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Tim Lancaster - One of the best experts on this subject based on the ideXlab platform.

  • Anxiolytics and antidepressants for smoking cessation.
    Cochrane Database of Systematic Reviews, 2003
    Co-Authors: Hughes, Lindsay F. Stead, Tim Lancaster
    Abstract:

    BACKGROUND: There are two reasons to believe antidepressants and Anxiolytics might help in smoking. First, anxiety and depression are symptoms of nicotine withdrawal, and smoking cessation sometimes precipitates depression. Second, smoking appears to be due, in part, to deficits in dopamine, serotonin and norepinephrine, all of which are increased by Anxiolytics and antidepressants. OBJECTIVES: The aim of this review is to assess the effectiveness of such drugs in aiding long term smoking cessation. The drugs include bupropion; buspirone; diazepam; doxepin; fluoxetine; imipramine; meprobamate; moclobemide; nortriptyline; tryptophan; ondansetron; venlafaxine and the beta-blockers metoprolol, oxprenolol and propanolol. SEARCH STRATEGY: We searched the Cochrane Tobacco Addiction Group trials register which includes trials indexed in Medline, Embase, SciSearch and PsycLit, and meetings abstracts. SELECTION CRITERIA: We considered randomized trials comparing anxiolytic or antidepressant drugs to placebo or an alternative therapeutic control for smoking cessation. We excluded trials with less than 6 months follow-up. DATA COLLECTION AND ANALYSIS: We extracted data in duplicate on the type of study population, the nature of the drug therapy, the outcome measures, method of randomisation, and completeness of follow-up. The main outcome measure was abstinence from smoking after at least six months follow-up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effects model. MAIN RESULTS: There was one trial each of the Anxiolytics diazepam, meprobamate, metoprolol and oxprenolol. There were two trials of the anxiolytic buspirone. None of these showed evidence of effectiveness in helping smokers to quit. There was one trial each of the antidepressants fluoxetine and moclobemide, two of nortriptyline, and four trials of bupropion. Nortriptyline and bupropion increased cessation and other antidepressants might also be effective. One trial found combined bupropion and nicotine patch produced higher quit rates than patch alone. REVIEWER'S CONCLUSIONS: There is little evidence that Anxiolytics aid smoking cessation. Some antidepressants (bupropion and nortriptyline) can aid smoking cessation. It is not clear whether these effects are specific for individual drugs, or a class effect.

  • The Cochrane Library - Anxiolytics for smoking cessation.
    Cochrane Database of Systematic Reviews, 2000
    Co-Authors: John R. Hughes, Lindsay F. Stead, Tim Lancaster
    Abstract:

    The aim of this review is to assess the effectiveness of anxiolytic pharmacotherapy in aiding long term smoking cessation. The drugs include buspirone; diazepam; doxepin; meprobamate; ondansetron; and the beta-blockers metoprolol, oxprenolol and propanolol. Conclusion: There is no consistent evidence that Anxiolytics aid smoking cessation, but the available evidence does not rule out a possible effect.

Andrzej Pilc - One of the best experts on this subject based on the ideXlab platform.

  • Glutamate receptor ligands as Anxiolytics.
    Current opinion in investigational drugs, 2001
    Co-Authors: Ewa Chojnacka-wójcik, Aleksandra Kłodzińska, Andrzej Pilc
    Abstract:

    : The glutamatergic system has received considerable attention over recent years as a potential target for anxiolytic drugs. In spite of the pronounced anxiolytic-like effects of competitive and non-competitive antagonists of NMDA receptors in animal models of anxiety, these substances can not be regarded as potential anxiolytic drugs, mainly due to their side-effect profiles (eg, ataxia, myorelaxation, impairment of learning and memory processes and psychotomimetic effects). Antagonists and partial agonists of the glycine, receptor inhibit function of the NMDA receptor complex and evoke in animals an anxiolytic-like response. Although data concerning anti-anxiety-like effects of glycine, receptor antagonists are not very promising, studies are underway to develop new, brain-penetrating agents devoid of side effects. Further developments are necessary to more fully elucidate the possible involvement of AMPA/kainate receptors in anxiety. The recent discovery of metabotropic glutamate receptors, which modulate the function of the glutamatergic system, offers new hope for discovery of a new generation of Anxiolytics. MPEP, a highly selective, brain penetrable, noncompetitive mGlu5 receptor antagonist, evokes anxiolytic-like effects in several animal models of anxiety, remaining remarkably free of side effects. LY-354740, a selective brain-penetrable group II mGlu receptor agonist, evokes marked anxiolytic-like effects in animal models of anxiety. LY-354740 causes mild sedation in mice, does not disturb motor coordination and has no potential to cause dependence. Therefore mGlu receptor ligands may become the Anxiolytics of the future, free from the side effects characteristic of benzodiazepines.

