Endocannabinoids blunt the augmentation of synaptic transmission by serotonin 2A receptors in the nucleus tractus solitarii (nTS).
Endocannabinoids blunt the augmentation of synaptic transmission by serotonin 2A receptors in the nucleus tractus solitarii (nTS).
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DOI：
10.1016/j.brainres.2013.09.006
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发表时间：
2013-11-06
期刊：
影响因子：
2.9
通讯作者：
Kline DD
中科院分区：
文献类型：
--
作者：
Austgen JR;Kline DD
5-羟色胺（5-羟色胺，5-HT）和5-HT2受体部分通过nTS的作用调节心血管和自主神经功能，nTS是脑干中心肺传入的主要终止和整合点。在其他脑区，5-HT2受体（5-HT2R）直接改变突触传递，也可通过5- ht2ar诱导内源性大麻素释放。本研究探讨了5-HT2AR在孤立束核（nTS）神经传递中的作用及其与内源性大麻素的相互作用。在激活和阻断5-HT2ARs的水平脑干切片上记录了单突触nTS神经元的兴奋性突触后电流（EPSCs）。5-HT2AR激活增强孤立束（TS）诱发EPSC幅值，而5-HT2AR阻断在低和高TS刺激率下抑制TS-EPSC幅值。内源性大麻素受体阻滞可降低5- ht2ar诱导的神经传递增加，并在高频而非低频TS刺激下增加突触间隙内源性内源性大麻素。内源性大麻素对EPSCs没有强直性影响。这些数据表明，5-羟色胺通过5-HT2AR在nTS中是一种兴奋性神经调节剂，其作用由内源性大麻素系统调节。
Serotonin (5-Hydroxytryptamine, 5-HT) and the 5-HT2 receptor modulate cardiovascular and autonomic function in part through actions in the nTS, the primary termination and integration point for cardiorespiratory afferents in the brainstem. In other brain regions, 5-HT2 receptors (5-HT2R) modify synaptic transmission directly, as well as through 5-HT2AR-induced endocannabinoid release. This study examined the role of 5-HT2AR as well as their interaction with endocannabinoids on neurotransmission in the nucleus tractus solitarii (nTS). Excitatory postsynaptic currents (EPSCs) in monosynaptic nTS neurons were recorded in the horizontal brainstem slice during activation and blockade of 5-HT2ARs. 5-HT2AR activation augmented solitary tract (TS) evoked EPSC amplitude whereas 5-HT2AR blockade depressed TS-EPSC amplitude at low and high TS stimulation rates. The 5-HT2AR-induced increase in neurotransmission was reduced by endocannabinoid receptor block and increased endogenous endocannabinoids in the synaptic cleft during high frequency, but not low, TS stimulation. Endocannabinoids did not tonically modify EPSCs. These data suggest 5-HT acting through the 5-HT2AR is an excitatory neuromodulator in the nTS and its effects are modulated by the endocannabinoid system.
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