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首页> 外文期刊>The European Journal of Neuroscience >Insulin promotes functional induction of silent synapses in differentiating rat neocortical neurons.
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Insulin promotes functional induction of silent synapses in differentiating rat neocortical neurons.

机译:胰岛素促进分化大鼠新皮层神经元沉默突触的功能诱导。

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摘要

Long-term synaptic plasticity is thought to underlie synaptic reorganization phenomena that occur during neocortical development. Recently, it has been proposed, that the functional induction of AMPA receptors at silent glutamatergic synapses is of major importance in activity-dependent, developmental plasticity. To investigate the mechanisms involved in the developmental regulation of silent synapses, we analysed the functional maturation of the thalamocortical projection in culture. A large proportion of the thalamocortical synapses were functionally silent at an early stage in vitro. During further differentiation, the incidence of silent synapses decreased drastically, indicating a conversion of silent into functional synapses. Chronic blockade of spontaneous network activity by addition of tetrodotoxin to the culture medium strongly impaired this developmental maturation. Moreover, the developmental decline in the proportion of silent synapses was dramatically accelerated by chronic addition of the neurotrophic factor, insulin. This effect of insulin was partly dependent on spontaneous activity. Thus, insulin appears to be involved in the modulation of long-term developmental plasticity at immature glutamatergic synapses.
机译:长期的突触可塑性被认为是新皮层发育期间发生的突触重组现象的基础。最近,有人提出,沉默的谷氨酸能突触对AMPA受体的功能诱导在依赖于活动的发育可塑性中具有重要意义。为了调查参与沉默突触的发育调节的机制,我们分析了丘脑皮层投射在文化中的功能成熟。大部分的丘脑皮层突触在体外早期是功能沉默的。在进一步的分化过程中,沉默突触的发生率急剧下降,表明沉默突触转变为功能性突触。通过向培养基中添加河豚毒素来慢性阻断自发性网络活动,严重损害了这种发育成熟。此外,通过长期添加神经营养因子胰岛素极大地加速了沉默突触比例的发育下降。胰岛素的这种作用部分取决于自发活动。因此,胰岛素似乎参与了未成熟谷氨酸能突触的长期发育可塑性的调节。

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