Introducing treatment strategy for cerebellar ataxia in mutant med mice: Combination of acetazolamide and 4-Aminopyridine
Abstract Purkinje neurons are the sole output neuron of the cerebellar cortex, and they generate high-frequency action potentials. Electrophysiological dysfunction of Purkinje neurons causes cerebellar ataxia. Mutant med mice have the lack of expression of the Scn8a gene. This gene encodes the NaV1....
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| Veröffentlicht in: | Computer methods and programs in biomedicine 2014-02, Vol.113 (2), p.697-704 |
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| creator | Abbasi, Samira Abbasi, Ataollah Sarbaz, Yashar |
| description | Abstract Purkinje neurons are the sole output neuron of the cerebellar cortex, and they generate high-frequency action potentials. Electrophysiological dysfunction of Purkinje neurons causes cerebellar ataxia. Mutant med mice have the lack of expression of the Scn8a gene. This gene encodes the NaV1.6 protein. In med Purkinje neurons, regular high-frequency firing is slowed, and med mice are ataxic. The aim of this study was to propose the neuroprotective drugs which could be useful for ataxia treatment in med mice, and to investigate the neuroprotective effects of these drugs by simulation. Simulation results showed that Kv4 channel inhibitors and BK channel activators restored the normal electrophysiological properties of the med Purkinje neurons. 4-Aminopyridine (4-AP) and acetazolamide (ACTZ) were proposed as neuroprotective drugs for Kv4 channel inhibitor and BK channel activator, respectively. |
| doi_str_mv | 10.1016/j.cmpb.2013.11.008 |
| format | Article |
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Electrophysiological dysfunction of Purkinje neurons causes cerebellar ataxia. Mutant med mice have the lack of expression of the Scn8a gene. This gene encodes the NaV1.6 protein. In med Purkinje neurons, regular high-frequency firing is slowed, and med mice are ataxic. The aim of this study was to propose the neuroprotective drugs which could be useful for ataxia treatment in med mice, and to investigate the neuroprotective effects of these drugs by simulation. Simulation results showed that Kv4 channel inhibitors and BK channel activators restored the normal electrophysiological properties of the med Purkinje neurons. 4-Aminopyridine (4-AP) and acetazolamide (ACTZ) were proposed as neuroprotective drugs for Kv4 channel inhibitor and BK channel activator, respectively.</description><identifier>ISSN: 0169-2607</identifier><identifier>EISSN: 1872-7565</identifier><identifier>DOI: 10.1016/j.cmpb.2013.11.008</identifier><identifier>PMID: 24326337</identifier><language>eng</language><publisher>Kidlington: Elsevier Ireland Ltd</publisher><subject>4-Aminopyridine - administration & dosage ; 4-Aminopyridine - pharmacology ; 4-Aminopyridine - therapeutic use ; Acetazolamide - administration & dosage ; Acetazolamide - pharmacology ; Acetazolamide - therapeutic use ; Action Potentials - drug effects ; Animals ; Ataxia ; Biological and medical sciences ; Cell physiology ; Cerebellar Ataxia - drug therapy ; Cerebellar Ataxia - physiopathology ; Disease Models, Animal ; Drug Therapy, Combination ; Fundamental and applied biological sciences. Psychology ; Internal Medicine ; Ion channels ; Mice ; Mice, Mutant Strains ; Modeling ; Molecular and cellular biology ; Muscle contraction ; Neuroprotective agents ; Neuroprotective Agents - administration & dosage ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Other ; Purkinje Cells - drug effects ; Therapeutics</subject><ispartof>Computer methods and programs in biomedicine, 2014-02, Vol.113 (2), p.697-704</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2013 