Abstract:
: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.
journal_name
Brain Struct Functjournal_title
Brain structure & functionauthors
Zhu W,Ge X,Gao P,Li M,Guan Y,Guan Xdoi
10.1007/s00429-017-1590-0subject
Has Abstractpub_date
2018-05-01 00:00:00pages
1829-1838issue
4eissn
1863-2653issn
1863-2661pii
10.1007/s00429-017-1590-0journal_volume
223pub_type
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