斑马鱼的触摸反应需要电压门控钙通道 2.1b。
Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b.
机构信息
Départment de Pathologie et Biologie Cellulaire, Groupe de Recherche sur le Système Nerveux Central et Centre d'Excellence en Neuromique de l'Université de Montéral, Université de Montréal, Montreal, Quebec, Canada.
出版信息
J Neurophysiol. 2012 Jul;108(1):148-59. doi: 10.1152/jn.00839.2011. Epub 2012 Apr 4.
Abstract
The molecular and physiological basis of the touch-unresponsive zebrafish mutant fakir has remained elusive. Here we report that the fakir phenotype is caused by a missense mutation in the gene encoding voltage-gated calcium channel 2.1b (CACNA1Ab). Injection of RNA encoding wild-type CaV2.1 restores touch responsiveness in fakir mutants, whereas knockdown of CACNA1Ab via morpholino oligonucleotides recapitulates the fakir mutant phenotype. Fakir mutants display normal current-evoked synaptic communication at the neuromuscular junction but have attenuated touch-evoked activation of motor neurons. NMDA-evoked fictive swimming is not affected by the loss of CaV2.1b, suggesting that this channel is not required for motor pattern generation. These results, coupled with the expression of CACNA1Ab by sensory neurons, suggest that CaV2.1b channel activity is necessary for touch-evoked activation of the locomotor network in zebrafish.
摘要
fakir 突变体的触觉无反应的分子和生理基础仍然难以捉摸。在这里，我们报告 fakir 表型是由电压门控钙通道 2.1b (CACNA1Ab) 基因编码的错义突变引起的。编码野生型 CaV2.1 的 RNA 的注射恢复了 fakir 突变体的触觉反应，而通过 morpholino 寡核苷酸对 CACNA1Ab 的敲低则再现了 fakir 突变体的表型。fakir 突变体在神经肌肉接头处显示正常的电流诱发的突触通讯，但触觉诱发的运动神经元激活减弱。NMDA 诱发的虚拟游泳不受 CaV2.1b 缺失的影响，表明该通道对于运动模式生成不是必需的。这些结果，加上感觉神经元表达 CACNA1Ab，表明 CaV2.1b 通道活性对于斑马鱼中触觉激活运动网络是必需的。
相似文献
1
Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b.斑马鱼的触摸反应需要电压门控钙通道 2.1b。
J Neurophysiol. 2012 Jul;108(1):148-59. doi: 10.1152/jn.00839.2011. Epub 2012 Apr 4.
2
Na(v)1.6a is required for normal activation of motor circuits normally excited by tactile stimulation.Na(v)1.6a 对于正常激活通常由触觉刺激激发的运动回路是必需的。
Dev Neurobiol. 2010 Jun;70(7):508-22. doi: 10.1002/dneu.20791.
3
Sensory gating of an embryonic zebrafish interneuron during spontaneous motor behaviors.自发运动行为期间胚胎斑马鱼中间神经元的感觉门控
Front Neural Circuits. 2014 Sep 30;8:121. doi: 10.3389/fncir.2014.00121. eCollection 2014.
4
scn1bb, a zebrafish ortholog of SCN1B expressed in excitable and nonexcitable cells, affects motor neuron axon morphology and touch sensitivity.scn1bb是SCN1B在斑马鱼中的直系同源基因，在可兴奋细胞和非可兴奋细胞中表达，影响运动神经元轴突形态和触觉敏感性。
J Neurosci. 2008 Nov 19;28(47):12510-22. doi: 10.1523/JNEUROSCI.4329-08.2008.
5
Ca2.2 Gates Calcium-Independent but Voltage-Dependent Secretion in Mammalian Sensory Neurons.钙离子通道钙非依赖性但电压依赖性分泌在哺乳动物感觉神经元中的作用。
Neuron. 2017 Dec 20;96(6):1317-1326.e4. doi: 10.1016/j.neuron.2017.10.028. Epub 2017 Nov 30.