  • Glutamate receptor ligands as Anxiolytics.
    Current opinion in investigational drugs, 2001
    Co-Authors: Ewa Chojnacka-wójcik, Aleksandra Kłodzińska, Andrzej Pilc
    Abstract:

    : The glutamatergic system has received considerable attention over recent years as a potential target for anxiolytic drugs. In spite of the pronounced anxiolytic-like effects of competitive and non-competitive antagonists of NMDA receptors in animal models of anxiety, these substances can not be regarded as potential anxiolytic drugs, mainly due to their side-effect profiles (eg, ataxia, myorelaxation, impairment of learning and memory processes and psychotomimetic effects). Antagonists and partial agonists of the glycine, receptor inhibit function of the NMDA receptor complex and evoke in animals an anxiolytic-like response. Although data concerning anti-anxiety-like effects of glycine, receptor antagonists are not very promising, studies are underway to develop new, brain-penetrating agents devoid of side effects. Further developments are necessary to more fully elucidate the possible involvement of AMPA/kainate receptors in anxiety. The recent discovery of metabotropic glutamate receptors, which modulate the function of the glutamatergic system, offers new hope for discovery of a new generation of Anxiolytics. MPEP, a highly selective, brain penetrable, noncompetitive mGlu5 receptor antagonist, evokes anxiolytic-like effects in several animal models of anxiety, remaining remarkably free of side effects. LY-354740, a selective brain-penetrable group II mGlu receptor agonist, evokes marked anxiolytic-like effects in animal models of anxiety. LY-354740 causes mild sedation in mice, does not disturb motor coordination and has no potential to cause dependence. Therefore mGlu receptor ligands may become the Anxiolytics of the future, free from the side effects characteristic of benzodiazepines.

R. J. E. Joordens - One of the best experts on this subject based on the ideXlab platform.

  • Fear-potentiated startle response is remarkably similar in two laboratories
    Psychopharmacology, 1996
    Co-Authors: R. J. E. Joordens, Theo H Hijzen, B. Olivier, B. W. M. M. Peeters
    Abstract:

    The fear-potentiated startle response paradigm is used to investigate anxiolytic properties of drugs. The first objective of the present study was to further investigate the predictive validity of this paradigm. The Anxiolytics chlordiazepoxide (2.5–10 mg/kg IP) and oxazepam (1–10 mg/kg PO) and the putative anxiolytic flesinoxan (1–10 mg/kg PO) decreased startle potentiation dose-dependently, indicating an anxiolytic effect. The antidepressant fluvoxamine (5–20 mg/kg PO) did not affect startle potentiation. Ideally, anxiolytic drugs attenuate startle potentiation without affecting control startle levels, although some studies report altered control startle amplitudes. The second objective was to investigate whether different effects on control startle amplitudes are related to different startle devices. Therefore, the drugs were tested in two laboratories. Results showed no significant differences between laboratories, indicating that equipment is not a critical factor in the drug-induced alteration of control startle levels. In an additional experiment, it was shown that flesinoxan (10 mg/kg PO) did not affect strychnine-induced startle potentiation, supporting the idea that the attenuating effect of flesinoxan on the fear-potentiated startle response is due to its anxiolytic properties. Thus, the fear-potentiated startle response paradigm appears a valid and reliable model for anxiolytic properties of drugs.

