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Vol. 54, Issue 3, 569-576, September 1998
2C-Adrenoceptor-Overexpressing Mice Are Impaired
in Executing Nonspatial and Spatial Escape Strategies
Department of Neurology and Neuroscience, University of Kuopio,
Kuopio, FIN-70211, Finland (M.B., J.P., P.J., P.R.),
A. I. Virtanen Institute, FIN-70211 Kuopio, Finland (J. Si.),
Department of Pharmacology and Clinical Pharmacology, University of
Turku, FIN-20520 Turku, Finland (J. Sa., M.S.),
Kuopio University
Hospital, FIN-70211 Kuopio, Finland (P.J., P.R.), and
Department of
Molecular and Cellular Physiology, Howard Hughes Medical Institute and
Division of Cardiovascular Medicine, Stanford University, Stanford,
California 94305 (R.K.K.)
Drugs acting via 
2-adrenoceptors modulate cognitive
functions mediated via frontostriatothalamic feedback loops. The
2C-adrenoceptor subtype is expressed in the basal
ganglia, hippocampus, and neocortex, areas that are involved in memory
and other cognitive functions. 2C-Overexpressing (OE)
mice were impaired in spatial or nonspatial water maze (WM) tests, and
2 antagonist treatment fully reversed the WM escape
defect in OE mice. However, 2C-overexpression did not
influence open field and passive avoidance behaviors or cortical EEG
arousal or the actions of 2 agonist or antagonist drugs
on these functions. Our results suggest that
2C-adrenoceptors can modulate navigation to a hidden or
visible escape platform, whereas many other actions of
2-adrenergic agents, such as sedation, are not mediated
via 2C-adrenoceptors. Therefore,
2-agonists lacking 2C-AR affinity or
2C-AR subtype-selective 2 antagonists could modulate functioning of frontostriatothalamic feedback loops more
effectively than the current subtype-nonselective drugs.
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