6
A hybrid electrical/chemical circuit in the spinal cord generates a transient embryonic motor behavior.脊髓中的混合电气/化学电路产生短暂的胚胎运动行为。
J Neurosci. 2014 Jul 16;34(29):9644-55. doi: 10.1523/JNEUROSCI.1225-14.2014.
7
A mutation in Ca2.1 linked to a severe neurodevelopmental disorder impairs channel gating.一种与严重神经发育障碍相关的 Ca2.1 突变会损害通道门控。
J Gen Physiol. 2019 Jun 3;151(6):850-859. doi: 10.1085/jgp.201812237. Epub 2019 Apr 23.
8
Zebrafish CaV2.1 calcium channels are tailored for fast synchronous neuromuscular transmission.斑马鱼CaV2.1钙通道专为快速同步神经肌肉传递而设计。
Biophys J. 2015 Feb 3;108(3):578-84. doi: 10.1016/j.bpj.2014.11.3484.
9
TRPM7 is required within zebrafish sensory neurons for the activation of touch-evoked escape behaviors.TRPM7 在斑马鱼感觉神经元中对于触摸引发的逃避行为的激活是必需的。
J Neurosci. 2011 Aug 10;31(32):11633-44. doi: 10.1523/JNEUROSCI.4950-10.2011.
10
Roles of high-voltage-activated calcium channel subtypes in a vertebrate spinal locomotor network.高压激活钙通道亚型在脊椎动物脊髓运动网络中的作用。
J Neurophysiol. 2000 Dec;84(6):2758-66. doi: 10.1152/jn.2000.84.6.2758.
引用本文的文献
1
Genetic modeling of degenerative diseases and mechanisms of neuronal regeneration in the zebrafish cerebellum.斑马鱼小脑退行性疾病的遗传建模及神经元再生机制
Cell Mol Life Sci. 2024 Dec 27;82(1):26. doi: 10.1007/s00018-024-05538-z.
2
Localization of Piezo 1 and Piezo 2 in Lateral Line System and Inner Ear of Zebrafish ().斑马鱼（）侧线系统和内耳中 Piezo1 和 Piezo2 的定位。
Int J Mol Sci. 2024 Aug 24;25(17):9204. doi: 10.3390/ijms25179204.
3
Developing a pathway to clinical trials for -related epilepsies: A patient organization perspective.为与……相关的癫痫症制定临床试验途径：患者组织视角
Ther Adv Rare Dis. 2024 Apr 25;5:26330040241245725. doi: 10.1177/26330040241245725. eCollection 2024 Jan-Dec.
4
Zebrafish Models of Rare Neurological Diseases like Spinocerebellar Ataxias (SCAs): Advantages and Limitations.诸如脊髓小脑共济失调（SCAs）等罕见神经疾病的斑马鱼模型：优势与局限性
Biology (Basel). 2023 Oct 10;12(10):1322. doi: 10.3390/biology12101322.
5
Towards Zebrafish Models of CNS Channelopathies.迈向中枢神经系统通道病的斑马鱼模型。
Int J Mol Sci. 2022 Nov 12;23(22):13979. doi: 10.3390/ijms232213979.
6
A forward genetic screen identifies Dolk as a regulator of startle magnitude through the potassium channel subunit Kv1.1.一项正向遗传学筛选发现 Dolk 是通过钾通道亚基 Kv1.1 调节惊跳幅度的调控因子。
PLoS Genet. 2021 Jun 1;17(6):e1008943. doi: 10.1371/journal.pgen.1008943. eCollection 2021 Jun.
7
Zebrafish Models of Autosomal Dominant Ataxias.常染色体显性遗传性共济失调症的斑马鱼模型。
Cells. 2021 Feb 17;10(2):421. doi: 10.3390/cells10020421.
8
Experimental Models to Study Autism Spectrum Disorders: hiPSCs, Rodents and Zebrafish.自闭症谱系障碍的实验模型：iPS 细胞、啮齿动物和斑马鱼。
Genes (Basel). 2020 Nov 20;11(11):1376. doi: 10.3390/genes11111376.