  • Predictive validity of the potentiated startle response as a behavioral model for anxiolytic drugs
    Psychopharmacology, 1995
    Co-Authors: Theo H Hijzen, R. J. E. Joordens, B. Olivier, S. W. J. Houtzager, J. L. Slangen
    Abstract:

    The fear-potentiated startle (PSR) paradigm is a putative behavioral model for the determination of anxiolytic properties of drugs. The present study further investigated the predictive validity of the model. Predictive validity is high, when only drugs clinically used as Anxiolytics attenuate PSR dose dependently. Results showed that startle potentiation decreased dose dependently after the administration of the Anxiolytics CDP (2.5–10 mg/kg, IP) and alprazolam (1–3 mg/kg, IP). After administration of the clinically non-anxiolytic drugs amitriptyline (2.5–10 mg/kg, IP), carbamazepine (5–20 mg/kg, IP), fentanyl (0.0025–0.04 mg/kg, SC), naloxone (2.5–10 mg/kg, IP), nicotine (0.4–1.6 mg/kg, IP), alcohol (500–2000 mg/kg, IP), and d -amphetamine (0.6–2.4 mg/kg, IP), a dose-dependent decrease in startle potentiation was not found. The PSR correctly discriminated most of the drugs tested in clinically anxiolytic and clinically non-anxiolytic drugs. However, haloperidol behaved as a false positive, and results of nicotine and alcohol were at variance with results reported by others.

Tamaki Hayase - One of the best experts on this subject based on the ideXlab platform.

  • Chronologically overlapping occurrences of nicotine-induced anxiety- and depression-related behavioral symptoms: effects of anxiolytic and cannabinoid drugs
    BMC Neuroscience, 2007
    Co-Authors: Tamaki Hayase
    Abstract:

    Background Anxiety and depression are among the most frequently-observed psychiatric symptoms associated with nicotine (NC). In addition to the similarity to other addictive drugs, these NC-induced symptoms are characteristic in that the opposite behavioral effects, i.e. anxiolytic and antidepressant effects, which may reinforce the habitual use of NC, have also been reported. In the present study, the time course of anxiety- and depression-related behavioral alterations was examined in mice. Furthermore, based on the reported similarity in the mechanisms responsible for NC-induced anxiety- and depression-related symptoms, as well as the contribution of brain cannabinoid (CB) receptors to these behavioral symptoms, the effects of Anxiolytics and CB receptor ligands (CBs) against these behavioral symptoms were investigated. Results Repeated subcutaneous NC treatments (0.3 mg/kg, 4 days), compared with a single treatment (0.5 mg/kg), caused both prolonged anxiogenic effects in the elevated plus-maze test, and prolonged depressive effects in the forced swimming test, even at 120 min time point after the last NC treatment. A transient anxiolytic preference for open arms was also observed in the elevated plus-maze test. Among the Anxiolytics and CBs, the serotonin 1A (5-HT1A) antagonist WAY 100135 and the endogenous mixed CB agonist/antagonist virodhamine (VD), when administered intraperitoneally before each NC treatment, provided the strongest antagonistic effects against the anxiety-related symptoms. However, against the depression-related symptoms, only VD provided significant antagonistic effects in both single and repeated treatment groups. Conclusion The present results support the presence of a chronological overlap of NC-induced anxiety- and depression-related behavioral symptoms, and the contribution of brain CB receptors to these behavioral symptoms. The repeated NC-induced prolongation of these behavioral symptoms and the early transient anxiolytic behavioral alterations support an increased possibility of the habitual use of NC. Furthermore, based on the antagonistic effects of VD, one can predict that the characteristic effects on brain CB receptors as a mixed CB agonist/antagonist contributed to its therapeutic effects as both an anxiolytic and an antidepressant.

  • Chronologically overlapping occurrences of nicotine-induced anxiety- and depression-related behavioral symptoms: effects of anxiolytic and cannabinoid drugs
    BMC neuroscience, 2007
    Co-Authors: Tamaki Hayase
    Abstract:

