CAFFEINE-INDUCED ANXIOGENESIS - THE ROLE OF ADENOSINE, BENZODIAZEPINE AND NORADRENERGIC RECEPTORS
CAFFEINE-INDUCED ANXIOGENESIS - THE ROLE OF ADENOSINE, BENZODIAZEPINE AND NORADRENERGIC RECEPTORS
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DOI：
10.1016/0091-3057(89)90230-x
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发表时间：
1989-01-01
影响因子：
3.6
通讯作者：
FILE, SE
中科院分区：
文献类型：
--
作者：
BALDWIN, HA;FILE, SE
这项研究的目的是确定咖啡因增加焦虑的机制。在单独施用咖啡因（20或40 mg/kg）或与各种化合物组合施用咖啡因后，在焦虑的社交互动测试中测试大鼠。为了研究腺苷受体的作用，咖啡因与2-氯腺苷（0.1和1 mg/kg）联合给药。为了研究苯二氮卓类受体的作用，使用了氯氮卓（5 mg/kg）、苯二氮卓类拮抗剂氟马西尼（RO 15-1788，1和10 mg/kg）和三唑苯二氮卓U-43，465（32 mg/kg）。最后，将α 2-受体激动剂可乐定（0.1和0.025mg/kg）和β-受体激动剂用肾上腺素能受体拮抗剂DL-心得安（5 mg/kg）研究去甲肾上腺素能系统在咖啡因作用中的作用。咖啡因（20和40 mg/kg）减少了社会交往的时间，这种作用被利氮卓、U-43，465和DL-普萘洛尔拮抗，但不被氟马西尼、2-氯腺苷或可乐定拮抗。因此得出结论，咖啡因的致焦虑作用不太可能是由于其对腺苷或苯二氮卓受体的作用。这表明利血平逆转咖啡因的作用可能是“功能性的”，即，这仅仅是两种相反效果的抵消。讨论了普萘洛尔和U-43，465对咖啡因作用的逆转是否是功能性的，或者反映了去甲肾上腺素能作用位点。
The purpose of this study was to determine the mechanism by which caffeine increases anxiety. Rats were tested in the social interaction test of anxiety after administration of caffeine (20 or 40 mg/kg) alone or in combination with various compounds. In order to investigate the role of adenosine receptors, caffeine was given in combination with 2-chloroadenosine (0.1 and 1 mg/kg). To investigate the role of benzodiazepine receptors, chlordiazepoxide (5 mg/kg), a benzodiazepine antagonist, flumazenil (RO 15-1788, 1 and 10 mg/kg) and a triazolobenzodiazepine U-43,465 (32 mg/kg) were used. Finally, an .alpha.2-receptor agonist, clonidine (0.1 and 0.025 mg/kg) and a .beta.-adrenoceptor antagonist, DL-propranolol (5 mg/kg), were used to study the role of noradrenergic systems in the effects of caffeine. Caffeine (20 and 40 mg/kg) reduced the time spent in social interaction and this effect was antagonized by chlordiazepoxide, U-43,465 and DL-propranolol, but not by flumazenil, 2-chloroadenosine or clonidine. It was therefore concluded that the anxiogenic effect of caffeine was unlikely to be due to its effects at adenosine or benzodiazepine receptors. It is suggested that the reversal of caffeine''s effects by chlordiazepoxide may have been "functional," i.e., merely a cancellation of two opposite effects. It is discussed whether the reversal of caffeine''s effects by propranolol and U-43,465 are functional, or reflect a noradrenergic site of action.