Aleksidze N G, Balavadze M V
Biull Eksp Biol Med. 1977 May;83(5):545-8.
The enhancement of the brain acetyl cholinesterase (ACHE) activity in rats by the intraventricular injection of adrenaline or dibutiryl analogue cyclic adenosine-3',5'-monophosphate (cAMP) was shown to be due to the enzyme inductive synthesis. ACHE induction manifests itself more in the subcortical white matter than in the cortex. The stimulating effect of adrenaline on the ACHE activity is suppressed under the beta-adrenoreceptor block, while the cAMP effect remains unchanged. On the contrary, the block of the alpha-adrenoreceptors stimulates the enzyme synthesis induction. The effects of adrenaline and cAMP are of the same direction and are realized through the beta-adrenoreceptors. The enhancement of ACHE activity during the block of the alpha-adrenoreceptors is accounted for by the elimination of their inhibitory influence on the beta-adrenoreceptors.
通过脑室内注射肾上腺素或二丁酰环磷腺苷（cAMP）类似物可使大鼠脑内乙酰胆碱酯酶（ACHE）活性增强，这一增强被证明是由于酶的诱导合成。ACHE诱导在皮层下白质中比在皮层中表现得更明显。在β-肾上腺素能受体阻断的情况下，肾上腺素对ACHE活性的刺激作用受到抑制，而cAMP的作用保持不变。相反，α-肾上腺素能受体的阻断会刺激酶合成的诱导。肾上腺素和cAMP的作用方向相同，且是通过β-肾上腺素能受体实现的。在α-肾上腺素能受体阻断期间ACHE活性的增强是由于消除了它们对β-肾上腺素能受体的抑制作用。