    Anxiety and depression are among the most frequently-observed psychiatric symptoms associated with nicotine (NC). In addition to the similarity to other addictive drugs, these NC-induced symptoms are characteristic in that the opposite behavioral effects, i.e. anxiolytic and antidepressant effects, which may reinforce the habitual use of NC, have also been reported. In the present study, the time course of anxiety- and depression-related behavioral alterations was examined in mice. Furthermore, based on the reported similarity in the mechanisms responsible for NC-induced anxiety- and depression-related symptoms, as well as the contribution of brain cannabinoid (CB) receptors to these behavioral symptoms, the effects of Anxiolytics and CB receptor ligands (CBs) against these behavioral symptoms were investigated. Repeated subcutaneous NC treatments (0.3 mg/kg, 4 days), compared with a single treatment (0.5 mg/kg), caused both prolonged anxiogenic effects in the elevated plus-maze test, and prolonged depressive effects in the forced swimming test, even at 120 min time point after the last NC treatment. A transient anxiolytic preference for open arms was also observed in the elevated plus-maze test. Among the Anxiolytics and CBs, the serotonin 1A (5-HT1A) antagonist WAY 100135 and the endogenous mixed CB agonist/antagonist virodhamine (VD), when administered intraperitoneally before each NC treatment, provided the strongest antagonistic effects against the anxiety-related symptoms. However, against the depression-related symptoms, only VD provided significant antagonistic effects in both single and repeated treatment groups. The present results support the presence of a chronological overlap of NC-induced anxiety- and depression-related behavioral symptoms, and the contribution of brain CB receptors to these behavioral symptoms. The repeated NC-induced prolongation of these behavioral symptoms and the early transient anxiolytic behavioral alterations support an increased possibility of the habitual use of NC. Furthermore, based on the antagonistic effects of VD, one can predict that the characteristic effects on brain CB receptors as a mixed CB agonist/antagonist contributed to its therapeutic effects as both an anxiolytic and an antidepressant.

Theo H Hijzen - One of the best experts on this subject based on the ideXlab platform.

  • Fear-potentiated startle response is remarkably similar in two laboratories
    Psychopharmacology, 1996
    Co-Authors: R. J. E. Joordens, Theo H Hijzen, B. Olivier, B. W. M. M. Peeters
    Abstract:

    The fear-potentiated startle response paradigm is used to investigate anxiolytic properties of drugs. The first objective of the present study was to further investigate the predictive validity of this paradigm. The Anxiolytics chlordiazepoxide (2.5–10 mg/kg IP) and oxazepam (1–10 mg/kg PO) and the putative anxiolytic flesinoxan (1–10 mg/kg PO) decreased startle potentiation dose-dependently, indicating an anxiolytic effect. The antidepressant fluvoxamine (5–20 mg/kg PO) did not affect startle potentiation. Ideally, anxiolytic drugs attenuate startle potentiation without affecting control startle levels, although some studies report altered control startle amplitudes. The second objective was to investigate whether different effects on control startle amplitudes are related to different startle devices. Therefore, the drugs were tested in two laboratories. Results showed no significant differences between laboratories, indicating that equipment is not a critical factor in the drug-induced alteration of control startle levels. In an additional experiment, it was shown that flesinoxan (10 mg/kg PO) did not affect strychnine-induced startle potentiation, supporting the idea that the attenuating effect of flesinoxan on the fear-potentiated startle response is due to its anxiolytic properties. Thus, the fear-potentiated startle response paradigm appears a valid and reliable model for anxiolytic properties of drugs.

  • Predictive validity of the potentiated startle response as a behavioral model for anxiolytic drugs
    Psychopharmacology, 1995
    Co-Authors: Theo H Hijzen, R. J. E. Joordens, B. Olivier, S. W. J. Houtzager, J. L. Slangen
    Abstract:

    The fear-potentiated startle (PSR) paradigm is a putative behavioral model for the determination of anxiolytic properties of drugs. The present study further investigated the predictive validity of the model. Predictive validity is high, when only drugs clinically used as Anxiolytics attenuate PSR dose dependently. Results showed that startle potentiation decreased dose dependently after the administration of the Anxiolytics CDP (2.5–10 mg/kg, IP) and alprazolam (1–3 mg/kg, IP). After administration of the clinically non-anxiolytic drugs amitriptyline (2.5–10 mg/kg, IP), carbamazepine (5–20 mg/kg, IP), fentanyl (0.0025–0.04 mg/kg, SC), naloxone (2.5–10 mg/kg, IP), nicotine (0.4–1.6 mg/kg, IP), alcohol (500–2000 mg/kg, IP), and d -amphetamine (0.6–2.4 mg/kg, IP), a dose-dependent decrease in startle potentiation was not found. The PSR correctly discriminated most of the drugs tested in clinically anxiolytic and clinically non-anxiolytic drugs. However, haloperidol behaved as a false positive, and results of nicotine and alcohol were at variance with results reported by others.