The safety and tolerability of zolpidem--an update.

Zolpidem belongs to a new class of hypnotic agents, chemically distinct from the pre-existing ones, and has a unique neuropharmacological profile. It induces sedative/hypnotic effects in rodents at doses much lower than those for anticonvulsant and myorelaxant activities. Clinically, zolpidem is indicated for the short term treatment of insomnia.

Comparison of continuous versus intermittent administration of zolpidem in chronic insomniacs: a double-blind, randomized pilot study.

The subjective efficacy and safety of intermittent administration of a hypnotic for insomnia was assessed, since such a regime may provide a potential means of reducing the risk of habituation and dependence. A total of 160 adult patients (mean 45 years) with chronic insomnia were treated for 2 weeks with zolpidem, 10 mg, either continuously or intermittently (five nights zolpidem, two consecutive nights placebo per week) in this multicentre, out-patient, pilot study. At the end of the 2-week treatment, patients subjectively estimated their nightly total sleep time as 6.

[Contribution of zolpidem in the management of sleep disorders].

Zolpidem is a nonbenzodiazepine hypnotic agent belonging to a new class of psychotropic drugs the imidazopyridines which enhance the GABAA receptor function by interacting with a specific receptor population. Zolpidem binds selectively to the Omega-1 receptor subtype and from a pharmacological point of view differs from benzodiazepines (BZD) by producing a strong sedative and hypnotic profile which predominates over the anticonvulsivant and anxiolytic activity and moreover appears practically devoid of myorelaxant properties. From a pharmacodynamic point of view, these results suggest that zolpidem facilitates more selectively than BZD, GABAA function and produces a selective hypnotic effect.

Behavioral indices of beta receptor subsensitivity after chronic treatment with viloxazine in the mouse.

The aim of the experiments was to determine whether chronic pretreatment with viloxazine decreased the sensitivity of mice to the sedative effects of a beta agonist clenbuterol. Mice were subjected to chronic oral treatment with viloxazine (128 mg/kg twice daily) and then given a single administration of 32 mg/kg PO followed by clenbuterol (0.125 mg/kg IP) before being tested in a standard photocell activity meter.