memory?
Michael D. Laing, Zafar I. Bashir
eNeuro 25 February 2015, 2 (1) ENEURO.0046-14.2015; DOI: 10.1523/ENEURO.0046-14.2015

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Presynaptic NR2A-Containing NMDARs Are Required for LTD between the Amygdala and the Perirhinal Cortex: A Potential Mechanism for the Emotional Modulation of Memory?
Michael D. Laing, Zafar I. Bashir
eNeuro 25 February 2015, 2 (1) ENEURO.0046-14.2015; DOI: 10.1523/ENEURO.0046-14.2015
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Keywords

  • amygdala
  • emotion
  • memory
  • perirhinal
  • plasticity
  • transmission

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