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电生理研究证明 ,焦虑与忧郁剂治疗的神经生物学机制取决于影响特异性的解剖区域对 5 -HT1A受体敏感的适应性。此外 ,临床上用相应的抗焦虑 /抗忧郁药剂重复处理 ,在前脑的作用表现为增进 5 -HT的神经传导 ,尤以海马最显著。药物处理 2～ 3周后 ,可减少抑制性体树突自动受体的敏感性 ,增加突触后的受体敏感性 ,或两者兼备。使用对氮 ,氮 -二丙基 -5 -氨基色胺刺激的鸟苷 -5 ’-氧-( 3-硫代 )三磷酸盐 ( [35S]GTPγS)结合体进行放射自显影照相的方法评估 ,测定了该假设。将大白鼠用生理盐水或药剂处理 2 1d ,每天处理 1次 (mg/kg :fluoxetine ,1 0 ;imipramine ,1 0 ;clorgyline ,1 )或每天处理 2次 (ipsapirone,2 0mg/kg)。检测了 3个富含 5 -HT1A受体的脑区 :背中缝核 (DR ;体树突 ) ,背侧海马 (DH)和外侧隔区 (LS) (突触后 )。只有imipramine( +1 7% )和fluoxetine( +5 4 % )显著地增加了背侧海马上激活剂结合在背侧海马。除了imipramine ,所有药剂均减少在背侧中缝核的结合 ( -1 9到-4 1 % )。尽管总的说来结果支持增进海马 5 -HT的神经传导的概念 ,但受体敏感性变化的模式与电生理的研究结果仍稍有不同。然而 ,最一致和最显著的结果是四种药剂处理均在外侧隔区 (LS)降低 [35S]GTPγS结合 ( -1 4到 -2
Electrophysiological studies have demonstrated that the neurobiological mechanisms of anxiety and depression treatment depend on the responsiveness of the specific anatomical region to the 5-HT1A receptor. In addition, the clinical treatment with the corresponding anti-anxiety / anti-depressant agents repeated treatment in the forebrain appears to enhance the 5-HT nerve conduction, especially in the most significant hippocampus. Drug treatment after 2 to 3 weeks, can reduce the sensitivity of dendritic auto-receptor inhibition, increased post-synaptic receptor sensitivity, or both. A method of autoradiography was performed using a guanosine-5 ’-oxy- (3-thio) triphosphate ([35S] GTPγS) conjugate stimulated with nitrogen, nitrogen-dipropyl-5-aminotriamine , This hypothesis was measured. The rats were treated for 21 days with saline or a drug, once a day (mg / kg: fluoxetine, 10; imipramine, 10; clorgyline, 1) or twice daily (ipsapirone, 20 mg / kg). Three brain regions rich in 5-HT1A receptors were examined: dorsal raphe (DR; dendrites), dorsal hippocampus (DH) and lateral septum (LS) (postsynaptic). Only imipramine (+1 7%) and fluoxetine (+5 4%) significantly increased dorsal hippocampus activation in the dorsal hippocampus. With the exception of imipramine, all agents reduced the dorsal raphe ligation (-1 9 to -4 1%). Although the results generally support the notion of promoting neurotransmission in 5-HT of the hippocampus, the pattern of changes in receptor sensitivity remains somewhat different from electrophysiological findings. However, the most consistent and significant result was that all four agents were reduced in the lateral compartment (LS) [35S] GTPγS binding (-1 4 to -2