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Effect of Noradrenergic Lesions on Subtypes of α~2~‐Adrenoceptors in Rat Brain by Gregory A. Ordway is a Neuroscience article available to read on EtoBox.

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Abstract: The binding of [^3^H]rauwolscine to α~2A~‐ (also referred to as α~2D~‐) and α~2C~‐adrenoceptors in homogenates of rat cerebral cortex was measured by exploiting the selectivity of oxymetazoline for α~2A~‐adrenoceptors. Inhibition of [^3^H]rauwolscine binding by oxymetazoline was modeled best assuming binding to two sites (__p__ < 0.001). Competition curves for oxymetazoline were shifted rightward by the addition of GTP (250 μ__M__) but were still fit best by a two‐site model (__p__ < 0.001). A concentration of oxymetazoline was calculated that would optimally antagonize [^3^H]rauwolscine binding (with GTP present) to oxymetazoline‐sensitive α~2A~‐adrenoceptors, minimally inhibiting binding to α~2C~‐adrenoceptors. Subsequently, [^3^H]rauwolscine binding to α~2A~‐ and α~2C~‐adrenoceptors in cortex was examined 3 weeks after destruction of noradrenergic terminals. Binding to α~2C~‐adrenoceptors was increased significantly after treatment with 6‐hydroxydopamine (6‐OHDA) compared with vehicle‐treated controls, whereas binding to α~2A~‐adrenoceptors was unchanged. Pretreatment of rats with desipramine before 6‐hydroxydopamine, to protect noradrenergic neurons, resulted in no ch

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Author

Gregory A. Ordway

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

1995

Language

EN

Field

Neuroscience (Life Sciences)