Cellular neuroscienceDopamine-dependent long term potentiation in the dorsal striatum is reduced in the R6/2 mouse model of Huntington’s disease
Section snippets
Animals
R6/2 transgenic mice were taken from a colony established in the Department of Pharmacology, University of Cambridge and maintained by backcrossing R6/2 males to CBA×C57BL/6 F1 females. Genotyping was confirmed by polymerase chain reaction as reported in Gibson et al. (2005). A common set of mice was used by Gibson et al. (2005) and in the present study both for electrophysiology and for measurement of the repeat lengths of the mutation carried by R6/2 mice, which were 243±3 (n=26 mice). The
Frequency-dependent bidirectional synaptic plasticity in the striatum
A recent study described frequency-dependent bidirectional synaptic plasticity in individual medium spiny neurons of the striatum from young rats (Fino et al., 2005). To determine whether frequency-dependent bidirectional plasticity could be evoked in the striatum of adult mice, we measured compound field potentials from populations of striatal neurons in the dorsolateral region of the striatum, evoked by stimulation of the overlying white matter. The field potential responses are likely to be
Discussion
We have found that striatal neurons of adult mice exhibit frequency-dependent bidirectional plasticity, with HFS inducing NMDA receptor- and dopamine D1 receptor-dependent LTP, and LFS inducing NMDA receptor-dependent LTD. Furthermore, we have found that LTP, but not LTD, is impaired in the striatum of adult R6/2 mice.
Our observation that evoked field potentials in the striatum of adult mice undergo frequency-dependent bidirectional plasticity is in agreement with the recent findings of Fino et
Acknowledgments
This work was supported by the Hereditary Disease Foundation USA, HighQ Foundation and CURE HD, USA; the Physiological Society and the Durham Fund, Kings College Cambridge (V.W.S.K.) and the Wellcome Trust (R.H.) provided vacation studentships.
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