“School of Cognitive Sciences”
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| Paper IPM / Cognitive Sciences / 12865 |
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| Abstract: | |||||||||||
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Nicotine, the major addictive substance in tobacco, increases the activity of the central amygdala (CeA).
Amygdala is directly implicated in anxiety modulation and sends projections to the vicinity of the midbrain
dopamine neurons, including the ventral tegmental area (VTA) which is a key area that controls nicotine dependence
processes. In this study, the role of dopamine D1 and D2/3 receptors of the VTA on anxiogenic-like
behavior induced with intra-CeA injection of nicotine has been investigated. Male Wistar rats with cannula
aimed to the left CeA and the left VTA were submitted to the elevated plus-maze (EPM). The nicotine injection
(1 μg/rat) into the CeA decreased the percentage of open arm time and open arm entries, but not locomotor
activity, indicating an anxiogenic-like response. Intra-VTA injection of a dopamine D1 receptor
antagonist, SCH23390 (0.25 μg/rat), and a dopamine D2/3 receptor antagonist, sulpiride (0.7 μg/rat),
inhibited the anxiogenic-like response caused by intra-CeA injection of nicotine. These results suggest that
the relationship between the VTA and the CeA may be involved in nicotine-induced anxiogenic-like behavior
via dopamine D1 and D2/3 receptors. An understanding of these cellular processes will be crucial for the development
of new intervention to combat nicotine effect.
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