Correction to: Regulation of TrkB receptor translocation to lipid rafts by adenosine A_2A receptors and its functional implications for BDNF-induced regulation of synaptic plasticity.

IF 3 4区医学 Q2 NEUROSCIENCES

Purinergic Signalling Pub Date : 2024-06-01 DOI:10.1007/s11302-024-10011-4

Natália Assaife-Lopes, Vasco C Sousa, Daniela B Pereira, Joaquim A Ribeiro, Ana M Sebastião

引用次数: 0

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更正：腺苷 A2A 受体对 TrkB 受体向脂质筏转运的调控及其对 BDNF 诱导的突触可塑性调控的功能性影响。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Purinergic Signalling 医学-神经科学

CiteScore

6.60

自引率

17.10%

发文量

审稿时长

6-12 weeks

期刊介绍： Nucleotides and nucleosides are primitive biological molecules that were utilized early in evolution both as intracellular energy sources and as extracellular signalling molecules. ATP was first identified as a neurotransmitter and later as a co-transmitter with all the established neurotransmitters in both peripheral and central nervous systems. Four subtypes of P1 (adenosine) receptors, 7 subtypes of P2X ion channel receptors and 8 subtypes of P2Y G protein-coupled receptors have currently been identified. Since P2 receptors were first cloned in the early 1990’s, there is clear evidence for the widespread distribution of both P1 and P2 receptor subtypes in neuronal and non-neuronal cells, including glial, immune, bone, muscle, endothelial, epithelial and endocrine cells.

Correction to: Regulation of TrkB receptor translocation to lipid rafts by adenosine A2A receptors and its functional implications for BDNF-induced regulation of synaptic plasticity.

Correction to: Regulation of TrkB receptor translocation to lipid rafts by adenosine A_2A receptors and its functional implications for BDNF-induced regulation of synaptic plasticity.