Lee K S, Schubert P, Heinemann U
Brain Res. 1984 Oct 29;321(1):160-4. doi: 10.1016/0006-8993(84)90694-2.
Neural afterdischarges generated in the presence of penicillin or low extracellular calcium concentrations were found to be inhibited by adenosine in the rat hippocampus in vitro. This anticonvulsant effect of adenosine is observed in the absence, as well as in the presence, of chemical synaptic transmission and apparently occurs at a postsynaptic site which is most sensitive in the apical dendritic region of the CA1 pyramidal cells. The methylxanthine theophylline antagonizes the effect of adenosine; and, the anticonvulsant action of the L-isomer of the adenosine analogue phenylisopropyladenosine (PIA) is substantially more potent than the D-isomer, findings which are characteristic of an A1 type adenosine receptor. The endogenous release of adenosine may therefore serve to tonically reduce the tendency for repetitive discharge in CA1 pyramidal cells via an interaction with a high affinity A1 receptor which appears to be preferentially localized in the apical dendrites.
在体外培养的大鼠海马体中发现,在青霉素存在或细胞外钙浓度较低的情况下产生的神经放电后发放会被腺苷抑制。腺苷的这种抗惊厥作用在化学突触传递存在和不存在的情况下均能观察到,并且显然发生在突触后位点,该位点在CA1锥体细胞的顶端树突区域最为敏感。甲基黄嘌呤茶碱可拮抗腺苷的作用;腺苷类似物苯异丙基腺苷(PIA)的L-异构体的抗惊厥作用明显比D-异构体更强,这些发现是A1型腺苷受体的特征。因此,内源性腺苷释放可能通过与高亲和力A1受体相互作用,来持续降低CA1锥体细胞重复放电的倾向,该受体似乎优先定位于顶端树突中。