Nicotine Activation of α4* Receptors: Sufficient for Reward, Tolerance, and Sensitization
By A. Tapper, S. Mckinney, R. Nashmi, J. Schwarz, P. Deshpande, C. Labarca, P. Whiteaker, M. Marks, A. C. Collins, H. Lester. Science, 2004
693 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/cfba7b74a4ef2cf78740a1ea2cd2e1badd8c1696
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- S. Hyman
- E. Nestler
- R. Malenka
- Mark T. Harnett
- Kent C. Berridge
- Nora D. Volkow
- G. Koob
- Anthony A. Grace
In Molecular Biology
Citations in the corpus
- Neural mechanisms of addiction: the role of reward-related learning and memory. (2006, background): “Whether acting directly or indirectly (Johnson & North 1992, Jones et al. 1998, Tapper et al. 2004, Waldhoer et al. 2004, Justinova et al. 2005), all addictive drugs increase levels of synaptic dopamine within the NAc.”
- Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function (2009, background): “Extensive measurements of these animals revealed that the 4(L:A) nAChR subunit mutation and enhanced receptor activation alone can account for nicotine reinforcement, sensitization, and the development of tolerance (461).”
- Ca2+ Permeability of the (α4)3(β2)2 Stoichiometry Greatly Exceeds That of (α4)2(β2)3 Human Acetylcholine Receptors (2006, background): “4 2* AChRs are sufficient for nicotine reward, tolerance, and sensitization (Tapper et al., 2004; Maskos et al., 2005).”