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Lu-ning Wang - One of the best experts on this subject based on the ideXlab platform.

  • gamma aminobutyric acid GABA Receptor Agonists for acute stroke
    Cochrane Database of Systematic Reviews, 2016
    Co-Authors: Jia Liu, Lu-ning Wang
    Abstract:

    Background Gamma aminobutyric acid (GABA) Receptor Agonists have been shown to have a neuroprotectant effect in reducing infarct size and improving functional outcome in animal models of cerebrovascular disease. However, the sedative effects of GABA Receptor Agonists have limited their wider application in people with acute stroke, due to the potential risk of stupor. This is an update of a Cochrane review first published in 2013, and previously updated in 2014. Objectives To determine the efficacy and safety of GABA Receptor Agonists in the treatment of acute stroke. Search methods We searched the Cochrane Stroke Group Trials Register (accessed March 2016), the Cochrane Central Register of Controlled Trials (CENTRAL) 2016, Issue 3, part of the Cochrane Library (accessed March 2016), MEDLINE (from 1949 to March 2016), Embase (from 1980 to March 2016), CINAHL (from 1982 to March 2016), AMED (from 1985 to March 2016), and 11 Chinese databases (accessed March 2016). In an effort to identify further published, unpublished, and ongoing trials we searched ongoing trials registers, reference lists, and relevant conference proceedings, and contacted authors and pharmaceutical companies. Selection criteria We included randomized controlled trials (RCTs) investigating GABA Receptor Agonists versus placebo for people with acute stroke (within 12 hours after stroke onset), with the primary outcomes of efficacy and safety. Data collection and analysis Two review authors independently screened the titles and abstracts of identified records, selected studies for inclusion, extracted eligible data, cross-checked the data for accuracy, and assessed the risk of bias. Main results We included five trials with 3838 participants (3758 analyzed). The methodological quality of the included trials was generally good, with an unclear risk for selection bias only. Four trials (N = 2909) measured death and dependency at three months for chlormethiazole versus placebo; pooled results did not find a significant difference (risk ratio (RR) 1.03, 95% confidence interval (CI) 0.96 to 1.11). One trial (N = 849) measured this outcome for diazepam versus placebo (RR 0.94, 95% CI 0.82 to 1.07). The most frequent adverse events related to chlormethiazole were somnolence (RR 4.56, 95% CI 3.50 to 5.95; two trials; N = 2527) and rhinitis (RR 4.75, 95% CI 2.67 to 8.46; two trials; N = 2527). Authors' conclusions This review provides moderate-quality evidence that fails to support the use of GABA Receptor Agonists (chlormethiazole or diazepam) for the treatment of people with acute stroke. More well-designed RCTs with large samples of participants with total anterior circulation syndrome are required to determine if there are benefits for this subgroup. Somnolence and rhinitis are frequent adverse events related to chlormethiazole.

  • The Cochrane Library - Gamma aminobutyric acid (GABA) Receptor Agonists for acute stroke
    The Cochrane database of systematic reviews, 2014
    Co-Authors: Jia Liu, Lu-ning Wang
    Abstract:

    Background Gamma aminobutyric acid (GABA) Receptor Agonists have been shown to have a neuroprotectant effect in reducing infarct size and improving functional outcome in animal models of cerebrovascular disease. However, the sedative effects of GABA Receptor Agonists have limited their wider application in people with acute stroke, due to the potential risk of stupor. This is an update of a Cochrane review first published in 2013, and previously updated in 2014. Objectives To determine the efficacy and safety of GABA Receptor Agonists in the treatment of acute stroke. Search methods We searched the Cochrane Stroke Group Trials Register (accessed March 2016), the Cochrane Central Register of Controlled Trials (CENTRAL) 2016, Issue 3, part of the Cochrane Library (accessed March 2016), MEDLINE (from 1949 to March 2016), Embase (from 1980 to March 2016), CINAHL (from 1982 to March 2016), AMED (from 1985 to March 2016), and 11 Chinese databases (accessed March 2016). In an effort to identify further published, unpublished, and ongoing trials we searched ongoing trials registers, reference lists, and relevant conference proceedings, and contacted authors and pharmaceutical companies. Selection criteria We included randomized controlled trials (RCTs) investigating GABA Receptor Agonists versus placebo for people with acute stroke (within 12 hours after stroke onset), with the primary outcomes of efficacy and safety. Data collection and analysis Two review authors independently screened the titles and abstracts of identified records, selected studies for inclusion, extracted eligible data, cross-checked the data for accuracy, and assessed the risk of bias. Main results We included five trials with 3838 participants (3758 analyzed). The methodological quality of the included trials was generally good, with an unclear risk for selection bias only. Four trials (N = 2909) measured death and dependency at three months for chlormethiazole versus placebo; pooled results did not find a significant difference (risk ratio (RR) 1.03, 95% confidence interval (CI) 0.96 to 1.11). One trial (N = 849) measured this outcome for diazepam versus placebo (RR 0.94, 95% CI 0.82 to 1.07). The most frequent adverse events related to chlormethiazole were somnolence (RR 4.56, 95% CI 3.50 to 5.95; two trials; N = 2527) and rhinitis (RR 4.75, 95% CI 2.67 to 8.46; two trials; N = 2527). Authors' conclusions This review provides moderate-quality evidence that fails to support the use of GABA Receptor Agonists (chlormethiazole or diazepam) for the treatment of people with acute stroke. More well-designed RCTs with large samples of participants with total anterior circulation syndrome are required to determine if there are benefits for this subgroup. Somnolence and rhinitis are frequent adverse events related to chlormethiazole.

