Dolezal V, Tucek S
Department of Neurochemistry, Czechoslovak Academy of Sciences, Prague.
Neurochem Res. 1990 Jan;15(1):41-5. doi: 10.1007/BF00969182.
The release of acetylcholine (ACh) from brain tissue is known to be inhibited by muscarinic autoreceptors on cholinergic nerve terminals but the mechanism of the inhibition is not understood. Atropine brings about an increase of ACh release by removing the inhibitory action of autoreceptors. We investigated whether the effect of atropine on the release of [14C]ACh newly synthesized during incubations from [U-14C] glucose depends on the concentration of Ca2+ in the medium. In rat striatal slices incubated in the presence of an inhibitor of cholinesterases and of 30 mmol/l K+, significant increases in the release of [14C]ACh elicited by atropine were only observed during incubations with very low concentrations of Ca2+. This finding supports the view that the activation of presynaptic muscarinic autoreceptors in the brain affects the release of ACh by reducing the availability of Ca2+ that is required for transmitter liberation.
已知胆碱能神经末梢上的毒蕈碱型自身受体可抑制脑组织中乙酰胆碱(ACh)的释放,但抑制机制尚不清楚。阿托品通过消除自身受体的抑制作用使ACh释放增加。我们研究了阿托品对[U-14C]葡萄糖孵育期间新合成的[14C]ACh释放的影响是否取决于培养基中Ca2+的浓度。在存在胆碱酯酶抑制剂和30 mmol/L K+的情况下孵育的大鼠纹状体切片中,仅在极低浓度Ca2+孵育期间观察到阿托品引起的[14C]ACh释放显著增加。这一发现支持了这样一种观点,即大脑中突触前毒蕈碱型自身受体的激活通过减少递质释放所需的Ca2+的可用性来影响ACh的释放。