MemberMagnolol, a major bioactive constituent of the bark of Magnolia officinalis, exerts antiepileptic effects via theGABA/benzodiazepine receptor complex in mice.
BACKGROUND AND PURPOSE:
The aim of this study was to evaluate the anti-convulsant effects of magnolol (6, 6', 7, 12-tetramethoxy-2, 2'-dimethyl-1-β-berbaman, C18H18O2) and the mechanisms involved.
EXPERIMENTAL APPROACH:
Mice were treated with magnolol (20, 40 and 80 mg·kg(-1)) 30 min before injection with pentylenetetrazol (PTZ, 60 mg·kg(-1), i.p.). The anti-seizure effects of magnolol were analysed using seizure models of behaviour, EEG and in vitro electrophysiology and c-Fos expression in the hippocampus and cortex.
KEY RESULTS:
Magnolol at doses of 40 and 80 mg·kg(-1) significantly delayed the onset of myoclonic jerks and generalized clonic seizures, and decreased the seizure stage and mortality compared with those of the vehicle-treated animals. EEG recordings showed that magnolol (40 and 80 mg·kg(-1)) prolonged the latency of seizure onset and decreased the number of seizure spikes. The anti-epileptic effect of magnolol was reversed by the GABA(A)/benzodiazepine receptor antagonist flumazenil. Pretreatment with flumazenil decreased the effects of magnolol on prolongation of seizure latency and decline of seizure stage. In a Mg(2+)-free model of epileptiform activity, using multi-electrode array recordings in mouse hippocampal slices, magnolol decreased spontaneous epileptiform discharges. Magnolol also significantly decreased seizure-induced Fos immunoreactivity in the piriform cortex, dentate gyrus and hippocampal area CA1. These effects were attenuated by pretreatment with flumazenil.
CONCLUSIONS AND IMPLICATIONS:
These findings indicate that the inhibitory effects of magnolol on epileptiform activity were mediated by theGABA(A) /benzodiazepine receptor complex.
http://www.ncbi.nlm.nih.gov/pubmed/21518336
Magnolol, a major bioactive constituent of the bark of Magnolia officinalis, induces sleep via the benzodiazepine site of GABA(A) receptor in mice.
Magnolia bark extract has powerful stress busting effects, largely due to "honokiol" a well-studied and potent anxiolytic. It works similarly to prescription medications like alprazolam (Xanax), chlordiazepoxide (Librium), diazepam (Valium), and lorazepam (Ativan). Both magnolia and prescription sedatives work by increasing levels of GABA, a relaxing hormone that helps calm and soothe an overactive brain. The difference is that honokiol is picky and works in specific areas of the brain (raising GABA). The net effect is relaxation. Prescription drugs affect GABA receptors throughout your entire body, causing systemic side effects such morning hangover effect, muscle weakness, daytime fatigue and more. Magnolia, being more selective, should not produce these problems, and should not make you feel doped up.
http://www.ncbi.nlm.nih.gov/pubmed/22771461
BACKGROUND AND PURPOSE:
The aim of this study was to evaluate the anti-convulsant effects of magnolol (6, 6', 7, 12-tetramethoxy-2, 2'-dimethyl-1-β-berbaman, C18H18O2) and the mechanisms involved.
EXPERIMENTAL APPROACH:
Mice were treated with magnolol (20, 40 and 80 mg·kg(-1)) 30 min before injection with pentylenetetrazol (PTZ, 60 mg·kg(-1), i.p.). The anti-seizure effects of magnolol were analysed using seizure models of behaviour, EEG and in vitro electrophysiology and c-Fos expression in the hippocampus and cortex.
KEY RESULTS:
Magnolol at doses of 40 and 80 mg·kg(-1) significantly delayed the onset of myoclonic jerks and generalized clonic seizures, and decreased the seizure stage and mortality compared with those of the vehicle-treated animals. EEG recordings showed that magnolol (40 and 80 mg·kg(-1)) prolonged the latency of seizure onset and decreased the number of seizure spikes. The anti-epileptic effect of magnolol was reversed by the GABA(A)/benzodiazepine receptor antagonist flumazenil. Pretreatment with flumazenil decreased the effects of magnolol on prolongation of seizure latency and decline of seizure stage. In a Mg(2+)-free model of epileptiform activity, using multi-electrode array recordings in mouse hippocampal slices, magnolol decreased spontaneous epileptiform discharges. Magnolol also significantly decreased seizure-induced Fos immunoreactivity in the piriform cortex, dentate gyrus and hippocampal area CA1. These effects were attenuated by pretreatment with flumazenil.
CONCLUSIONS AND IMPLICATIONS:
These findings indicate that the inhibitory effects of magnolol on epileptiform activity were mediated by theGABA(A) /benzodiazepine receptor complex.
http://www.ncbi.nlm.nih.gov/pubmed/21518336
Magnolol, a major bioactive constituent of the bark of Magnolia officinalis, induces sleep via the benzodiazepine site of GABA(A) receptor in mice.
Magnolia bark extract has powerful stress busting effects, largely due to "honokiol" a well-studied and potent anxiolytic. It works similarly to prescription medications like alprazolam (Xanax), chlordiazepoxide (Librium), diazepam (Valium), and lorazepam (Ativan). Both magnolia and prescription sedatives work by increasing levels of GABA, a relaxing hormone that helps calm and soothe an overactive brain. The difference is that honokiol is picky and works in specific areas of the brain (raising GABA). The net effect is relaxation. Prescription drugs affect GABA receptors throughout your entire body, causing systemic side effects such morning hangover effect, muscle weakness, daytime fatigue and more. Magnolia, being more selective, should not produce these problems, and should not make you feel doped up.
http://www.ncbi.nlm.nih.gov/pubmed/22771461
