Basic Mechanisms of Gabitril (Tiagabine) and Future Potential Developments
Gabitril (tiagabine) is a potent selective inhibitor of the principal neuronal γ‐aminobutyric acid (GABA) transporter (GAT‐1) in the cortex and hippocampus. By slowing the reuptake of synaptically‐released GABA, it prolongs inhibitory postsynaptic potentials. In animal models of epilepsy, tiagabine...
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| Veröffentlicht in: | Epilepsia (Copenhagen) 1999-01, Vol.40 (s9), p.S2-S6 |
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| creator | Meldrum, Brian S. Chapman, Astrid G. |
| description | Gabitril (tiagabine) is a potent selective inhibitor of the principal neuronal γ‐aminobutyric acid (GABA) transporter (GAT‐1) in the cortex and hippocampus. By slowing the reuptake of synaptically‐released GABA, it prolongs inhibitory postsynaptic potentials. In animal models of epilepsy, tiagabine is particularly effective against kindled (limbic) seizures and against reflexly‐induced generalized convulsive seizures. These data are predictive of its efficacy in complex partial seizures in humans. Possible clinical applications outside the field of epilepsy include bipolar disorder and pain. |
| doi_str_mv | 10.1111/j.1528-1157.1999.tb02087.x |
| format | Article |
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By slowing the reuptake of synaptically‐released GABA, it prolongs inhibitory postsynaptic potentials. In animal models of epilepsy, tiagabine is particularly effective against kindled (limbic) seizures and against reflexly‐induced generalized convulsive seizures. These data are predictive of its efficacy in complex partial seizures in humans. Possible clinical applications outside the field of epilepsy include bipolar disorder and pain.</description><identifier>ISSN: 0013-9580</identifier><identifier>EISSN: 1528-1167</identifier><identifier>DOI: 10.1111/j.1528-1157.1999.tb02087.x</identifier><identifier>PMID: 10612355</identifier><identifier>CODEN: EPILAK</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Anticonvulsants - pharmacology ; Anticonvulsants - therapeutic use ; Anticonvulsants. Antiepileptics. Antiparkinson agents ; Antiepileptic ; Biological and medical sciences ; Bipolar Disorder - drug therapy ; Carrier Proteins - drug effects ; Epilepsy ; Epilepsy - drug therapy ; Epilepsy - metabolism ; Epilepsy - physiopathology ; GABA ; GABA Antagonists - pharmacology ; GABA Antagonists - therapeutic use ; GABA Plasma Membrane Transport Proteins ; gamma-Aminobutyric Acid - metabolism ; Humans ; Kindling, Neurologic - drug effects ; Kindling, Neurologic - physiology ; Limbic System - drug effects ; Limbic System - physiology ; Medical sciences ; Membrane Proteins - drug effects ; Membrane Transport Proteins ; Mice ; Mode of action ; Neuropharmacology ; Nipecotic Acids - pharmacology ; Nipecotic Acids - therapeutic use ; Organic Anion Transporters ; Pain - drug therapy ; Pharmacology. 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By slowing the reuptake of synaptically‐released GABA, it prolongs inhibitory postsynaptic potentials. In animal models of epilepsy, tiagabine is particularly effective against kindled (limbic) seizures and against reflexly‐induced generalized convulsive seizures. These data are predictive of its efficacy in complex partial seizures in humans. Possible clinical applications outside the field of epilepsy include bipolar disorder and pain.</description><subject>Animals</subject><subject>Anticonvulsants - pharmacology</subject><subject>Anticonvulsants - therapeutic use</subject><subject>Anticonvulsants. Antiepileptics. Antiparkinson agents</subject><subject>Antiepileptic</subject><subject>Biological and medical sciences</subject><subject>Bipolar Disorder - drug therapy</subject><subject>Carrier Proteins - drug effects</subject><subject>Epilepsy</subject><subject>Epilepsy - drug therapy</subject><subject>Epilepsy - metabolism</subject><subject>Epilepsy - physiopathology</subject><subject>GABA</subject><subject>GABA Antagonists - pharmacology</subject><subject>GABA Antagonists - therapeutic use</subject><subject>GABA Plasma Membrane Transport Proteins</subject><subject>gamma-Aminobutyric Acid - metabolism</subject><subject>Humans</subject><subject>Kindling, Neurologic - drug effects</subject><subject>Kindling, Neurologic - physiology</subject><subject>Limbic System - drug effects</subject><subject>Limbic System - physiology</subject><subject>Medical sciences</subject><subject>Membrane Proteins - drug effects</subject><subject>Membrane Transport Proteins</subject><subject>Mice</subject><subject>Mode of action</subject><subject>Neuropharmacology</subject><subject>Nipecotic Acids - pharmacology</subject><subject>Nipecotic Acids - therapeutic use</subject><subject>Organic Anion Transporters</subject><subject>Pain - drug therapy</subject><subject>Pharmacology. 