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Transgenic Mice with Chronic NGF Deprivation and Alzheimer's Disease-Like Pathology Display Hippocampal Region-Specific Impairments in Short- and Long-Term Plasticities

Gry Houeland, Armando Romani, Cristina Marchetti, Gianluca Amato, Simona Capsoni, Antonino Cattaneo and Hélène Marie
Journal of Neuroscience 29 September 2010, 30 (39) 13089-13094; DOI: https://doi.org/10.1523/JNEUROSCI.0457-10.2010
Gry Houeland
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Armando Romani
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Cristina Marchetti
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Gianluca Amato
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Simona Capsoni
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Antonino Cattaneo
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Hélène Marie
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    Figure 1.

    Short-term plasticity deficits at the SC–CA1 and MPP–DG synapses of fully symptomatic (11–13 months) AD11 mice. A, SC–CA1 synapse input–output curves (fEPSP slopes versus increasing afferent FV amplitudes) were similar in aged-matched WT and AD11 mice (n = slices, N= mice). B, SC–CA1 synapse PPRs (fEPSP2 slope/fEPSP1 slope) were similar in WT and AD11 mice at all ISIs examined. C, Synaptic facilitation during repeated stimulation (15 pulses at 40 Hz) was significantly reduced at the SC–CA1 synapse from the fifth stimulus onwards in AD11 compared to WT mice (normalized to first response of train). D, MPP–DG synapse input–output curves were similar in WT and AD11 mice. E, PPR was altered, displaying increased depression, at the MPP–DG synapse of AD11 compared to WT mice. F, Synaptic depression during repeated stimulation (15 pulses at 40 Hz) was increased at the MPP–DG synapse from the fifth stimulus onwards in AD11 compared to WT mice (normalized to first response of train). Representative traces of fEPSP recordings of responses at FV intensities 100–300 μV (A, D), of PPR (all ISIs) (B, E), and of the train of fEPSPs (C, F) are shown above graphs for WT and AD11 mice. *p < 0.05; **p < 0.01.

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    Figure 2.

    LTP was normal at the SC–CA1 synapse, but defective at the MPP–DG synapse in fully symptomatic (11–13 months) AD11 mice. A, Summary graphs of TBS-LTP (arrow) elicited at the SC–CA1 synapse of AD11 and WT mice (n = slices, N= mice). B, Summary of fEPSP magnitude 0–20 min and 40–60 min after LTP induction (time 0) at the SC–CA1 synapse as percentage of baseline. C, Summary graphs of TBS-LTP (arrow) elicited at the MPP–DG synapse of AD11 and WT mice. D, Summary of fEPSP magnitude 0–20 min and 40–60 min after LTP induction (time 0) at the MPP–DG synapse as percentage of baseline. Traces in A and C show sample fEPSPs before LTP induction (1) and after LTP induction (2; 10–20 min after induction). **p < 0.01.

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    Figure 3.

    AD11 mice display enhanced synaptic transmission at both synapses under conditions of low release probability. Recordings of hippocampal slices were performed in [Ca2+]o of 1 mm (n = slices, N= mice), leading to conditions of low release probability. A, The input–output curve was significantly altered, displaying enhanced transmission, at the SC–CA1 synapse of 11- to 13-month-old AD11 compared to WT mice. B, The input–output curve was significantly altered, displaying enhanced transmission, at the MPP–DG synapse of 11- to 13-month-old AD11 compared to WT mice. C, The input–output curve at the SC–CA1 synapse of AD11 was similar to WT mice at 1 month of age. D, The input–output curve at the MPP–DG synapse of AD11 was similar to WT mice at 1 month of age. Representative fEPSP recordings are shown with each graph for FV intensities 100–300 μV.

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The Journal of Neuroscience: 30 (39)
Journal of Neuroscience
Vol. 30, Issue 39
29 Sep 2010
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Transgenic Mice with Chronic NGF Deprivation and Alzheimer's Disease-Like Pathology Display Hippocampal Region-Specific Impairments in Short- and Long-Term Plasticities
Gry Houeland, Armando Romani, Cristina Marchetti, Gianluca Amato, Simona Capsoni, Antonino Cattaneo, Hélène Marie
Journal of Neuroscience 29 September 2010, 30 (39) 13089-13094; DOI: 10.1523/JNEUROSCI.0457-10.2010

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Transgenic Mice with Chronic NGF Deprivation and Alzheimer's Disease-Like Pathology Display Hippocampal Region-Specific Impairments in Short- and Long-Term Plasticities
Gry Houeland, Armando Romani, Cristina Marchetti, Gianluca Amato, Simona Capsoni, Antonino Cattaneo, Hélène Marie
Journal of Neuroscience 29 September 2010, 30 (39) 13089-13094; DOI: 10.1523/JNEUROSCI.0457-10.2010
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