Tiapride-induced catalepsy is potentiated by gamma-hydroxybutyric acid administration

Navarro, José Francisco; Pedraza, Carmen; Martin, M. Garcia; Manzaneque, Juan M.; Dávila, Guadalupe; Maldonado, E.

doi:10.1016/s0278-5846(98)00043-8

Cited by 15 publications

(13 citation statements)

References 21 publications

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“…in SpraqueDawley rats (Sevak et al 2004), 200 mg/kg GHB i.p. in OF.1 mice (Navarro et al 1998), 300 mg/kg GHB i.p. in Swiss-Webster mice (Itzhak and Ali 2002), and 320 mg/kg GHB i.p.…”

Section: Discussionmentioning

confidence: 99%

Cataleptic effects of γ-hydroxybutyrate (GHB) and baclofen in mice: mediation by GABAB receptors, but differential enhancement by N-methyl-d-aspartate (NMDA) receptor antagonists

Koek

2008

Psychopharmacology

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Rationale-Gamma-hydroxybutyrate (GHB) is a gamma-aminobutyric acid (GABA) analog that is used to treat narcolepsy but that is also abused. GHB has many actions in common with the GABA B receptor agonist baclofen, but their underlying GABA B receptor mechanisms may be different.Objective-The aim of this study is to further investigate a possible differential role of glutamate in GABA B receptor-mediated effects of GHB and baclofen. Materials and methods-The experiments examined the effects of non-competitive antagonists at the N-methyl-d-asparate (NMDA) subtype of glutamate receptors on GHB-induced catalepsy and compared these effects with those on baclofen-induced catalepsy.Results-In C57BL/6J mice, ketamine, phencyclidine (PCP), and dizocilpine (MK-801) all enhanced GHB-induced catalepsy. They did so with a potency order (i.e., MK-801 > PCP > ketamine) consistent with their relative potencies as NMDA antagonists but not as inhibitors of dopamine or organic cation transporters. Ketamine, PCP, and MK-801 enhanced catalepsy along inverted U-shaped dose-response curves likely because higher doses affected motor coordination, which limited their catalepsy-enhancing effects. Doses that were maximally effective to enhance GHB-induced catalepsy did not affect the cataleptic effects of baclofen.Conclusions-The finding that NMDA receptor antagonists enhance the cataleptic effects of GHB but not those of baclofen is further evidence that the GABA B receptor mechanisms mediating the effects of GHB and GABA B agonists are not identical. Differential interactions of glutamate with the GABA B receptor mechanisms mediating the effects of GHB and baclofen may explain why GHB is effective for treating narcolepsy and is abused, whereas baclofen is not.

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“…in SpraqueDawley rats (Sevak et al 2004), 200 mg/kg GHB i.p. in OF.1 mice (Navarro et al 1998), 300 mg/kg GHB i.p. in Swiss-Webster mice (Itzhak and Ali 2002), and 320 mg/kg GHB i.p.…”

Section: Discussionmentioning

confidence: 99%

Cataleptic effects of γ-hydroxybutyrate (GHB) and baclofen in mice: mediation by GABAB receptors, but differential enhancement by N-methyl-d-aspartate (NMDA) receptor antagonists

Koek

2008

Psychopharmacology

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“…in Spraque-Dawley rats (Sevak et al 2004), 200 mg/kg of GHB i.p. in OF.1 mice (Navarro et al 1998), 300 mg/kg of GHB i.p. in Swiss-Webster mice (Itzhak and Ali 2002), and 320 mg/kg of GHB i.p.…”

Section: Discussionmentioning

confidence: 99%

Cataleptic effects of γ-hydroxybutyrate (GHB), its precursor γ-butyrolactone (GBL), and GABAB receptor agonists in mice: differential antagonism by the GABAB receptor antagonist CGP35348

2007

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The finding that CGP35348 was about threefold less potent to antagonize GHB and GBL than baclofen and SKF97541 is further evidence that the mechanisms mediating the effects of GHB and GABA(B) agonists are not identical. Differential involvement of GABA(B) receptor subtypes, or differential interactions with GABA(B) receptors, may possibly explain why GHB is effective for treating narcolepsy and is abused whereas baclofen is not.

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“…Possible interactions may occur between sodium oxybate and drugs that induce or inhibit the GHB dehydrogenase enzyme; these could include antiepileptics such as sodium valproate, phenytoin and ethosuximide (Gerot Lannach, 2007). Whereas Navarro et al (1998) suggested a synergistic interaction between GHB and the neuroleptic haloperidol, Sevak et al (2004) did not. SSRIs, such as the antidepressants citalopram and fluoxetine were here prescribed to a number of decedents; however the literature does not suggest any SSRI/GHB interactions.…”

Section: Drug Interactionsmentioning

confidence: 94%

Gamma hydroxybutyrate (GHB), gamma butyrolactone (GBL) and 1,4-butanediol (1,4-BD; BDO): A literature review with a focus on UK fatalities related to non-medical use

Corkery

Loi

Claridge

et al. 2015

Neuroscience & Biobehavioral Reviews

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Misuse of gamma hydroxybutrate (GHB) and gamma butyrolactone (GBL) has increased greatly since the early 1990s, being implicated in a rising number of deaths. This paper reviews knowledge on GHB and derivatives, and explores the largest series of deaths associated with their non-medical use. Descriptive analyses of cases associated with GHB/GBL and 1,4-butanediol (1,4-BD) use extracted from the UK's National Programme on Substance Abuse Deaths database. From 1995 to September 2013, 159 GHB/GBL-associated fatalities were reported. Typical victims: White (92%); young (mean age 32 years); male (82%); with a drug misuse history (70%). Most deaths (79%) were accidental or related to drug use, the remainder (potential) suicides. GHB/GBL alone was implicated in 37%; alcohol 14%; other drugs 28%; other drugs and alcohol 15%. Its endogenous nature and rapid elimination limit toxicological detection. Post-mortem blood levels: mean 482 (range 0-6500; SD 758)mg/L. Results suggest significant caution is needed when ingesting GHB/GBL, particularly with alcohol, benzodiazepines, opiates, stimulants, and ketamine. More awareness is needed about risks associated with consumption.

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Tiapride-induced catalepsy is potentiated by gamma-hydroxybutyric acid administration

Cited by 15 publications

References 21 publications

Cataleptic effects of γ-hydroxybutyrate (GHB) and baclofen in mice: mediation by GABAB receptors, but differential enhancement by N-methyl-d-aspartate (NMDA) receptor antagonists

Cataleptic effects of γ-hydroxybutyrate (GHB) and baclofen in mice: mediation by GABAB receptors, but differential enhancement by N-methyl-d-aspartate (NMDA) receptor antagonists

Cataleptic effects of γ-hydroxybutyrate (GHB), its precursor γ-butyrolactone (GBL), and GABAB receptor agonists in mice: differential antagonism by the GABAB receptor antagonist CGP35348

Gamma hydroxybutyrate (GHB), gamma butyrolactone (GBL) and 1,4-butanediol (1,4-BD; BDO): A literature review with a focus on UK fatalities related to non-medical use

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