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Antiepileptics. Antiparkinson agents</topic><topic>Antiepileptic</topic><topic>Biological and medical sciences</topic><topic>Bipolar Disorder - drug therapy</topic><topic>Carrier Proteins - drug effects</topic><topic>Epilepsy</topic><topic>Epilepsy - drug therapy</topic><topic>Epilepsy - metabolism</topic><topic>Epilepsy - physiopathology</topic><topic>GABA</topic><topic>GABA Antagonists - pharmacology</topic><topic>GABA Antagonists - therapeutic use</topic><topic>GABA Plasma Membrane Transport Proteins</topic><topic>gamma-Aminobutyric Acid - metabolism</topic><topic>Humans</topic><topic>Kindling, Neurologic - drug effects</topic><topic>Kindling, Neurologic - physiology</topic><topic>Limbic System - drug effects</topic><topic>Limbic System - physiology</topic><topic>Medical sciences</topic><topic>Membrane Proteins - drug effects</topic><topic>Membrane Transport Proteins</topic><topic>Mice</topic><topic>Mode of action</topic><topic>Neuropharmacology</topic><topic>Nipecotic Acids - pharmacology</topic><topic>Nipecotic Acids - therapeutic use</topic><topic>Organic Anion Transporters</topic><topic>Pain - drug therapy</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Tiagabine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meldrum, Brian S.</creatorcontrib><creatorcontrib>Chapman, Astrid G.</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><jtitle>Epilepsia (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meldrum, Brian S.</au><au>Chapman, Astrid G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Basic Mechanisms of Gabitril (Tiagabine) and Future Potential Developments</atitle><jtitle>Epilepsia (Copenhagen)</jtitle><addtitle>Epilepsia</addtitle><date>1999-01-01</date><risdate>1999</risdate><volume>40</volume><issue>s9</issue><spage>S2</spage><epage>S6</epage><pages>S2-S6</pages><issn>0013-9580</issn><eissn>1528-1167</eissn><coden>EPILAK</coden><abstract>Gabitril (tiagabine) is a potent selective inhibitor of the principal neuronal γ‐aminobutyric acid (GABA) transporter (GAT‐1) in the cortex and hippocampus. By slowing the reuptake of synaptically‐released GABA, it prolongs inhibitory postsynaptic potentials. In animal models of epilepsy, tiagabine is particularly effective against kindled (limbic) seizures and against reflexly‐induced generalized convulsive seizures. These data are predictive of its efficacy in complex partial seizures in humans. Possible clinical applications outside the field of epilepsy include bipolar disorder and pain.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10612355</pmid><doi>10.1111/j.1528-1157.1999.tb02087.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Epilepsia (Copenhagen), 1999-01, Vol.40 (s9), p.S2-S6 |
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| language | eng |
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| source | MEDLINE; Wiley Online Library; Wiley Online Library Journals; Free E-Journal (出版社公開部分のみ）; Alma/SFX Local Collection |
| subjects | Animals Anticonvulsants - pharmacology Anticonvulsants - therapeutic use Anticonvulsants. Antiepileptics. Antiparkinson agents Antiepileptic Biological and medical sciences Bipolar Disorder - drug therapy Carrier Proteins - drug effects Epilepsy Epilepsy - drug therapy Epilepsy - metabolism Epilepsy - physiopathology GABA GABA Antagonists - pharmacology GABA Antagonists - therapeutic use GABA Plasma Membrane Transport Proteins gamma-Aminobutyric Acid - metabolism Humans Kindling, Neurologic - drug effects Kindling, Neurologic - physiology Limbic System - drug effects Limbic System - physiology Medical sciences Membrane Proteins - drug effects Membrane Transport Proteins Mice Mode of action Neuropharmacology Nipecotic Acids - pharmacology Nipecotic Acids - therapeutic use Organic Anion Transporters Pain - drug therapy Pharmacology. Drug treatments Rats Tiagabine |
| title | Basic Mechanisms of Gabitril (Tiagabine) and Future Potential Developments |
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