Katz R J, Sibel M
Pharmacol Biochem Behav. 1982 Jun;16(6):979-82. doi: 10.1016/0091-3057(82)90056-9.
In previous papers we reported that chronic stress elicited reductions in selected forms of open field activity resembled endogenomorphic depression upon behavioral, motivational, neuroendocrine, and neuropharmacological grounds. In particular, the loss of acute stress elicited activity proved to be exclusively reversible by antidepressant treatments. Insofar as clinically ineffective compounds were tested, the deficit proved refractory to treatment, further suggesting the model reflected just those processes which were disrupted in depression. A number of ineffective compounds are known to yield false positives upon other related tests, but have yet to be examined in the present model. Three such compounds, an antihistamine (tripelennamine), a neuroleptic (haloperidol), and an anxiolytic (oxazepam) were examined for their behavioral and neuroendocrine effects. Although other stress related phenomena were replicated, none of the above compounds was effective in restoring the activation deficit or in eliminating the endocrine abnormality. This suggests the depression model is relatively selective pharmacologically and not critically dependent upon receptor blocking properties of the above drugs.
在之前的论文中我们报道，基于行为、动机、神经内分泌和神经药理学依据，慢性应激引发的特定形式旷场活动减少类似于内源性抑郁症。特别是，抗抑郁治疗被证明可完全逆转急性应激引发活动的丧失。就测试临床无效化合物而言，这种缺陷被证明对治疗具有抗性，这进一步表明该模型反映的正是那些在抑郁症中受到干扰的过程。已知许多无效化合物在其他相关测试中会产生假阳性，但尚未在当前模型中进行研究。研究了三种此类化合物，一种抗组胺药（曲吡那敏）、一种抗精神病药（氟哌啶醇）和一种抗焦虑药（奥沙西泮）的行为和神经内分泌作用。尽管其他与应激相关的现象得到了重复，但上述化合物均未能有效恢复激活缺陷或消除内分泌异常。这表明抑郁症模型在药理学上具有相对选择性，并不严重依赖于上述药物的受体阻断特性。
