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Altered cortico-striatal crosstalk underlies object recognition memory deficits in the sub-chronic phencyclidine model of schizophrenia

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posted on 2017-05-12, 11:22 authored by Aman Asif-Malik, Daniel Dautan, Andrew M. Young, Todor V. Gerdjikov
The neural mechanisms underlying cognitive deficits in schizophrenia are poorly understood. Sub-chronic treatment with the NMDA antagonist phencyclidine (PCP) produces cognitive abnormalities in rodents that reliably model aspects of the neurocognitive alterations observed in schizophrenia. Given that network activity across regions encompassing medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) plays a significant role in motivational and cognitive tasks, we measured activity across cortico-striatal pathways in PCP-treated rats to characterize neural enabling and encoding of task performance in a novel object recognition task. We found that PCP treatment impaired task performance and concurrently (1) reduced tonic NAc neuronal activity, (2) desynchronized cross-activation of mPFC and NAc neurons, and (3) prevented the increase in mPFC and NAc neural activity associated with the exploration of a novel object in relation to a familiar object. Taken together, these observations reveal key neuronal and network-level adaptations underlying PCP-induced cognitive deficits, which may contribute to the emergence of cognitive abnormalities in schizophrenia.

History

Citation

Brain Structure and Function, 2017, doi:10.1007/s00429-017-1393-3

Author affiliation

/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/MBSP Non-Medical Departments/Neuroscience, Psychology and Behaviour

Version

  • VoR (Version of Record)

Published in

Brain Structure and Function

Publisher

Springer Verlag

issn

1863-2653

eissn

1863-2661

Acceptance date

2017-02-22

Copyright date

2017

Available date

2017-05-12

Publisher version

https://link.springer.com/article/10.1007/s00429-017-1393-3

Language

en

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