Long-term potentiation of excitatory inputs to brain reward areas by nicotine.

By Huibert D. Mansvelder, D. McGehee. Neuron, 2000

745 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e2469cfbc2757094b3179d3ef157931310df6469

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Citations in the corpus

Addiction and the brain: The neurobiology of compulsion and its persistence (2001, methodology): “When applied to a slice preparation of the VTA, nicotine also elicits LTP in dopaminergic cells when paired with postsynaptic depolarizatio”
Ultrastructural Distribution of the α7 Nicotinic Acetylcholine Receptor Subunit in Rat Hippocampus (2001, background): “The actual sampled region was the synaptic cleft plus the adjoining 30-nmwide presynaptic and postsynaptic zones, because the separation between a labeled epitope and a gold particle attached to a secondary antibody can extend up to 28 nm (Matsubara et al., 1996).”
Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function (2009, background): “Other levels of regulation of dopaminergic transmission arise from ␣7 nAChRs located on cortical glutamatergic terminals; activation of these receptors increases glutamate release onto dopaminergic neurons in the VTA and, consequently, increases the their firing (344).”
Getting formal with dopamine and reward. (2002, positive): “Nicotine enhances glutamate-evoked longas seen with the administration of amphetamine (Westterm potentiation at dopamine neurons (Mansvelder and McGehee, 2000) and shifts dopamine neurons toward et al., 1997).”
The Brain Metabolite Kynurenic Acid Inhibits α7 Nicotinic Receptor Activity and Increases Non-α7 Nicotinic Receptor Expression: Physiopathological Implications (2001, background): “…of 7 nAChRs to inhibition by KYNA (Hilmas et al., 2000), and (2) like NMDA receptors, nAChRs are involved in regulating neuronal plasticity (Albuquerque et al., 1997; Broide and Leslie, 1999; Mansvelder and McGehee, 2000) and survival in the brain (Zoli et al., 1999; Kihara et al., 2001).”
Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons (2001, background): “Second, application of nicotine in vitro to slices of the VTA when paired with postsynaptic depolarization can elicit LT”
Neural mechanisms of addiction: the role of reward-related learning and memory. (2006, background): “Nicotine both directly excites VTA dopamine neurons (Calabresi et al. 1989, Pidoplichko et al. 1997) and enhances glutamate release from excitatory afferents to the VTA (Mansvelder & McGehee 2000).”
Synaptic mechanisms underlie nicotine-induced excitability of brain reward areas. (2002, methodology): “Our results on nicotine-induced synaptic modula- the 7 subunit (Mansvelder and McGehee, 2000).”
Drug Addiction as a Pathology of Staged Neuroplasticity (2008, background): “For example, changes in dopamine transporters are associated with amphetamine-like psychostimulants (Daws et al, 2002), GABA-A receptor changes have been noted after chronic alcohol (Charlton et al, 1997), and nicotine desensitizes nicotinic receptors (Mansvelder and McGehee, 2000).”
Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior (2012, background): “The MHb-interpeduncular pathway is cholinergic, and it has been proposed that its effects on VTA neuron firing are mediated indirectly through inhibition of the PPTg (Maskos, 2008).”