Tseng Kuei Y, O'Donnell Patricio
Center for Neuropharmacology and Neuroscience, 47 New Scotland Avenue, Albany Medical College (MC-136), Albany, New York 12208, USA.
Cereb Cortex. 2005 Jan;15(1):49-57. doi: 10.1093/cercor/bhh107. Epub 2004 Jun 24.
Dopamine-glutamate interactions may contribute to persistent electrical activity in the prefrontal cortex (PFC). We tested whether a D1 modulation of NMDA function can result in persistent depolarization in vitro. D1-NMDA co-activation yielded depolarizing plateaus resembling in vivo up states in PFC pyramidal neurons recorded in slices from adult (PD 45-65), but not pre-pubertal (PD 29-38) rats. These plateaus required intracellular Ca2+, activation of L-type Ca2+ channels and protein kinase A. These events were eliminated by intracellular administration of the voltage-gated Na+ channel blocker QX-314 or by interrupting synaptic activity with bath application of tetrodotoxin or the AMPA antagonist CNQX, suggesting that they require both intrinsic and synaptic mechanisms. These recurrent depolarizations could constitute important elements in cortical information processing, allowing synaptic plasticity and memory functions. Acquiring these PFC D1-NMDA interactions after puberty may be a critical element for developing mature cognitive abilities.
多巴胺 - 谷氨酸相互作用可能导致前额叶皮质（PFC）的持续性电活动。我们测试了NMDA功能的D1调节是否能在体外导致持续性去极化。D1 - NMDA共同激活在成年（出生后第45 - 65天）而非青春期前（出生后第29 - 38天）大鼠脑片记录的PFC锥体神经元中产生了类似于体内上行状态的去极化平台。这些平台需要细胞内Ca2 +、L型Ca2 +通道的激活和蛋白激酶A。通过细胞内给予电压门控Na +通道阻滞剂QX - 314或通过在浴中应用河豚毒素或AMPA拮抗剂CNQX中断突触活动可消除这些事件，这表明它们需要内在和突触机制。这些反复的去极化可能构成皮质信息处理中的重要元素，允许突触可塑性和记忆功能。青春期后获得这些PFC D1 - NMDA相互作用可能是发展成熟认知能力的关键因素。
