Literature DB >> 29427204

Reduced cooperativity of voltage-gated sodium channels in the hippocampal interneurons of an aged mouse model of Alzheimer's disease.

Carlos Perez1, Ghanim Ullah2.   

Abstract

Beta amyloid (A[Formula: see text] ) associated with Alzheimer's disease (AD) leads to abnormal behavior in inhibitory neurons, resulting in hyperactive neuronal networks, epileptiform behavior, disrupted gamma rhythms, and aberrant synaptic plasticity. Previously, we used a dual modeling-experimental approach to explain several observations, including failure to reliably produce action potentials (APs), smaller AP amplitudes, higher resting membrane potential, and higher membrane depolarization in response to a range of stimuli in hippocampal inhibitory neurons from 12- to 16-month-old female AP Pswe/PSEN1DeltaE9 (APdE9) AD mice as compared to age-matched non-transgenic (NTG) mice. Our experimental results also showed that AP initiation in interneurons from APdE9 mice are significantly different from that of NTG mice. APs in interneurons from NTG mice are characterized by abrupt onset and an upstroke that is much steeper and occurs with larger variability as compared to cells from APdE9 mice. The phase plot (the rate of change of membrane potential versus the instantaneous membrane potential) of APs produced by interneurons from APdE9 mice shows a biphasic behavior, whereas that from NTG mice shows a monophasic behavior. Here we show that using the classic Hodgkin-Huxley (HH) formalism for the gating of voltage-gated sodium channels (VGSCs) in a single-compartment neuron, we cannot reproduce these features, and a model that takes into account a cooperative activation of VGSCs is needed. We also argue that considering a realistic multi-compartment neuron where the kinetics of VGSC is modeled by HH formalism, as done in the past, would not explain our observations when APs from both NTG and APdE9 mice are considered simultaneously. We further show that VGSCs in interneurons from APdE9 mice exhibit significantly lower cooperativity in their activation as compared to those from NTG mice.

Entities:  

Keywords:  Alzheimer’s disease; Beta amyloid; Channelopathy; Cooperative gating of Na channels; Interneurons

Mesh:

Substances:

Year:  2018        PMID: 29427204      PMCID: PMC6008176          DOI: 10.1007/s00249-017-1274-y

Source DB:  PubMed          Journal:  Eur Biophys J        ISSN: 0175-7571            Impact factor:   1.733


  31 in total

1.  Active dendrites and spike propagation in multi-compartment models of oriens-lacunosum/moleculare hippocampal interneurons.

Authors:  F Saraga; C P Wu; L Zhang; F K Skinner
Journal:  J Physiol       Date:  2003-08-15       Impact factor: 5.182

2.  Gamma oscillation by synaptic inhibition in a hippocampal interneuronal network model.

Authors:  X J Wang; G Buzsáki
Journal:  J Neurosci       Date:  1996-10-15       Impact factor: 6.167

3.  AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss.

Authors:  Helen Hsieh; Jannic Boehm; Chihiro Sato; Takeshi Iwatsubo; Taisuke Tomita; Sangram Sisodia; Roberto Malinow
Journal:  Neuron       Date:  2006-12-07       Impact factor: 17.173

4.  Reduced sodium channel Na(v)1.1 levels in BACE1-null mice.

Authors:  Doo Yeon Kim; Manuel T Gersbacher; Perrine Inquimbert; Dora M Kovacs
Journal:  J Biol Chem       Date:  2010-12-29       Impact factor: 5.157

5.  Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model.

Authors:  Laure Verret; Edward O Mann; Giao B Hang; Albert M I Barth; Inma Cobos; Kaitlyn Ho; Nino Devidze; Eliezer Masliah; Anatol C Kreitzer; Istvan Mody; Lennart Mucke; Jorge J Palop
Journal:  Cell       Date:  2012-04-27       Impact factor: 41.582

6.  Amyloid beta-induced neuronal hyperexcitability triggers progressive epilepsy.

Authors:  Rimante Minkeviciene; Sylvain Rheims; Marton B Dobszay; Misha Zilberter; Jarmo Hartikainen; Lívia Fülöp; Botond Penke; Yuri Zilberter; Tibor Harkany; Asla Pitkänen; Heikki Tanila
Journal:  J Neurosci       Date:  2009-03-18       Impact factor: 6.167

7.  Beta-amyloid protein (25-35) disrupts hippocampal network activity: role of Fyn-kinase.

Authors:  Fernando Peña; Benito Ordaz; Hugo Balleza-Tapia; Ramón Bernal-Pedraza; Abraham Márquez-Ramos; Liliana Carmona-Aparicio; Magda Giordano
Journal:  Hippocampus       Date:  2010-01       Impact factor: 3.899

Review 8.  The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

Authors:  John Hardy; Dennis J Selkoe
Journal:  Science       Date:  2002-07-19       Impact factor: 47.728

9.  Cortical action potential backpropagation explains spike threshold variability and rapid-onset kinetics.

Authors:  Yuguo Yu; Yousheng Shu; David A McCormick
Journal:  J Neurosci       Date:  2008-07-16       Impact factor: 6.167

Review 10.  Calcium regulation of neural rhythms, memory and Alzheimer's disease.

Authors:  Michael J Berridge
Journal:  J Physiol       Date:  2013-06-10       Impact factor: 5.182

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.