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Acute cocaine exposure alters spine density and long‐term potentiation in the ventral tegmental area
Author(s) -
Sarti Federica,
Borgland Stephanie L.,
Kharazia Viktor N.,
Bonci Antonello
Publication year - 2007
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2007.05689.x
Subject(s) - ventral tegmental area , long term potentiation , dendritic spine , neuroscience , ampa receptor , glutamatergic , synaptic plasticity , dopaminergic , neuroplasticity , nmda receptor , biology , dopamine , glutamate receptor , receptor , hippocampal formation , biochemistry
Growing evidence indicates that the expression of synaptic plasticity in the central nervous system results in dendritic reorganization and spine remodeling. Although long‐term potentiation of glutamatergic synapses after cocaine exposure in the ventral tegmental area (VTA) has been proposed as a cellular mechanism underlying addictive behaviors, the relationship between long‐term potentiation and dendritic remodeling induced by cocaine on the dopaminergic neurons of the VTA has not been demonstrated. Here we report that rat VTA cells classified as type I and II showed distinct morphological responses to cocaine, as a single cocaine exposure significantly increased dendritic spine density in type I but not in type II cells. Further, only type I cells had a significant increase in the AMPA receptor : NMDA receptor ratio after a single cocaine exposure. Taken together, our data provide evidence that increased spine density and synaptic plasticity are coexpressed within the same VTA neuronal population and that only type I neurons are structurally and synaptically modified by cocaine.