Functional characterization of central α-adrenoceptors by yohimbine diastereomers
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2015, PsychoneuroendocrinologyCitation Excerpt :To mimic abnormal processes of fear learning and memory, the noradrenergic system can be stimulated during or immediately after fear conditioning, either directly through the central administration of noradrenaline (LaLumiere et al., 2003), or indirectly through the administration of the α2-adrenoceptor antagonist yohimbine HCl (Gazarini et al., 2013, 2014; Soeter and Kindt, 2011, 2012). By blocking the α2-adrenergic autoreceptor, yohimbine interrupts the negative feedback control of noradrenaline release, thereby increasing noradrenergic activity (Hedler et al., 1981; Langer, 1974; Wemer et al., 1979). This experimental model has been shown to strengthen fear memory, characterized by the persistence and overgeneralization of fear (Gazarini et al., 2013, 2014; Soeter and Kindt, 2011, 2012).
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2003, Brain ResearchCitation Excerpt :cAMP levels were calculated as picomoles of cAMP formed per milligram of protein. In some experiments, tissues were incubated with α2-adrenoceptor antagonists, prazosin (1×10−7 M) [18] or yohimbine (1×10−5 M) [14] for 30 min at 37 °C in a shaking water bath. The density of α2-adrenoceptors in cortical membranes was measured using [3H]yohimbine.
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