PMID- 28777881
OWN - NLM
STAT- MEDLINE
DCOM- 20190301
LR  - 20190301
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 144
IP  - 5
DP  - 2018 Mar
TI  - Early-stage attenuation of phase-amplitude coupling in the hippocampus and medial 
      prefrontal cortex in a transgenic rat model of Alzheimer's disease.
PG  - 669-679
LID - 10.1111/jnc.14136 [doi]
AB  - Alzheimer's disease (AD) is pathologically characterized by amyloid-beta peptide 
      (Abeta) accumulation, neurofibrillary tangle formation, and neurodegeneration. 
      Preclinical studies on neuronal impairments associated with progressive 
      amyloidosis have demonstrated some Abeta-dependent neuronal dysfunction including 
      modulation of gamma-aminobutyric acid-ergic signaling. The present work focuses 
      on the early stage of disease progression and uses TgF344-AD rats that 
      recapitulate a broad repertoire of AD-like pathologies to investigate the 
      neuronal network functioning using simultaneous intracranial recordings from the 
      hippocampus (HPC) and the medial prefrontal cortex (mPFC), followed by 
      pathological analyses of gamma-aminobutyric acid (GABA(A) ) receptor subunits 
      alpha1(,) alpha5, and delta, and glutamic acid decarboxylases (GAD65 and GAD67). Concomitant 
      to amyloid deposition and tau hyperphosphorylation, low-gamma band power was 
      strongly attenuated in the HPC and mPFC of TgF344-AD rats in comparison to those 
      in non-transgenic littermates. In addition, the phase-amplitude coupling of the 
      neuronal networks in both areas was impaired, evidenced by decreased modulation 
      of theta band phase on gamma band amplitude in TgF344-AD animals. Finally, the 
      gamma coherence between HPC and mPFC was attenuated as well. These results 
      demonstrate significant neuronal network dysfunction at an early stage of AD-like 
      pathology. This network dysfunction precedes the onset of cognitive deficits and 
      is likely driven by Abeta and tau pathologies. This article is part of the Special 
      Issue "Vascular Dementia".
CI  - (c) 2017 Her Majesty the Queen in Right of Canada Journal of Neurochemistry (c) 2017 
      International Society for Neurochemistry.
FAU - Bazzigaluppi, Paolo
AU  - Bazzigaluppi P
AD  - Physical Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
AD  - Fundamental Neurobiology, Krembil Research Institute, Toronto, Ontario, Canada.
FAU - Beckett, Tina L
AU  - Beckett TL
AD  - Physical Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
FAU - Koletar, Margaret M
AU  - Koletar MM
AD  - Physical Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
FAU - Lai, Aaron Y
AU  - Lai AY
AD  - Department of Laboratory Medicine and Pathobiology, University of Toronto, 
      Toronto, Ontario, Canada.
FAU - Joo, Illsung L
AU  - Joo IL
AD  - Physical Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
FAU - Brown, Mary E
AU  - Brown ME
AD  - Department of Laboratory Medicine and Pathobiology, University of Toronto, 
      Toronto, Ontario, Canada.
FAU - Carlen, Peter L
AU  - Carlen PL
AD  - Fundamental Neurobiology, Krembil Research Institute, Toronto, Ontario, Canada.
FAU - McLaurin, JoAnne
AU  - McLaurin J
AD  - Department of Laboratory Medicine and Pathobiology, University of Toronto, 
      Toronto, Ontario, Canada.
AD  - Biological Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
FAU - Stefanovic, Bojana
AU  - Stefanovic B
AUID- ORCID: 0000-0002-8439-7601
AD  - Physical Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
AD  - Department of Medical Biophysics, University of Toronto, Ontario, Canada.
LA  - eng
GR  - CAN-137794/CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171010
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Receptors, GABA-A)
RN  - EC 4.1.1.15 (Glutamate Decarboxylase)
RN  - EC 4.1.1.15 (glutamate decarboxylase 1)
RN  - EC 4.1.1.15 (glutamate decarboxylase 2)
SB  - IM
MH  - Alzheimer Disease/pathology/*physiopathology
MH  - Animals
MH  - Brain Waves
MH  - Disease Models, Animal
MH  - Female
MH  - Glutamate Decarboxylase/metabolism
MH  - Hippocampus/metabolism/pathology/*physiopathology
MH  - Male
MH  - Neural Pathways/physiopathology
MH  - Neurons/*physiology
MH  - Plaque, Amyloid/metabolism
MH  - Prefrontal Cortex/pathology/*physiopathology
MH  - Rats, Inbred F344
MH  - Rats, Transgenic
MH  - Receptors, GABA-A/metabolism
OTO - NOTNLM
OT  - GABA
OT  - Alzheimer's disease
OT  - TgF344
OT  - cross-frequency coupling
OT  - hippocampus
OT  - prefrontal cortex
EDAT- 2017/08/05 06:00
MHDA- 2019/03/02 06:00
CRDT- 2017/08/05 06:00
PHST- 2017/03/13 00:00 [received]
PHST- 2017/06/27 00:00 [revised]
PHST- 2017/07/26 00:00 [accepted]
PHST- 2017/08/05 06:00 [pubmed]
PHST- 2019/03/02 06:00 [medline]
PHST- 2017/08/05 06:00 [entrez]
AID - 10.1111/jnc.14136 [doi]
PST - ppublish
SO  - J Neurochem. 2018 Mar;144(5):669-679. doi: 10.1111/jnc.14136. Epub 2017 Oct 10.