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-99091cc611c090be852ab639d79f51cbf104dac1dfcec6c1d0557f4b681968d83</citedby><cites>FETCH-LOGICAL-c474t-99091cc611c090be852ab639d79f51cbf104dac1dfcec6c1d0557f4b681968d83</cites><orcidid>0000-0001-6572-8711</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0169260713003805$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28150499$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24326337$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Abbasi, Samira</creatorcontrib><creatorcontrib>Abbasi, Ataollah</creatorcontrib><creatorcontrib>Sarbaz, Yashar</creatorcontrib><title>Introducing treatment strategy for cerebellar ataxia in mutant med mice: Combination of acetazolamide and 4-Aminopyridine</title><title>Computer methods and programs in biomedicine</title><addtitle>Comput Methods Programs Biomed</addtitle><description>Abstract Purkinje neurons are the sole output neuron of the cerebellar cortex, and they generate high-frequency action potentials. Electrophysiological dysfunction of Purkinje neurons causes cerebellar ataxia. Mutant med mice have the lack of expression of the Scn8a gene. This gene encodes the NaV1.6 protein. In med Purkinje neurons, regular high-frequency firing is slowed, and med mice are ataxic. The aim of this study was to propose the neuroprotective drugs which could be useful for ataxia treatment in med mice, and to investigate the neuroprotective effects of these drugs by simulation. Simulation results showed that Kv4 channel inhibitors and BK channel activators restored the normal electrophysiological properties of the med Purkinje neurons. 4-Aminopyridine (4-AP) and acetazolamide (ACTZ) were proposed as neuroprotective drugs for Kv4 channel inhibitor and BK channel activator, respectively.</description><subject>4-Aminopyridine - administration & dosage</subject><subject>4-Aminopyridine - pharmacology</subject><subject>4-Aminopyridine - therapeutic use</subject><subject>Acetazolamide - administration & dosage</subject><subject>Acetazolamide - pharmacology</subject><subject>Acetazolamide - therapeutic use</subject><subject>Action Potentials - drug effects</subject><subject>Animals</subject><subject>Ataxia</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Cerebellar Ataxia - drug therapy</subject><subject>Cerebellar Ataxia - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Drug Therapy, Combination</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Internal Medicine</subject><subject>Ion channels</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Modeling</subject><subject>Molecular and cellular biology</subject><subject>Muscle contraction</subject><subject>Neuroprotective agents</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Other</subject><subject>Purkinje Cells - drug effects</subject><subject>Therapeutics</subject><issn>0169-2607</issn><issn>1872-7565</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk2LFDEQhoMo7jr6BzxILoKXHlPdnXRHZGEZ_FhY8KCeQzqpXjJ2J2OSFsdfb5oZFTzoqS5PVSXvU4Q8BbYFBuLlfmvmw7CtGTRbgC1j_T1yCX1XVx0X_D65LJCsasG6C_IopT1jrOZcPCQXddvUomm6S3K88TkGuxjn72iOqPOMPtOUo854d6RjiNRgxAGnSUeqs_7uNHWezkvWBZzR0tkZfEV3YR6c19kFT8NItcGsf4RJz84i1d7StrqenQ-HY3TWeXxMHox6SvjkXDfk89s3n3bvq9sP725217eVabs2V1IyCcYIAMMkG7DntR5EI20nRw5mGIG1Vhuwo0EjSmWcd2M7iB6k6G3fbMiL09xDDF8XTFnNLpn1Ox7DkhRwEB0H1rX_R1tZdyD6Et2G1CfUxJBSxFEdopt1PCpgarWj9mq1o1Y7CkAVO6Xp2Xn-MpTgfrf80lGA52dAJ6OnMWpvXPrD9cBZK2XhXp84LMF9cxhVMg69QesimqxscP9-x9Vf7WZy3pWNX_CIaR-W6IsSBSrViqmP6x2tZwQNY03PePMTFKrDdQ</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Abbasi, Samira</creator><creator>Abbasi, Ataollah</creator><creator>Sarbaz, Yashar</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><orcidid>https://orcid.org/0000-0001-6572-8711</orcidid></search><sort><creationdate>20140201</creationdate><title>Introducing treatment strategy for cerebellar ataxia in mutant med mice: Combination of acetazolamide and 4-Aminopyridine</title><author>Abbasi, Samira ; Abbasi, Ataollah ; Sarbaz, Yashar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-99091cc611c090be852ab639d79f51cbf104dac1dfcec6c1d0557f4b681968d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>4-Aminopyridine - administration & dosage</topic><topic>4-Aminopyridine - pharmacology</topic><topic>4-Aminopyridine - therapeutic use</topic><topic>Acetazolamide - administration & dosage</topic><topic>Acetazolamide - pharmacology</topic><topic>Acetazolamide - therapeutic use</topic><topic>Action Potentials - drug effects</topic><topic>Animals</topic><topic>Ataxia</topic><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Cerebellar Ataxia - drug therapy</topic><topic>Cerebellar Ataxia - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Drug Therapy, Combination</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Internal Medicine</topic><topic>Ion channels</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Modeling</topic><topic>Molecular and cellular biology</topic><topic>Muscle contraction</topic><topic>Neuroprotective agents</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Other</topic><topic>Purkinje Cells - drug effects</topic><topic>Therapeutics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Abbasi, Samira</creatorcontrib><creatorcontrib>Abbasi, Ataollah</creatorcontrib><creatorcontrib>Sarbaz, Yashar</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Computer methods and programs in biomedicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abbasi, Samira</au><au>Abbasi, Ataollah</au><au>Sarbaz, Yashar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Introducing treatment strategy for cerebellar ataxia in mutant med mice: Combination of acetazolamide and 4-Aminopyridine</atitle><jtitle>Computer methods and programs in biomedicine</jtitle><addtitle>Comput Methods Programs Biomed</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>113</volume><issue>2</issue><spage>697</spage><epage>704</epage><pages>697-704</pages><issn>0169-2607</issn><eissn>1872-7565</eissn><abstract>Abstract Purkinje neurons are the sole output neuron of the cerebellar cortex, and they generate high-frequency action potentials. Electrophysiological dysfunction of Purkinje neurons causes cerebellar ataxia. Mutant med mice have the lack of expression of the Scn8a gene. This gene encodes the NaV1.6 protein. In med Purkinje neurons, regular high-frequency firing is slowed, and med mice are ataxic. The aim of this study was to propose the neuroprotective drugs which could be useful for ataxia treatment in med mice, and to investigate the neuroprotective effects of these drugs by simulation. Simulation results showed that Kv4 channel inhibitors and BK channel activators restored the normal electrophysiological properties of the med Purkinje neurons. 4-Aminopyridine (4-AP) and acetazolamide (ACTZ) were proposed as neuroprotective drugs for Kv4 channel inhibitor and BK channel activator, respectively.</abstract><cop>Kidlington</cop><pub>Elsevier Ireland Ltd</pub><pmid>24326337</pmid><doi>10.1016/j.cmpb.2013.11.008</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-6572-8711</orcidid></addata></record> |
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| subjects | 4-Aminopyridine - administration & dosage 4-Aminopyridine - pharmacology 4-Aminopyridine - therapeutic use Acetazolamide - administration & dosage Acetazolamide - pharmacology Acetazolamide - therapeutic use Action Potentials - drug effects Animals Ataxia Biological and medical sciences Cell physiology Cerebellar Ataxia - drug therapy Cerebellar Ataxia - physiopathology Disease Models, Animal Drug Therapy, Combination Fundamental and applied biological sciences. Psychology Internal Medicine Ion channels Mice Mice, Mutant Strains Modeling Molecular and cellular biology Muscle contraction Neuroprotective agents Neuroprotective Agents - administration & dosage Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Other Purkinje Cells - drug effects Therapeutics |
| title | Introducing treatment strategy for cerebellar ataxia in mutant med mice: Combination of acetazolamide and 4-Aminopyridine |
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