The Interaction between Dopaminergic and Noradrenergic Neurons in the Medial Prefrontal Cortex

碩士 === 國立陽明大學 === 藥理學研究所 === 87 === Noradrenergic and dopaminergic projections converge in the medial prefrontal cortex (mPFC) and there is growing evidence of an interaction between dopamine (DA) and norepinephrine (NE). In our study, local infusion of NE (90 nM、150 nM and 300...

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Bibliographic Details
Main Authors: Sze-Yuan Yang, 楊思源
Other Authors: Wynn H. T. Pan
Format: Others
Language:zh-TW
Published: 1999
Online Access:http://ndltd.ncl.edu.tw/handle/35236850289138697906
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Summary:碩士 === 國立陽明大學 === 藥理學研究所 === 87 === Noradrenergic and dopaminergic projections converge in the medial prefrontal cortex (mPFC) and there is growing evidence of an interaction between dopamine (DA) and norepinephrine (NE). In our study, local infusion of NE (90 nM、150 nM and 300 nM) into the mPFC concentration-dependently increased extracellular DA (110±2%、160±4% and 183±6%) in chloral hydrate anaesthetized rats. The a1 receptor antagonist prazosin (10 mM) could block the 300 nM NE-induced increase of DA in the mPFC; but not the 2 receptor antagonist, piperoxan (100 mM). Local application of NE uptake inhibitor, desipramine (DMI; 1 mM), into the mPFC increased extracellular DA (158±5%) as well as NE (194±9%) in this area. Co-infusion of DMI and the a1 receptor antagonist prazosin (10 M) could decrease the DMI-induced increase of DA (125±5%) and NE (130±6%). On the other hand, local application of DA (12 nM、20 nM and 40 nM) into the mPFC concentration-dependently increased extracellular NE (119±3%、135±6% and 160±6%) in the mPFC. The D1 receptor antagonist SCH 23390 (10nM), but not D2 receptor antagonist eticlopride (1nM), could block the increase of extracellular NE, which was induced by local infusion of 40 nM DA. These results suggest that in the mPFC (1) when the extracellular NE concentration increased, the DA concentration would also increase, which may be due to the action of NE on a1 receptors (heteroreceptor regulation) and the competitive effect of DA with NE for reuptake sites on the NE terminals (heterotransporter regulation); (2) DA terminals can regulate extracellular NE and this is due to the action of DA on D1 receptors to enhance NE release (heteroreceptor regulation).