Introini-Collison I B, Dalmaz C, McGaugh J L
Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717-3800, USA.
Neurobiol Learn Mem. 1996 Jan;65(1):57-64. doi: 10.1006/nlme.1996.0006.
These experiments examined the involvement of the amygdaloid complex as a site of interaction of adrenergic and muscarinic cholinergic influences on memory storage. Male Sprague-Dawley rats (60 days old; 250-300 g) were given a single training trial in an inhibitory avoidance task and a retention test trial 48 h later. Immediately after training buffer control or drug solutions (0.5 microliter) were infused into the amygdala and, in the first experiment only, other drugs were administered intraperitoneally (ip). The first experiment examined the effects of post-training systemic injections of the muscarinic agonist oxotremorine (100.0 micrograms/kg) administered alone or together with intraamygdala injections of either the muscarinic antagonist atropine (1.0 microgram) or the beta-noradrenergic antagonist propranolol (0.3 microgram). Oxotremorine enhanced retention and atropine, but not propranolol, attenuated the effects of oxotremorine. In the second experiment intraamygdala infusions of the beta-noradrenergic agonist clenbuterol (10.0 ng) were administered either alone or together with atropine (1.0 microgram). Clenbuterol enhanced retention and atropine blocked the effects of clenbuterol. In the third experiment intraamygdala infusions of oxotremorine (3, 10, 30, or 100 ng) were administered either alone or together with propranolol (0.3 microgram). Oxotremorine (3.0 and 10.0 ng) enhanced retention and propranolol did not block the effects of oxotremorine. These findings are consistent with the view that memory storage is regulated by an interaction of beta-noradrenergic and cholinergic influences and suggest that the noradrenergic influences are mediated by the release of acetylcholine and activation of muscarinic cholinergic receptors within the amygdala.
这些实验研究了杏仁核复合体作为肾上腺素能和毒蕈碱胆碱能对记忆存储影响的相互作用位点的作用。雄性斯普拉格-道利大鼠（60日龄；250-300克）在抑制性回避任务中进行单次训练试验，并在48小时后进行记忆保持测试试验。训练后立即将缓冲液对照或药物溶液（0.5微升）注入杏仁核，并且仅在第一个实验中，其他药物通过腹腔注射（ip）给药。第一个实验研究了训练后全身注射毒蕈碱激动剂氧化震颤素（100.0微克/千克）单独使用或与杏仁核内注射毒蕈碱拮抗剂阿托品（1.0微克）或β-去甲肾上腺素能拮抗剂普萘洛尔（0.3微克）联合使用的效果。氧化震颤素增强了记忆保持，而阿托品而非普萘洛尔减弱了氧化震颤素的作用。在第二个实验中，杏仁核内注入β-去甲肾上腺素能激动剂克伦特罗（10.0纳克）单独使用或与阿托品（1.0微克）联合使用。克伦特罗增强了记忆保持，阿托品阻断了克伦特罗的作用。在第三个实验中，杏仁核内注入氧化震颤素（3、10、30或100纳克）单独使用或与普萘洛尔（0.3微克）联合使用。氧化震颤素（3.0和10.0纳克）增强了记忆保持，普萘洛尔未阻断氧化震颤素的作用。这些发现与记忆存储受β-去甲肾上腺素能和胆碱能影响相互作用调节的观点一致，并表明去甲肾上腺素能影响是由杏仁核内乙酰胆碱的释放和毒蕈碱胆碱能受体的激活介导的。
