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Synaptic dysfunction in hippocampus of transgenic mouse models of Alzheimer's disease: a multi-electrode array study.
Neurobiol Dis. 2011 Dec; 44(3):284-91.ND

Abstract

APP.V717I and Tau.P301L transgenic mice develop Alzheimer's disease pathology comprising important aspects of human disease including increased levels of amyloid peptides, cognitive and motor impairment, amyloid plaques and neurofibrillary tangles. The combined model, APP.V717I×Tau.P301L bigenic mice (biAT mice) exhibit aggravated amyloid and tau pathology with severe cognitive and behavioral defects. In the present study, we investigated early changes in synaptic function in the CA1 and CA3 regions of acute hippocampal slices of young APP.V717I, Tau.P301L and biAT transgenic animals. We have used planar multi-electrode arrays (MEA) and improved methods for simultaneous multi-site recordings from two hippocampal sub-regions. In the CA1 region, long-term potentiation (LTP) was severely impaired in all transgenic animals when compared with age-matched wild-type controls, while basal synaptic transmission and paired-pulse facilitation were minimally affected. In the CA3 region, LTP was normal in Tau.P301L and APP.V717I but clearly impaired in biAT mice. Surprisingly, frequency facilitation in CA3 was significantly enhanced in Tau.P301L mice, while not affected in APP.V717I mice and depressed in biAT mice. The findings demonstrate important synaptic changes that differ considerably in the hippocampal sub-regions already at young age, well before the typical amyloid or tau pathology is evident.

Authors+Show Affiliations

Bio-Electronic Systems, Imec, Kapeldreef 75, Leuven, Belgium.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21807097

Citation

Chong, Seon-Ah, et al. "Synaptic Dysfunction in Hippocampus of Transgenic Mouse Models of Alzheimer's Disease: a Multi-electrode Array Study." Neurobiology of Disease, vol. 44, no. 3, 2011, pp. 284-91.
Chong SA, Benilova I, Shaban H, et al. Synaptic dysfunction in hippocampus of transgenic mouse models of Alzheimer's disease: a multi-electrode array study. Neurobiol Dis. 2011;44(3):284-91.
Chong, S. A., Benilova, I., Shaban, H., De Strooper, B., Devijver, H., Moechars, D., Eberle, W., Bartic, C., Van Leuven, F., & Callewaert, G. (2011). Synaptic dysfunction in hippocampus of transgenic mouse models of Alzheimer's disease: a multi-electrode array study. Neurobiology of Disease, 44(3), 284-91. https://doi.org/10.1016/j.nbd.2011.07.006
Chong SA, et al. Synaptic Dysfunction in Hippocampus of Transgenic Mouse Models of Alzheimer's Disease: a Multi-electrode Array Study. Neurobiol Dis. 2011;44(3):284-91. PubMed PMID: 21807097.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Synaptic dysfunction in hippocampus of transgenic mouse models of Alzheimer's disease: a multi-electrode array study. AU - Chong,Seon-Ah, AU - Benilova,Iryna, AU - Shaban,Hamdy, AU - De Strooper,Bart, AU - Devijver,Herman, AU - Moechars,Dieder, AU - Eberle,Wolfgang, AU - Bartic,Carmen, AU - Van Leuven,Fred, AU - Callewaert,Geert, Y1 - 2011/07/18/ PY - 2011/02/15/received PY - 2011/05/19/revised PY - 2011/07/06/accepted PY - 2011/8/3/entrez PY - 2011/8/3/pubmed PY - 2012/2/7/medline SP - 284 EP - 91 JF - Neurobiology of disease JO - Neurobiol. Dis. VL - 44 IS - 3 N2 - APP.V717I and Tau.P301L transgenic mice develop Alzheimer's disease pathology comprising important aspects of human disease including increased levels of amyloid peptides, cognitive and motor impairment, amyloid plaques and neurofibrillary tangles. The combined model, APP.V717I×Tau.P301L bigenic mice (biAT mice) exhibit aggravated amyloid and tau pathology with severe cognitive and behavioral defects. In the present study, we investigated early changes in synaptic function in the CA1 and CA3 regions of acute hippocampal slices of young APP.V717I, Tau.P301L and biAT transgenic animals. We have used planar multi-electrode arrays (MEA) and improved methods for simultaneous multi-site recordings from two hippocampal sub-regions. In the CA1 region, long-term potentiation (LTP) was severely impaired in all transgenic animals when compared with age-matched wild-type controls, while basal synaptic transmission and paired-pulse facilitation were minimally affected. In the CA3 region, LTP was normal in Tau.P301L and APP.V717I but clearly impaired in biAT mice. Surprisingly, frequency facilitation in CA3 was significantly enhanced in Tau.P301L mice, while not affected in APP.V717I mice and depressed in biAT mice. The findings demonstrate important synaptic changes that differ considerably in the hippocampal sub-regions already at young age, well before the typical amyloid or tau pathology is evident. SN - 1095-953X UR - https://www.unboundmedicine.com/medline/citation/21807097/Synaptic_dysfunction_in_hippocampus_of_transgenic_mouse_models_of_Alzheimer's_disease:_a_multi_electrode_array_study_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0969-9961(11)00232-4 DB - PRIME DP - Unbound Medicine ER -