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The binding of [³H]‐yohimbine and [³H]‐idazoxan to rat cortex and hippocampus is rapid, reversible and of high affinity. Saturation data indicate that a single population of binding sites exist for [³H]‐yohimbine in the cortex (B_max 121 ± 10 fmol mg⁻¹, protein; K_d 5.2 ± 0.9 nm) and hippocampus (B_max 72 ± 6 fmol mg⁻¹ protein; K_d 5.8 ± 0.7 nm). [³H]‐idazoxan labels one site in the cortex (B_max 87 ± 8 fmol mg⁻¹ protein; K_d 4.1± 0.9 nm) and hippocampus (B_max 30 ± 6 fmol mg⁻¹ protein; K_d 3.5 + 0.5 nm), when 3 μm phentolamine is used to define non‐specific binding. A second distinct [³H]‐idazoxan binding site (B_max 110 ± 21fmolmg^_1 protein; K_d 3.6 ± 0.07 nm) is identified in rat cortex if 0.3 μm cirazoline is used to define non‐specific binding and 3 μm yohimbine is included to prevent binding to α₂‐adrenoceptors.

Displacement studies indicate that the α₁‐adrenoceptor antagonist prazosin and the 5‐HT₁ …