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10.1111/j.1369-1600.2009.00186.x http://scihub22266oqcxt.onion/10.1111/j.1369-1600.2009.00186.x 20002022/?report=reader!3038569!20002022     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Addict+Biol 2010 ; 15 (1): 45-61 Nephropedia Template TP {{tp|p=20002022|t=2010. Mice lacking Gad2 show altered behavioral effects of ethanol, flurazepam and gabaxadol |pdf=|usr=}}{{20002022}} gab.com Text Mice lacking Gad2 show altered behavioral effects of ethanol, flurazepam and gabaxadol JO: Addict Biol http://www.kidney.de/pget.php?&tw=1&pmid=20002022 #FOAvip Gamma-aminobutyric acid (GABA) is synthesized in brain by two isoforms of glutamic acid decarboxylase (Gad), Gad1 and Gad2. Gad1 provides most of the GABA in brain, but Gad2 can be rapidly activated in times of high GABA demand. Mice lacking Gad2 are viable whereas deletion of Gad1 is lethal. We produced null mutant mice for Gad2 on three different genetic backgrounds: predominantly C57BL/6J and one or two generations of backcrossing to 129S1/SvimJ (129N1, 129N2). We used these mice to determine if actions of alcohol are regulated by synthesis of GABA from this isoform. We also studied behavioral responses to a benzodiazepine (flurazepam) and a GABAA receptor agonist (gabaxadol). Deletion of Gad2 increased ethanol palatability and intake and slightly reduced the severity of ethanol-induced withdrawal, but these effects depended strongly on genetic background. Mutant mice on the 129N2 background showed the above three ethanol behavioral phenotypes, but the C57BL/6J inbred background did not show any of these phenotypes. Effects on ethanol consumption also depended on the test as the mutation did not alter consumption in limited access models. Deletion of Gad2 reduced the effect of flurazepam on motor incoordination and increased the effect of extrasynaptic GABAA receptor agonist gabaxadol without changing the duration of loss of righting reflex produced by these drugs. These results are consistent with earlier proposals that deletion of Gad2 (on 129N2 background) reduces synaptic GABA but also suggest changes in extrasynaptic receptor function. Twit Text FOAVip Mice lacking Gad2 show altered behavioral effects of ethanol, flurazepam and gabaxadol ????Addict Biol http://www.kidney.de/pget.php?&tw=1&pmid=20002022 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20002022 #FOAvip English Wikipedia <ref>{{Cite pmid|20002022}}</ref> Mice lacking Gad2 show altered behavioral effects of ethanol, flurazepam and gabaxadol #MMPMID20002022 Blednov YA; Walker DL; Iyer SV; Homanics G; Harris AR Addict Biol 2010[Jan]; 15 (1): 45-61 PMID20002022show ga Gamma-aminobutyric acid (GABA) is synthesized in brain by two isoforms of glutamic acid decarboxylase (Gad), Gad1 and Gad2. Gad1 provides most of the GABA in brain, but Gad2 can be rapidly activated in times of high GABA demand. Mice lacking Gad2 are viable whereas deletion of Gad1 is lethal. We produced null mutant mice for Gad2 on three different genetic backgrounds: predominantly C57BL/6J and one or two generations of backcrossing to 129S1/SvimJ (129N1, 129N2). We used these mice to determine if actions of alcohol are regulated by synthesis of GABA from this isoform. We also studied behavioral responses to a benzodiazepine (flurazepam) and a GABAA receptor agonist (gabaxadol). Deletion of Gad2 increased ethanol palatability and intake and slightly reduced the severity of ethanol-induced withdrawal, but these effects depended strongly on genetic background. Mutant mice on the 129N2 background showed the above three ethanol behavioral phenotypes, but the C57BL/6J inbred background did not show any of these phenotypes. Effects on ethanol consumption also depended on the test as the mutation did not alter consumption in limited access models. Deletion of Gad2 reduced the effect of flurazepam on motor incoordination and increased the effect of extrasynaptic GABAA receptor agonist gabaxadol without changing the duration of loss of righting reflex produced by these drugs. These results are consistent with earlier proposals that deletion of Gad2 (on 129N2 background) reduces synaptic GABA but also suggest changes in extrasynaptic receptor function. |Alcohol Drinking/*genetics[MESH] |Alcohol Withdrawal Delirium/genetics[MESH] |Animals[MESH] |Benzodiazepines/*toxicity[MESH] |Brain/drug effects[MESH] |Crosses, Genetic[MESH] |Ethanol/blood/*toxicity[MESH] |Flurazepam/*toxicity[MESH] |GABA Agonists/*toxicity[MESH] |Genotype[MESH] |Glutamate Decarboxylase/*genetics[MESH] |Isoxazoles/*toxicity[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Inbred Strains[MESH] |Mice, Knockout[MESH] |Mice, Neurologic Mutants[MESH] |Motor Skills/*drug effects[MESH] |Phenotype[MESH] |Postural Balance/*drug effects/*genetics[MESH] |Species Specificity[MESH]Mice lacking Gad2 show altered behavioral effects of ethanol, flurazep(epmc).pdf DeepDyve Pubget Overpricing