Literature DB >> 19617884

Transfection of rat or mouse neurons by biolistics or electroporation.

Sulayman D Dib-Hajj1, Jin Sung Choi, Lawrence J Macala, Lynda Tyrrell, Joel A Black, Theodore R Cummins, Stephen G Waxman.   

Abstract

Properties of ion channels are affected by the background of the cells in which they are expressed. Thus, it is important for investigators interested in neuronal function to study these proteins in post-mitotic neurons. However, post-mitotic neurons, and many cell lines, are difficult to transfect by standard methods. Here we provide detailed protocols for two different procedures, biolistic and electroporation, which have been used to transfect peripheral sensory neurons from mice or rats with expression constructs of voltage-gated sodium channels. Neurons can be prepared, transfected and currents recorded within 48 h. Using these methods, primary sensory neurons can be transfected with an efficiency of 5-20%, which has permitted studying biophysical properties of sodium channels and their naturally occurring mutants in a native neuronal cell background. Although we have used sodium channels for the examples that we show here, these methods can also be used to study other types of molecules.

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Year:  2009        PMID: 19617884     DOI: 10.1038/nprot.2009.90

Source DB:  PubMed          Journal:  Nat Protoc        ISSN: 1750-2799            Impact factor:   13.491


  57 in total

Review 1.  Techniques for gene transfer into neurons.

Authors:  Philip Washbourne; A Kimberley McAllister
Journal:  Curr Opin Neurobiol       Date:  2002-10       Impact factor: 6.627

Review 2.  Inherited disorders of voltage-gated sodium channels.

Authors:  Alfred L George
Journal:  J Clin Invest       Date:  2005-08       Impact factor: 14.808

Review 3.  International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels.

Authors:  William A Catterall; Alan L Goldin; Stephen G Waxman
Journal:  Pharmacol Rev       Date:  2005-12       Impact factor: 25.468

4.  A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons.

Authors:  Anthony M Rush; Sulayman D Dib-Hajj; Shujun Liu; Theodore R Cummins; Joel A Black; Stephen G Waxman
Journal:  Proc Natl Acad Sci U S A       Date:  2006-05-15       Impact factor: 11.205

5.  Primary structure and functional expression of a mammalian skeletal muscle sodium channel.

Authors:  J S Trimmer; S S Cooperman; S A Tomiko; J Y Zhou; S M Crean; M B Boyle; R G Kallen; Z H Sheng; R L Barchi; F J Sigworth
Journal:  Neuron       Date:  1989-07       Impact factor: 17.173

Review 6.  Erythermalgia: molecular basis for an inherited pain syndrome.

Authors:  Stephen G Waxman; Sulayman Dib-Hajj
Journal:  Trends Mol Med       Date:  2005-11-08       Impact factor: 11.951

Review 7.  Pathomechanisms in channelopathies of skeletal muscle and brain.

Authors:  Stephen C Cannon
Journal:  Annu Rev Neurosci       Date:  2006       Impact factor: 12.449

8.  Altered subthreshold sodium currents and disrupted firing patterns in Purkinje neurons of Scn8a mutant mice.

Authors:  I M Raman; L K Sprunger; M H Meisler; B P Bean
Journal:  Neuron       Date:  1997-10       Impact factor: 17.173

9.  Vinpocetine is a potent blocker of rat NaV1.8 tetrodotoxin-resistant sodium channels.

Authors:  Xiaoping Zhou; Xiao-Wei Dong; James Crona; Maureen Maguire; Tony Priestley
Journal:  J Pharmacol Exp Ther       Date:  2003-05-01       Impact factor: 4.030

10.  Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable.

Authors:  Sulayman D Dib-Hajj; Mark Estacion; Brian W Jarecki; Lynda Tyrrell; Tanya Z Fischer; Mark Lawden; Theodore R Cummins; Stephen G Waxman
Journal:  Mol Pain       Date:  2008-09-19       Impact factor: 3.395

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  52 in total

Review 1.  Transfection techniques for neuronal cells.

Authors:  Daniela Karra; Ralf Dahm
Journal:  J Neurosci       Date:  2010-05-05       Impact factor: 6.167

2.  Probing localized neural mechanotransduction through surface-modified elastomeric matrices and electrophysiology.

Authors:  Chao-Min Cheng; Yi-Wen Lin; Robert M Bellin; Robert L Steward; Yuan-Ren Cheng; Philip R LeDuc; Chih-Cheng Chen
Journal:  Nat Protoc       Date:  2010-03-25       Impact factor: 13.491

3.  Nonlinear effects of hyperpolarizing shifts in activation of mutant Nav1.7 channels on resting membrane potential.

Authors:  Mark Estacion; Stephen G Waxman
Journal:  J Neurophysiol       Date:  2017-02-01       Impact factor: 2.714

4.  Synthesis and characterization of glycol chitosan DNA nanoparticles for retinal gene delivery.

Authors:  Rajendra N Mitra; Zongchao Han; Miles Merwin; Muhammed Al Taai; Shannon M Conley; Muna I Naash
Journal:  ChemMedChem       Date:  2013-11-07       Impact factor: 3.466

5.  Voltage-clamp and current-clamp recordings from mammalian DRG neurons.

Authors:  Theodore R Cummins; Anthony M Rush; Mark Estacion; Sulayman D Dib-Hajj; Stephen G Waxman
Journal:  Nat Protoc       Date:  2009-07-09       Impact factor: 13.491

6.  Reverse pharmacogenomics: carbamazepine normalizes activation and attenuates thermal hyperexcitability of sensory neurons due to Nav 1.7 mutation I234T.

Authors:  Yang Yang; Talia Adi; Philip R Effraim; Lubin Chen; Sulayman D Dib-Hajj; Stephen G Waxman
Journal:  Br J Pharmacol       Date:  2017-07-30       Impact factor: 8.739

7.  De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP.

Authors:  Krishna R Veeramah; Janelle E O'Brien; Miriam H Meisler; Xiaoyang Cheng; Sulayman D Dib-Hajj; Stephen G Waxman; Dinesh Talwar; Santhosh Girirajan; Evan E Eichler; Linda L Restifo; Robert P Erickson; Michael F Hammer
Journal:  Am J Hum Genet       Date:  2012-02-23       Impact factor: 11.025

8.  Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitability.

Authors:  Mark Estacion; Stephen G Waxman; Sulayman D Dib-Hajj
Journal:  Mol Pain       Date:  2010-06-08       Impact factor: 3.395

9.  Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders.

Authors:  Xiaoyang Cheng; Sulayman D Dib-Hajj; Lynda Tyrrell; Dowain A Wright; Tanya Z Fischer; Stephen G Waxman
Journal:  Mol Pain       Date:  2010-04-29       Impact factor: 3.395

10.  A gain-of-function mutation in Nav1.6 in a case of trigeminal neuralgia.

Authors:  Brian S Tanaka; Peng Zhao; Fadia B Dib-Hajj; Valerie Morisset; Simon Tate; Stephen G Waxman; Sulayman D Dib-Hajj
Journal:  Mol Med       Date:  2016-08-03       Impact factor: 6.354

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