Cocaine self-administration reduces excitatory responses in the mouse nucleus accumbens shell. Neuropsychopharmacology 2006 Jul;31(7):1444-51
Date
10/06/2005Pubmed ID
16205778DOI
10.1038/sj.npp.1300918Scopus ID
2-s2.0-33745207548 (requires institutional sign-in at Scopus site) 47 CitationsAbstract
Drugs of abuse affect behavior by altering neuronal communication within the brain. Previous research examining the effects of intraperitoneally administered cocaine has revealed that cocaine alters excitatory glutamatergic signaling, both directly through regulation of synaptic function, and indirectly through regulation of cellular excitability in areas of the drug reward circuitry such as the nucleus accumbens (NAcc) and ventral tegmental area. We have now extended these findings by testing the hypothesis that self-administration of cocaine might elicit similar alterations in excitatory signaling in the NAcc shell. We observed that cocaine self-administration reduces synaptically evoked excitatory responses recorded extracellularly in the NAcc shell compared to saline self-administration. This alteration was not accompanied by alterations in paired pulse ratio of synaptically evoked responses or in potentiation of these responses by application of the adenylyl cyclase activator forskolin. This reduction in glutamatergic signaling may be one mechanism by which cocaine exerts its long-term behavioral effects.
Author List
Schramm-Sapyta NL, Olsen CM, Winder DGAuthor
Christopher M. Olsen PhD Associate Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBehavior, Animal
Cocaine
Colforsin
Dopamine Uptake Inhibitors
Dose-Response Relationship, Drug
Drug Interactions
Evoked Potentials
Excitatory Amino Acid Agonists
Glutamic Acid
Male
Mice
Mice, Inbred C57BL
Nucleus Accumbens
Self Administration
Time Factors