9
Zebrafish as a Model System for the Study of Severe Ca2.1 (α) Channelopathies.斑马鱼作为研究严重Ca2.1（α）通道病的模型系统
Front Mol Neurosci. 2020 Feb 7;12:329. doi: 10.3389/fnmol.2019.00329. eCollection 2019.
10
Phenotypic Characterization of Larval Zebrafish (Danio rerio) with Partial Knockdown of the cacna1a Gene.部分敲低 cacna1a 基因的斑马鱼幼虫表型特征。
Mol Neurobiol. 2020 Apr;57(4):1904-1916. doi: 10.1007/s12035-019-01860-x. Epub 2019 Dec 26.
本文引用的文献
1
Disruption of Eaat2b, a glutamate transporter, results in abnormal motor behaviors in developing zebrafish.谷氨酸转运体 Eaat2b 的破坏导致发育中的斑马鱼出现异常运动行为。
Dev Biol. 2012 Feb 15;362(2):162-71. doi: 10.1016/j.ydbio.2011.11.001. Epub 2011 Nov 6.
2
Ensembl 2012.Ensembl 2012.
Nucleic Acids Res. 2012 Jan;40(Database issue):D84-90. doi: 10.1093/nar/gkr991. Epub 2011 Nov 15.
3
Connexin 39.9 protein is necessary for coordinated activation of slow-twitch muscle and normal behavior in zebrafish.连接蛋白 39.9 蛋白对于协调慢肌激活和斑马鱼正常行为是必需的。
J Biol Chem. 2012 Jan 6;287(2):1080-9. doi: 10.1074/jbc.M111.308205. Epub 2011 Nov 10.
4
TRPM7 is required within zebrafish sensory neurons for the activation of touch-evoked escape behaviors.TRPM7 在斑马鱼感觉神经元中对于触摸引发的逃避行为的激活是必需的。
J Neurosci. 2011 Aug 10;31(32):11633-44. doi: 10.1523/JNEUROSCI.4950-10.2011.
5
Forward and reverse genetic approaches for the analysis of vertebrate development in the zebrafish.利用斑马鱼进行脊椎动物发育的正向和反向遗传学分析。
Dev Cell. 2011 Jul 19;21(1):48-64. doi: 10.1016/j.devcel.2011.06.007.
6
Movement, technology and discovery in the zebrafish.斑马鱼中的运动、技术和发现。
Curr Opin Neurobiol. 2011 Feb;21(1):110-5. doi: 10.1016/j.conb.2010.09.011. Epub 2010 Oct 20.
7
Identification and modulation of voltage-gated Ca2+ currents in zebrafish Rohon-Beard neurons.鉴定和调制斑马鱼罗氏神经元中的电压门控 Ca2+ 电流。
J Neurophysiol. 2011 Jan;105(1):442-53. doi: 10.1152/jn.00625.2010. Epub 2010 Oct 20.
8
touché Is required for touch-evoked generator potentials within vertebrate sensory neurons.触须对于脊椎动物感觉神经元中的触诱发电机位是必需的。
J Neurosci. 2010 Jul 14;30(28):9359-67. doi: 10.1523/JNEUROSCI.1639-10.2010.
9
Biogenesis of GPI-anchored proteins is essential for surface expression of sodium channels in zebrafish Rohon-Beard neurons to respond to mechanosensory stimulation.糖基磷脂酰肌醇锚定蛋白的生物发生对于斑马鱼 Rohon-Beard 神经元表面钠离子通道的表达至关重要，以响应机械感觉刺激。
Development. 2010 May;137(10):1689-98. doi: 10.1242/dev.047464. Epub 2010 Apr 14.
10
Na(v)1.6a is required for normal activation of motor circuits normally excited by tactile stimulation.Na(v)1.6a 对于正常激活通常由触觉刺激激发的运动回路是必需的。
Dev Neurobiol. 2010 Jun;70(7):508-22. doi: 10.1002/dneu.20791.
Zotero 插件