Journal
NEURON
Volume 27, Issue 2, Pages 349-357Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(00)00042-8
Keywords
-
Categories
Funding
- NINDS NIH HHS [NS 35090] Funding Source: Medline
Ask authors/readers for more resources
Nicotine reinforces smoking behavior by activating nicotinic acetylcholine receptors (nAChRs) in the mid-brain dopaminergic (DA) reward centers, including the ventral tegmental area (VTA). Although nicotine induces prolonged excitation of the VTA in vivo, the nAChRs on the DA neurons desensitize in seconds. Here, we show that activation of nAChRs on presynaptic terminals in the VTA enhances glutamatergic inputs to DA neurons. Under conditions where the released glutamate can activate NMDA receptors, long-term potentiation (LTP) of the excitatory inputs is induced. Both the short- and the long-term effects of nicotine required activation of presynaptic alpha 7 subunit-containing nAChRs. These results can explain the long-term excitation of brain reward areas induced by a brief nicotine exposure. They also show that nicotine alters synaptic function through mechanisms that are linked to learning and memory.
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