Knockdown of zif268 in the posterior dorsolateral striatum does not enduringly disrupt a response memory of a rewarded T-maze task
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Cahill, E., Vousden, G., Exton-McGuinness, M., Beh, I., Swerner, C., Macak, M., Abas, S., et al. (2017). Knockdown of zif268 in the posterior dorsolateral striatum does not enduringly disrupt a response memory of a rewarded T-maze task. Neuroscience https://doi.org/10.1016/j.neuroscience.2017.07.014
Under certain conditions pavlovian memories undergo reconsolidation, whereby the reactivated memory can be disrupted by manipulations such as knockdown of zif268. For instrumental memories, reconsolidation disruption is less well established. Our previous, preliminary data identified that there was an increase in Zif268 in the posterior dorsolateral striatum (pDLS) after expression of an instrumental habit-like ‘response’ memory, but not an instrumental goal-directed ‘place’ memory on a T-maze task. Here, the requirement for Zif268 in the reconsolidation of a response memory was tested by knockdown of Zif268, using antisense oligodeoxynucleotide infusion into the pDLS, at memory reactivation. Zif268 knockdown reduced response memory expression 72H, but not 7d later. Western blotting revealed a non-significant increase in Zif268 in the pDLS in rats using response memories, but there was no change in Zif268 expression in the hippocampus following retrieval of a place memory. Zif268 expression increased in the basolateral amygdala after memory reactivation whether a response or place strategy was used during reactivation. We propose that Zif268 expression in the basolateral amygdala may be linked to prediction error, generated by the absence of reward at reactivation. Taken together, these results suggest a complex role for Zif268 in the maintenance of instrumental memories.
zif268, memory, striatum, amygdala, hippocampus, T-Maze
This work was conducted within the Behavioural and Clinical Neuroscience Institute (BCNI), a joint initiative funded by the Wellcome Trust and the UK Medical Research Council, in the Department of Psychology at the University of Cambridge. This work was funded by a UK Medical Research Council programme grant (no. G1002231) awarded to B.J.E. and A.L.M. G.H.V. was supported by a doctoral training grant from the BCNI. A.L.M. is the Ferreras-Willetts Fellow in Neuroscience at Downing College, Cambridge. E.N.C is a BBSRC Anniversary Future Leaders Fellow.
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External DOI: https://doi.org/10.1016/j.neuroscience.2017.07.014
This record's URL: https://www.repository.cam.ac.uk/handle/1810/265627
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