salsolinol facilitates glutamatergic transmission to dopamine neurons in the posterior ventral tegmental area of ratssalsolinol促进glutamatergic传播后腹侧被盖区多巴胺神经元的老鼠.pdfVIP
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salsolinol facilitates glutamatergic transmission to dopamine neurons in the posterior ventral tegmental area of ratssalsolinol促进glutamatergic传播后腹侧被盖区多巴胺神经元的老鼠
Salsolinol Facilitates Glutamatergic Transmission to
Dopamine Neurons in the Posterior Ventral Tegmental
Area of Rats
Guiqin Xie, Jiang-Hong Ye*
Department of Anesthesiology, Pharmacology and Physiology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey,
United States of America
Abstract
Although in vivo evidence indicates that salsolinol, the condensation product of acetaldehyde and dopamine, has properties
that may contribute to alcohol abuse, the underlying mechanisms have not been fully elucidated. We have reported previously
that salsolinol stimulates dopamine neurons in the posterior ventral tegmental area (p-VTA) partly by reducing inhibitory
GABAergic transmission, and that ethanol increases glutamatergic transmission to VTA-dopamine neurons via the activation of
dopamine D receptors (D Rs). In this study, we tested the hypothesis that salsolinol stimulates dopamine neurons involving
1 1
activation of D1Rs. By using whole-cell recordings on p-VTA-dopamine neurons in acute brain slices of rats, we found that
salsolinol-induced increase in spike frequency of dopamine neurons was substantially attenuated by DL-2-amino-5-
phosphono-valeric acid and 6, 7-dinitroquinoxaline-2, 3-dione, the antagonists of glutamatergic N-Methyl-D-aspartic acid and
a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. Moreover, salsolinol increased the amplitude of evoked
excitatory postsynaptic currents (EPSCs) and the frequency but not the amplitude of spontaneous EPSCs. Additionally,
SKF83566, a D1R antagonist attenuated the salsolinol-induced facilitation of EPSCs and of spontaneous firing of dopamine
neurons. Our data reveal that salsolinol enhances glutamatergic transmission onto dopamine neurons via activation of D1Rs
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