期刊
CELL REPORTS
卷 15, 期 4, 页码 735-747出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.03.062
关键词
-
类别
资金
- ERC [ENDOSWITCH 261286]
- Swedish Research Council [2010-3250]
- Novo Nordisk Fonden
- Strategic Research Programme in Diabetes at Karolinska Institutet
- Novo Nordisk Fonden [NNF15OC0016258, NNF14OC0011061, NNF16OC0021482] Funding Source: researchfish
How autoreceptors contribute to maintaining a stable output of rhythmically active neuronal circuits is poorly understood. Here, we examine this issue in a dopamine population, spontaneously oscillating hypothalamic rat (TIDA) neurons, that underlie neuroendocrine control of reproduction and neuroleptic side effects. Activation of dopamine receptors of the type 2 family (D2Rs) at the cell-body level slowed TIDA oscillations through two mechanisms. First, they prolonged the depolarizing phase through a combination of presynaptic increases in inhibition and postsynaptic hyperpolarization. Second, they extended the discharge phase through presynaptic attenuation of calcium currents and decreased synaptic inhibition. Dopamine reuptake blockade similarly reconfigured the oscillation, indicating that ambient somatodendritic transmitter concentration determines electrical behavior. In the absence of D2R feedback, however, discharge was abolished by depolarization block. These results indicate the existence of an ultra-short feedback loop whereby neuroendocrine dopamine neurons tune network behavior to echoes of their own activity, reflected in ambient somatodendritic dopamine, and also suggest a mechanism for antipsychotic side effects.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据