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K369I Tau Mice Demonstrate a Shift Towards Striatal Neuron Burst Firing and Goal-directed Behaviour by Max Mo; Marie E. Jönsson; Miranda A. Mathews; Daniel Johnstone; Yazi D. Ke; Lars M. Ittner; Bernard W. Balleine; Teri M. Furlong; Aaron J. Camp is a Neuroscience article available to read on EtoBox.

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Pathological forms of the microtubule-associated protein tau are involved in a large group of neurodegenerative diseases named tauopathies, including frontotemporal lobar degeneration (FTLD-tau). K369I mutant tau transgenic mice (K3 mice) recapitulate neural and behavioural symptoms of FTLD, including tau aggregates in the cortex, alterations to nigrostriatum, memory deficits and parkinsonism. The aim of this study was to further characterise the K3 mouse model by examining functional alterations to the striatum. Whole-cell patch-clamp electrophysiology was used to investigate the properties of striatal neurons in K3 mice and wildtype controls. Additionally, striatal-based instrumental learning tasks were conducted to assess goal-directed versus habitual behaviours (i.e., by examining sensitivity to outcome devaluation and progressive ratios). The K3 model demonstrated significant alterations in the discharge properties of striatal neurons relative to wildtype mice, which manifested as a shift in neuronal output towards a burst firing state. K3 mice acquired goal-directed responding faster than control mice and were goal-directed at test unlike wildtype mice, which is likely to ind

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Author

Max Mo; Marie E. Jönsson; Miranda A. Mathews; Daniel Johnstone; Yazi D. Ke; Lars M. Ittner; Bernard W. Balleine; Teri M. Furlong; Aaron J. Camp

Publisher

Elsevier BV

Published

2020

Language

EN

Field

Neuroscience (Life Sciences)