Journal
NATURE NEUROSCIENCE
Volume 12, Issue 2, Pages 190-199Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2245
Keywords
-
Categories
Funding
- National Institute on Drug Abuse [R01-DA24040, T32-DA7290]
- NIDA K [K-01DA017750]
- NARSAD
- Onassis Public Benefit Foundation
- US Department of Veterans Affairs and Veterans Affairs IDIQ [VA549-P-0027]
Ask authors/readers for more resources
The intrinsic properties of neurons that enable them to maintain depolarized, persistently activated states in the absence of sustained input are poorly understood. In short-term memory tasks, individual prefrontal cortical (PFC) neurons can maintain persistent action potential output during delay periods between informative cues and behavioral responses. Dopamine and drugs of abuse alter PFC function and working memory, possibly by modulating intrinsic neuronal properties. Here we used patch-clamp recording of layer 5 PFC pyramidal neurons to identify a postsynaptic depolarization that was evoked by action potential bursts and mediated by metabotropic glutamate receptor 5 (mGluR5). This depolarization occurred in the absence of recurrent synaptic activity and was reduced by a dopamine D1 receptor (D1R) protein kinase A pathway. After behavioral sensitization to cocaine, the depolarization was substantially diminished and D1R modulation was lost. We propose that burst-evoked intrinsic depolarization is a form of short-term cellular memory that is modulated by dopamine and cocaine experience.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available