期刊
JOURNAL OF NEUROSCIENCE
卷 36, 期 2, 页码 350-363出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2151-15.2016
关键词
GABA; intrinsic properties; place cell; resonance; synaptic plasticity
资金
- Medical Research Council funded CASE students
- EPSRC [EP/N014391/1, EP/L000296/1] Funding Source: UKRI
- MRC [G1100623, G1002064] Funding Source: UKRI
- Alzheimers Research UK [ARUK-SRF2012-6] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [EP/N014391/1, EP/L000296/1] Funding Source: researchfish
- Medical Research Council [G1100623, G1002064] Funding Source: researchfish
The formation and deposition of tau protein aggregates is proposed to contribute to cognitive impairments in dementia by disrupting neuronal function in brain regions, including the hippocampus. We used a battery of in vivo and in vitro electrophysiological recordings in the rTg4510 transgenic mouse model, which overexpresses a mutant form of human tau protein, to investigate the effects of tau pathology on hippocampal neuronal function in area CA1 of 7- to 8-month-old mice, an age point at which rTg4510 animals exhibit advanced tau pathology and progressive neurodegeneration. In vitro recordings revealed shifted theta-frequency resonance properties of CA1 pyramidal neurons, deficits in synaptic transmission at Schaffer collateral synapses, and blunted plasticity and imbalanced inhibition at temporoammonic synapses. These changes were associated with aberrant CA1 network oscillations, pyramidal neuron bursting, and spatial information coding in vivo. Our findings relate tauopathy-associated changes in cellular neurophysiology to altered behavior-dependent network function.
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