Power A E, Roozendaal B, McGaugh J L
Center for the Neurobiology of Learning and Memory, and Department of Neurobiology and Behavior, University of California, Irvine, CA 92697-3800, USA.
Eur J Neurosci. 2000 Oct;12(10):3481-7. doi: 10.1046/j.1460-9568.2000.00224.x.
Glucocorticoid-induced memory enhancement is known to depend on beta-adrenoceptor activation in the basolateral amygdala (BLA). Additionally, inactivation of muscarinic cholinergic receptors in the rat amygdala blocks memory enhancement induced by concurrent beta-adrenergic activation. Together, these findings suggest that glucocorticoid-induced modulation of memory consolidation requires cholinergic as well as adrenergic activation in the BLA. Two experiments investigated this issue. The first experiment examined whether blockade of muscarinic cholinergic receptors in the BLA with atropine alters the memory-enhancing effects of the systemically administered glucocorticoid dexamethasone. Dexamethasone (0.3, 1.0 or 3.0 mg/kg, s.c.) administered to rats immediately after inhibitory avoidance training produced dose-dependent enhancement of 48-h retention. Concurrent bilateral infusions of the muscarinic cholinergic antagonist atropine (0.5 microg in 0.2 microL per side) into the BLA blocked the memory enhancement. The second experiment investigated whether the BLA is a locus of interaction between glucocorticoid and muscarinic activation. The specific glucocorticoid receptor (GR or type II) agonist RU 28362 (1.0, 3.0 or 10 ng) was infused into the BLA either alone or together with atropine immediately after training. The GR agonist produced dose-dependent memory enhancement and atropine blocked the memory enhancement. These findings indicate that muscarinic cholinergic activation within the BLA is critical for enabling glucocorticoid enhancement of memory consolidation and that enhancement of memory induced by GR activation in the BLA requires cholinergic activation within the BLA.
已知糖皮质激素诱导的记忆增强依赖于基底外侧杏仁核（BLA）中的β-肾上腺素能受体激活。此外，大鼠杏仁核中M胆碱能受体的失活会阻断由同时发生的β-肾上腺素能激活诱导的记忆增强。这些发现共同表明，糖皮质激素诱导的记忆巩固调节需要BLA中的胆碱能以及肾上腺素能激活。两项实验研究了这个问题。第一个实验研究了用阿托品阻断BLA中的M胆碱能受体是否会改变全身给予糖皮质激素地塞米松的记忆增强作用。在抑制性回避训练后立即给大鼠皮下注射地塞米松（0.3、1.0或3.0mg/kg），产生了48小时记忆保持的剂量依赖性增强。同时双侧向BLA注入M胆碱能拮抗剂阿托品（每侧0.2μL中含0.5μg）可阻断记忆增强。第二个实验研究了BLA是否是糖皮质激素和M胆碱能激活之间相互作用的位点。在训练后立即将特异性糖皮质激素受体（GR或II型）激动剂RU 28362（1.0、3.0或10ng）单独或与阿托品一起注入BLA。GR激动剂产生了剂量依赖性的记忆增强，而阿托品阻断了记忆增强。这些发现表明，BLA内的M胆碱能激活对于糖皮质激素增强记忆巩固至关重要，并且BLA中GR激活诱导的记忆增强需要BLA内的胆碱能激活。