  • The Cochrane Library - Gamma Aminobutyric Acid Receptor Agonists for Acute Stroke
    Stroke, 2013
    Co-Authors: Jia Liu, Lu-ning Wang
    Abstract:

    Gamma aminobutyric acid (GABA) Receptor Agonists have shown to be effective in reducing infarct size and improving functional outcome in animal models of cerebral ischemia. However, the sedation effects of GABA Receptor Agonists limited the application in acute stroke patients because of the potential risk of stupor. ### Objective The aim of this study is to determine the efficacy and safety of GABA Receptor Agonists in the treatment of acute stroke. ### Types of Studies Randomized controlled trials. ### Types of Participants Acute stroke patients within 12 hours after stroke onset. ### Types of Interventions GABA Receptor Agonists in …

  • Gamma Aminobutyric Acid Receptor Agonists for Acute Stroke
    Stroke, 2013
    Co-Authors: Jia Liu, Lu-ning Wang
    Abstract:

    Gamma aminobutyric acid (GABA) Receptor Agonists have shown to be effective in reducing infarct size and improving functional outcome in animal models of cerebral ischemia. However, the sedation effects of GABA Receptor Agonists limited the application in acute stroke patients because of the potential risk of stupor. ### Objective The aim of this study is to determine the efficacy and safety of GABA Receptor Agonists in the treatment of acute stroke. ### Types of Studies Randomized controlled trials. ### Types of Participants Acute stroke patients within 12 hours after stroke onset. ### Types of Interventions GABA Receptor Agonists in …

Shuchun Wang - One of the best experts on this subject based on the ideXlab platform.

  • GABA Receptor Agonists eliminate the effect of NO synthase inhibitor on the sleep/waking cycle of the rat
    Henan Medical Research, 2003
    Co-Authors: Xiangli Chu, Yuruo Wang, Qian Zhang, Shuchun Wang
    Abstract:

    Objective: To testify the effect of N G nitro L arginine methyl ester (L NAME) (an inhibitor of nitric oxide synthase) and GABA on the regulation of the sleep/waking cycle in adult rats implanted for chronic sleep recordings.Methods: L NAME, muscilmol(an agonist of the Receptor of GABA A) and baclofen (an agonist of the Receptor of GABA B) were injected subcutaneously, and their effects on sleep/waking cycle were observed. The effects of pretreatment with muscimol or baclofen on the changes of sleep and waking induced by L NAME were also observed. Results: Subcutaneous administration of L NAME reduced slow wave sleep (SWS), rapide eye movement sleep (REMS) and the number of REMS periods.Subcutaneous adminstration of muscimol or baclofen did not induce significant changes of SWS, but both of them reduced REMS and the nulmber of REMS periods. Pretreatment with muscimol or baclofen eliminated the reduction of REMS induced by subcutaneous administration of L NAME.Conclusion: It seems that the Agonists of GABA Receptors can antagonize the suppression of sleep induced by L NAME.

  • GABA Receptor Agonists eliminate the effect of no synthase inhibitor on the sleep waking cycle of the rat
    Henan Medical Research, 2003
    Co-Authors: Xiangli Chu, Yuruo Wang, Qian Zhang, Shuchun Wang
    Abstract:

    Objective: To testify the effect of N G nitro L arginine methyl ester (L NAME) (an inhibitor of nitric oxide synthase) and GABA on the regulation of the sleep/waking cycle in adult rats implanted for chronic sleep recordings.Methods: L NAME, muscilmol(an agonist of the Receptor of GABA A) and baclofen (an agonist of the Receptor of GABA B) were injected subcutaneously, and their effects on sleep/waking cycle were observed. The effects of pretreatment with muscimol or baclofen on the changes of sleep and waking induced by L NAME were also observed. Results: Subcutaneous administration of L NAME reduced slow wave sleep (SWS), rapide eye movement sleep (REMS) and the number of REMS periods.Subcutaneous adminstration of muscimol or baclofen did not induce significant changes of SWS, but both of them reduced REMS and the nulmber of REMS periods. Pretreatment with muscimol or baclofen eliminated the reduction of REMS induced by subcutaneous administration of L NAME.Conclusion: It seems that the Agonists of GABA Receptors can antagonize the suppression of sleep induced by L NAME.

