Charney D S, Innis R B, Duman R S, Woods S W, Heninger G R
Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06508.
Psychopharmacology (Berl). 1989;98(1):102-7. doi: 10.1007/BF00442014.
The function of the alpha-2-receptor and intracellular effector systems was examined in 39 panic disorder patients and 30 healthy subjects using the platelet as a model system. Alpha-2-receptor density, as reflected by 3H-yohimbine binding, was not different between the two groups. Platelet alpha-2-receptor affinity was decreased (higher Kd) in the panic disorder patients. Other significant abnormalities in the patients included a decreased basal adenylate cyclase activity, reduced EC50 for the epinephrine inhibition of adenylate cyclase activity, and decreased stimulation of adenylate cyclase activity by prostaglandin E1 and sodium fluoride. These results are consistent with a dysfunction in some panic disorder patients at the level of the stimulatory GTP binding regulatory protein, Gs, or the adenylate cyclase catalytic unit. The relationship of these findings to previous studies of noradrenergic function in panic disorder patients is discussed.
以血小板作为模型系统,对39例惊恐障碍患者和30名健康受试者的α2受体及细胞内效应系统功能进行了研究。两组之间,由3H-育亨宾结合反映出的α2受体密度并无差异。惊恐障碍患者血小板α2受体亲和力降低(解离常数Kd更高)。患者的其他显著异常包括基础腺苷酸环化酶活性降低、肾上腺素对腺苷酸环化酶活性抑制的半数有效浓度(EC50)降低,以及前列腺素E1和氟化钠对腺苷酸环化酶活性的刺激减弱。这些结果与部分惊恐障碍患者在刺激性GTP结合调节蛋白Gs或腺苷酸环化酶催化单位水平的功能障碍一致。本文讨论了这些发现与既往惊恐障碍患者去甲肾上腺素能功能研究的关系。