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Exposure of nicotine to ventral tegmental area slices induces glutamatergic synaptic plasticity on dopamine neurons.
Synapse. 2011 Apr; 65(4):332-8.S

Abstract

Nicotine promotes glutamatergic synaptic plasticity in dopaminergic (DA) neurons in the ventral tegmental area (VTA), which is thought to be an important mechanism underlying nicotine reward. However, it is unclear whether exposure of nicotine alone to VTA slice is sufficient to increase glutamatergic synaptic strength on DA neurons and which nicotinic acetylcholine receptor (nAChR) subtype mediates this effect. Here, we report that the incubation of rat VTA slices with 500 nM nicotine induces glutamatergic synaptic plasticity in DA neurons. We measure the ratio of AMPA and NMDA receptor-mediated currents (AMPA/NMDA) and compare these ratios between nicotine-treated and -untreated slices. Our results demonstrate that the incubation of VTA slices with 500 nM nicotine for 1 h (but not for 10 min) significantly increases the AMPA/NMDA ratio when compared with controls. Preincubation with 10 nM of the α7-nAChR antagonist, methyllycaconitine (MLA) but not 1 μM α4-containing nAChR antagonist, dihydro-β-erythroidine (DHβE) prevents nicotinic effect, suggesting that α7-nAChRs are mainly mediated this nicotinic effect. This finding is further supported by the disappearance of this nicotinic effect in nAChR α7 knockout (KO) mice. Furthermore, nicotine reduced paired-pulse ratio (PPR) of evoked excitatory postsynaptic potential (eEPSP) in the VTA slices prepared from wild-type (WT) mice but not α7 KO mice. Collectively, these findings suggest that exposure of smoking-relevant concentrations of nicotine to VTA slices is sufficient to increase glutamatergic synaptic strength on DA neurons and that α7-nAChRs likely mediate this nicotinic effect through increasing presynaptic release of glutamate.

Authors+Show Affiliations

Department of Respiratory Medicine, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210029, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20730803

Citation

Jin, Yu, et al. "Exposure of Nicotine to Ventral Tegmental Area Slices Induces Glutamatergic Synaptic Plasticity On Dopamine Neurons." Synapse (New York, N.Y.), vol. 65, no. 4, 2011, pp. 332-8.
Jin Y, Yang K, Wang H, et al. Exposure of nicotine to ventral tegmental area slices induces glutamatergic synaptic plasticity on dopamine neurons. Synapse. 2011;65(4):332-8.
Jin, Y., Yang, K., Wang, H., & Wu, J. (2011). Exposure of nicotine to ventral tegmental area slices induces glutamatergic synaptic plasticity on dopamine neurons. Synapse (New York, N.Y.), 65(4), 332-8. https://doi.org/10.1002/syn.20850
Jin Y, et al. Exposure of Nicotine to Ventral Tegmental Area Slices Induces Glutamatergic Synaptic Plasticity On Dopamine Neurons. Synapse. 2011;65(4):332-8. PubMed PMID: 20730803.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exposure of nicotine to ventral tegmental area slices induces glutamatergic synaptic plasticity on dopamine neurons. AU - Jin,Yu, AU - Yang,Kechun, AU - Wang,Hong, AU - Wu,Jie, Y1 - 2010/11/11/ PY - 2010/05/01/received PY - 2010/07/22/accepted PY - 2010/8/24/entrez PY - 2010/8/24/pubmed PY - 2011/12/21/medline SP - 332 EP - 8 JF - Synapse (New York, N.Y.) JO - Synapse VL - 65 IS - 4 N2 - Nicotine promotes glutamatergic synaptic plasticity in dopaminergic (DA) neurons in the ventral tegmental area (VTA), which is thought to be an important mechanism underlying nicotine reward. However, it is unclear whether exposure of nicotine alone to VTA slice is sufficient to increase glutamatergic synaptic strength on DA neurons and which nicotinic acetylcholine receptor (nAChR) subtype mediates this effect. Here, we report that the incubation of rat VTA slices with 500 nM nicotine induces glutamatergic synaptic plasticity in DA neurons. We measure the ratio of AMPA and NMDA receptor-mediated currents (AMPA/NMDA) and compare these ratios between nicotine-treated and -untreated slices. Our results demonstrate that the incubation of VTA slices with 500 nM nicotine for 1 h (but not for 10 min) significantly increases the AMPA/NMDA ratio when compared with controls. Preincubation with 10 nM of the α7-nAChR antagonist, methyllycaconitine (MLA) but not 1 μM α4-containing nAChR antagonist, dihydro-β-erythroidine (DHβE) prevents nicotinic effect, suggesting that α7-nAChRs are mainly mediated this nicotinic effect. This finding is further supported by the disappearance of this nicotinic effect in nAChR α7 knockout (KO) mice. Furthermore, nicotine reduced paired-pulse ratio (PPR) of evoked excitatory postsynaptic potential (eEPSP) in the VTA slices prepared from wild-type (WT) mice but not α7 KO mice. Collectively, these findings suggest that exposure of smoking-relevant concentrations of nicotine to VTA slices is sufficient to increase glutamatergic synaptic strength on DA neurons and that α7-nAChRs likely mediate this nicotinic effect through increasing presynaptic release of glutamate. SN - 1098-2396 UR - https://www.unboundmedicine.com/medline/citation/20730803/Exposure_of_nicotine_to_ventral_tegmental_area_slices_induces_glutamatergic_synaptic_plasticity_on_dopamine_neurons_ L2 - https://doi.org/10.1002/syn.20850 DB - PRIME DP - Unbound Medicine ER -