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正常和同侧多巴胺耗竭大鼠网状丘脑核放电活动中局部激活和阻断多巴胺 D4 受体的影响。

Effects of local activation and blockade of dopamine D4 receptors in the spiking activity of the reticular thalamic nucleus in normal and in ipsilateral dopamine-depleted rats.

机构信息

Academia de Fisiología, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Casco de Santo Tomás, CdMx 11340, Mexico; Sección de Investigación y Posgrado de la Escuela Superior de Medicina del IPN, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Casco de Santo Tomás, CdMx 11340, Mexico.

Academia de Fisiología, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Casco de Santo Tomás, CdMx 11340, Mexico.

出版信息

Brain Res. 2019 Jun 1;1712:34-46. doi: 10.1016/j.brainres.2019.01.042. Epub 2019 Feb 1.

Abstract

The reticular thalamic nucleus (RTn) controls the overall activity of thalamo-cortical neurons information processing. GABAergic RTn neurons have one of the highest densities of D4-type dopamine receptors in subcortical structures. The unitary electrical activity of RTn neurons was recorded in vivo in Wistar rats in order to study the effects of local activation and blockade of D4 receptors under both conditions, normal and ipsilateral lesion of the dopaminergic pathways. Our data suggest that: i) there is a tonic dopaminergic input to the RTn; ii) local activation of D4 receptors increases the basal firing rate of RTn neurons in normal and lesioned rats, and iii) local blockade of D4 receptors diminishes the firing rate in normal but not in lesioned rats. Altogether, our findings support that dopamine contributes to the spontaneous basal firing of the RTn neurons through D4-type dopamine receptors.

摘要

网状丘脑核(RTn)控制丘脑-皮质神经元信息处理的整体活动。GABA 能 RTn 神经元在皮质下结构中具有最高密度的 D4 型多巴胺受体之一。为了研究多巴胺能通路正常和单侧损伤两种情况下局部激活和阻断 D4 受体的影响,我们在 Wistar 大鼠体内记录了 RTn 神经元的单位电活动。我们的数据表明:i)RTn 存在紧张性多巴胺能输入;ii)在正常和损伤大鼠中,局部激活 D4 受体增加 RTn 神经元的基础放电率,iii)在正常大鼠中局部阻断 D4 受体可降低放电率,但在损伤大鼠中则不然。总之,我们的发现支持多巴胺通过 D4 型多巴胺受体促进 RTn 神经元的自发基础放电。

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