TY - JOUR
T1 - Adolescent cocaine exposure induces prolonged synaptic modifications in medial prefrontal cortex of adult rats
AU - Zhu, Wei
AU - Ge, Xuhui
AU - Gao, Peng
AU - Li, Min
AU - Guan, Yun
AU - Guan, Xiaowei
N1 - Funding Information:
Acknowledgements This work was supported by the National Natural Science Foundation of China (no. 81571303). We thank Prof. Gang Chen and Dr. Wenda Xue, Nanjing University of Chinese Medicine, China, for their assistance in behavioral tests.
Funding Information:
This work was supported by the National Natural Science Foundation of China (no. 81571303). We thank Prof. Gang Chen and Dr. Wenda Xue, Nanjing University of Chinese Medicine, China, for their assistance in behavioral tests. The authors declare no competing financial interests.
Publisher Copyright:
© 2017, Springer-Verlag GmbH Germany, part of Springer Nature.
PY - 2018/5/1
Y1 - 2018/5/1
N2 - Substance used during adolescent period increases the risk of psychiatric disorders in later life, but the underlying neural mechanisms remain unclear. We hypothesize that synaptic remodeling and changes of homeostasis in the medial prefrontal cortex (mPFC) following adolescent cocaine exposure may last for a long time, and these modifications may contribute to behavioral deficiencies in adulthood. To address this hypothesis, rats were exposed to cocaine hydrochloride from postnatal day 28 (P28) to P42. When reared to adulthood, rats were subjected to behavioral tests. On P75 and P76, cocaine-experienced rats exhibited increased locomotive and anxiety-like behaviors, as well as impaired non-selective attention. In the cocaine-experienced rats, both levels of synapse-related proteins (synapsin I and PSD-95) and density of synapse and dendrite spine in mPFC were significantly decreased when compared to controls. Unexpected, the expression of molecules related to oxidative stress, inflammation and apoptosis showed no significant changes in mPFC following adolescent cocaine exposure. These findings suggested that adolescent exposure to cocaine induce long-term modification on synapses in mPFC, which might contribute to long-term behavioral outcomes in adulthood.
AB - Substance used during adolescent period increases the risk of psychiatric disorders in later life, but the underlying neural mechanisms remain unclear. We hypothesize that synaptic remodeling and changes of homeostasis in the medial prefrontal cortex (mPFC) following adolescent cocaine exposure may last for a long time, and these modifications may contribute to behavioral deficiencies in adulthood. To address this hypothesis, rats were exposed to cocaine hydrochloride from postnatal day 28 (P28) to P42. When reared to adulthood, rats were subjected to behavioral tests. On P75 and P76, cocaine-experienced rats exhibited increased locomotive and anxiety-like behaviors, as well as impaired non-selective attention. In the cocaine-experienced rats, both levels of synapse-related proteins (synapsin I and PSD-95) and density of synapse and dendrite spine in mPFC were significantly decreased when compared to controls. Unexpected, the expression of molecules related to oxidative stress, inflammation and apoptosis showed no significant changes in mPFC following adolescent cocaine exposure. These findings suggested that adolescent exposure to cocaine induce long-term modification on synapses in mPFC, which might contribute to long-term behavioral outcomes in adulthood.
KW - Abnormal behaviors
KW - Adolescent exposure
KW - Cocaine
KW - Dendrite spine
KW - Medial prefrontal cortex
KW - Synapse
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U2 - 10.1007/s00429-017-1590-0
DO - 10.1007/s00429-017-1590-0
M3 - Article
C2 - 29247260
AN - SCOPUS:85038090255
VL - 223
SP - 1829
EP - 1838
JO - Brain Structure and Function
JF - Brain Structure and Function
SN - 1863-2653
IS - 4
ER -