Ståhle L
Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.
Psychopharmacology (Berl). 1992;106(1):1-13. doi: 10.1007/BF02253581.
The hypothesis that stimulation of dopamine autoreceptors is the mechanism by which dopamine agonists induce yawning and suppression of exploration is critically examined. It is shown that the relation between reduced extracellular dopamine levels, assessed by microdialysis, and behavioural effects of dopamine agonists, a dopamine synthesis inhibitor and a granule storage blocker is highly inconsistent. The time-course and duration of the behavioural effects of dopamine agonists differ from the reduction of extracellular dopamine. Amphetamine cotreatment is shown to increase dopamine levels, while yawning and suppression of exploration can still be induced. The data strongly indicate that autoreceptors are not the mediators of these behavioural effects. It is proposed that postsynaptic receptors mediate dopamine agonist induced yawning and suppression of exploration. Evidence is also presented showing that yawning and suppression of exploration are not functionally equivalent.
多巴胺自身受体的刺激是多巴胺激动剂诱发打哈欠和抑制探索行为的机制这一假说受到了批判性检验。结果表明，通过微透析评估的细胞外多巴胺水平降低与多巴胺激动剂、多巴胺合成抑制剂和颗粒储存阻断剂的行为效应之间的关系极不一致。多巴胺激动剂行为效应的时间进程和持续时间与细胞外多巴胺的降低情况不同。安非他命联合治疗可增加多巴胺水平，但仍可诱发打哈欠和抑制探索行为。这些数据有力地表明，自身受体并非这些行为效应的介导因素。有人提出，突触后受体介导多巴胺激动剂诱发的打哈欠和抑制探索行为。还提供了证据表明打哈欠和抑制探索行为在功能上并不等同。
