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Prenatal exposure to cocaine is associated with increased number of spine synapses in rat prelimbic cortex
Author(s) -
Morrow Bret A.,
Hajszan Tibor,
Leranth Csaba,
Elsworth John D.,
Roth Robert H.
Publication year - 2007
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20430
Subject(s) - dendritic spine , infralimbic cortex , prenatal cocaine exposure , neuroscience , prefrontal cortex , excitatory postsynaptic potential , cortex (anatomy) , spine (molecular biology) , psychology , prenatal exposure , medicine , biology , cognition , gestation , pregnancy , inhibitory postsynaptic potential , hippocampal formation , microbiology and biotechnology , genetics
Prenatal exposure to cocaine has been associated with cognitive deficits in children and in animal models. An excess activation of pyramidal neurons in the prefrontal cortex has been proposed as a potential cause for these deficits based on previous studies. The goal of this study was to determine if prenatal exposure to cocaine was associated with an increase in the number of excitatory synapses on dendritic spines in layer II/III of the prelimbic cortex. Frontal cortex of young adult male and female rats, exposed to either saline or cocaine (3 mg/kg i.e., twice a day, embryonic day 10–20), were examined using electron microscopy and the number of asymmetric spines synapses were estimated using the physical disector method. Both male and female rats prenatally exposed to cocaine had about twice as many synapses on dendritic spines as the prenatal saline controls. The increase in number of excitatory synaptic inputs associated with prenatal cocaine exposure could contribute to the increased neuronal activation and cognitive deficits noted. Synapse 61:862–865, 2007. © 2007 Wiley‐Liss, Inc.