Giuseppe Bartholini - One of the best experts on this subject based on the ideXlab platform.

  • GABA Receptor Agonists: pharmacological spectrum and therapeutic actions.
    Medicinal Research Reviews, 2006
    Co-Authors: Giuseppe Bartholini
    Abstract:

    Abstract From the data discussed in this review it appears that GABA Receptor Agonists exhibit a variety of actions in the central nervous system, some of which are therapeutically useful (Table V). GABA Receptor Agonists, by changing the firing rate of the corresponding neurons accelerate noradrenaline turnover without changes in postsynaptic Receptor density and diminish serotonin liberation with an up-regulation of 5HT2 Receptors. These effects differ from those of tricyclic antidepressants which primarily block monoamine re-uptake and cause down-regulation of beta-adrenergic and 5HT2 Receptors. The GABA Receptor agonist progabide has been shown to exert an antidepressant action which is indistinguishable from that of imipramine in patients with major affective disorders. The fact that: (a) GABA Receptor Agonists and tricyclic antidepressants affect noradrenergic and serotonergic transmission differently; and (b) tricyclic antidepressants alter GABA-related parameters challenges the classical monoamine hypothesis of depression and suggests that GABA-mediated mechanisms play a role in mood disorders. Decreases in cellular excitability produced by GABAergic stimulation leads to control of seizures in practically all animal models of epilepsy. GABA Receptor Agonists have a wide spectrum as they antagonize not only seizures which are dependent on decreased GABA synaptic activity but also convulsant states which are apparently independent of alterations in GABA-mediated events. These results in animals are confirmed in a wide range of human epileptic syndromes. GABA Receptor Agonists decrease dopamine turnover in the basal ganglia and antagonize neuroleptic-induced increase in dopamine release. On repeated treatment, progabide prevents or reverses the neuroleptic-induced up-regulation of dopamine Receptors in the rat striatum and antagonizes the concomitant supersensitivity to dopaminomimetics. Behaviorally, GABA Receptor Agonists diminish the stereotypies induced by apomorphine or L-DOPA suggesting that GABAergic stimulation results also in an antidopaminergic action which is exerted beyond the dopamine synapse. These effects of GABA Receptor Agonists may represent the basis of the antidyskinetic action of these compounds which, however, remains to be fully confirmed. GABA Receptor Agonists reduce striatal acetylcholine turnover, an effect which occurs at doses much lower than those which affect dopamine neurons. Since hyperactivity of cholinergic neurons plays a determinant role in the pathogenesis of some parkinsonian symptoms, it is conceivable that GABAergic stimulation is effective in ameliorating Parkinson's disease.(ABSTRACT TRUNCATED AT 400 WORDS)

A Urban Höglund - One of the best experts on this subject based on the ideXlab platform.

  • Involvement of spinal GABA Receptors in the regulation of intraspinal acetylcholine release.
    European journal of pharmacology, 2005
    Co-Authors: Mahinda Kommalage, A Urban Höglund
    Abstract:

    It has been shown that analgesics such as morphine, lidocaine and clonidine increase the release of spinal acetylcholine. Acetylcholine may therefore play an important role in the regulation of spinal pain threshold. Since behavioral as well as in vitro studies have shown a clear involvement of GABA (gamma-amino butyric acid) Receptors in the regulation of spinal nociceptive mechanisms, the present study focused on the role of GABA Receptors for spinal acetylcholine release control. GABA Receptor Agonists and antAgonists were infused via a spinal microdialysis probe and acetylcholine release was measured. The GABA(A) Receptor agonist muscimol decreased acetylcholine release and the antagonist bicuculline increased acetylcholine release. The GABA(B) Receptor agonist baclofen decreased acetylcholine release whereas the antagonist saclofen did not change acetylcholine release. The results suggest that both GABA Receptor subtypes have an inhibitory role on spinal dorsal horn acetylcholine release and that the GABA(A) Receptors are tonically regulating acetylcholine release.

Yoshihiro Kosaka - One of the best experts on this subject based on the ideXlab platform.