Galarraga E, Hernández-López S, Reyes A, Barral J, Bargas J
Dept de Biofisica, UNAM, México City, México.
Neuroreport. 1997 Jul 7;8(9-10):2183-6. doi: 10.1097/00001756-199707070-00019.
When synaptic activity is evoked from relatively depolarized membrane potentials, D1 receptor agonists enhance the depolarization level and slow the decay of synaptic responses recorded from neostriatal spiny neurons. The population spikes' amplitude is also increased. These D1 actions facilitate firing and are evident in the presence of both NMDA and GABA selective blockers. Thus, dopaminergic D1 receptor activation facilitates the AMPA-mediated EPSP in these conditions. This facilitatory effect could be suppressed by L-type Ca2+ channel antagonists (200 nM calciseptine and 5 microM nicardipine), suggesting that it is mediated by an increase in L-current. D1-receptor activation thus mediates orthodromic facilitation of neostriatal neurons when evoked from depolarized membrane potentials. This reinforces the dopamine facilitation mediated through NMDA responses.
当从相对去极化的膜电位诱发突触活动时，D1受体激动剂可提高去极化水平，并减缓从新纹状体棘状神经元记录到的突触反应的衰减。群体峰电位的幅度也会增加。这些D1作用促进放电，并且在同时存在NMDA和GABA选择性阻滞剂的情况下也很明显。因此，在这些条件下，多巴胺能D1受体激活促进了AMPA介导的兴奋性突触后电位（EPSP）。这种促进作用可被L型Ca2+通道拮抗剂（200 nM钙调蛋白和5 μM尼卡地平）抑制，表明它是由L电流增加介导的。因此，当从去极化膜电位诱发时，D1受体激活介导新纹状体神经元的顺向促进作用。这加强了通过NMDA反应介导的多巴胺促进作用。
