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首页> 外文期刊>Journal of Neurophysiology >BDNF-endocannabinoid interactions at neocortical inhibitory synapses require phospholipase C signaling
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BDNF-endocannabinoid interactions at neocortical inhibitory synapses require phospholipase C signaling

机译：在新皮层抑制性突触中的BDNF-内源性大麻素相互作用需要磷脂酶C信号传导

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摘要

Endogenous cannabinoids (endo-cannabinoids) and neurotrophins, particularly brain-derived neu-rotrophic factor (BDNF), are potent synaptic modulators that are expressed throughout the forebrain and play critical roles in many behavioral processes. Although the effects of BDNF at excitatory synapses have been well characterized, the mechanisms of action of BDNF at inhibitory synapses are not well understood. Previously we have found that BDNF suppresses presynaptic GABA release in layer 2/3 of the neocortex via postsynaptic tropomyosin-related kinase receptor B (trkB) receptor-induced release of endocannabinoids. To examine the intracellular signaling pathways that underlie this effect, we used pharmacological approaches and whole cell patch-clamp techniques in layer 2/3 pyramidal neurons of somatosensory cortex in brain slices from iuvenile Swiss CD1 mice.
机译：内源性大麻素（内源性大麻素）和神经营养蛋白，尤其是脑源性中性营养因子（BDNF），是有效的突触调节剂，在整个前脑表达，并在许多行为过程中起关键作用。尽管已经很好地表征了BDNF在兴奋性突触中的作用，但是对BDNF在抑制性突触中的作用机理尚不十分了解。以前我们发现BDNF通过突触后原肌球蛋白相关激酶受体B（trkB）受体诱导的内源性大麻素释放来抑制新皮层2/3层中突触前GABA的释放。为了检查这种作用的基础细胞内信号传导途径，我们使用药理学方法和全细胞膜片钳技术在来自幼年瑞士CD1小鼠脑切片的体感皮层的2/3层锥体神经元中。

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