Ambien online research references
Alcohol Alcohol. 1999 Jul-Aug;34(4):511-9.
Zolpidem involvement on memory and hypnotic effect of ethanol in chronically ethanol-treated rats.
Mikolajczak P, Okulicz-Kozaryn I, Szczawinska K, Kaminska E, Kus K.
Department of Pharmacology, University of Medical Sciences in Poznan, Poland.
Multiple (10x) treatment of zolpidem (1.0 or 2.0 mg/kg, orally, p.o.) led to different effects in chronically ethanol-treated and control rats. In control rats, after repeated zolpidem administration, a weaker, when compared to single administration, hypnotic effect of ethanol was observed, which may be the result of tolerance developed towards the inhibitory effect of zolpidem. However, in chronically ethanol-treated rats, the multiple zolpidem treatment led to prolongation of ethanol-induced sleep similar to the values observed in non-zolpidem-treated control animals. This suggests that zolpidem multiple administration may inhibit tolerance towards ethanol in chronically ethanol-treated rats. In the experiment with zolpidem, there were effects on performance in a memory test and the impairment of passive avoidance task after multiple drug treatment when compared to the effects after single administration in control rats. In contrast, in chronically ethanol-treated rats, amplification of latency (especially after 2.0 mg/kg) was observed. The possible relationship between ethanol-induced sedation and latency values would be consistent with a higher contribution of the inhibitory effect of zolpidem, than a direct influence on memory processes in chronically ethanol-treated rats.
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Chest. 1990 Mar;97(3 Suppl):51S-52S.
Comparison of zolpidem (Z), triazolam (T), and flunitrazepam (F) effects on arterial blood gases and control of breathing in patients with severe chronic obstructive pulmonary disease (COPD).
Murciano D, Aubier M, Palacios S, Pariente R.
Clinique Pneumologique, INSERM U 226, Hopital Beaujon, Clichy, France.
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Rev Med Interne. 1989 Sep-Oct;10(5):466.
[Acute poisoning by zolpidem]
[Article in French]
Meram D, Descotes J.
Centre anti-poisons, hopital Edouard-Herriot, Lyon.
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Eur J Pharmacol. 1989 Feb 28;161(2-3):173-80.
Enhancement of GABAergic transmission by zolpidem, an imidazopyridine with preferential affinity for type I benzodiazepine receptors.
Biggio G, Concas A, Corda MG, Serra M.
Department of Experimental Biology, University of Cagliari, Italy.
The effect of zolpidem, an imidazopyridine derivative with high affinity at the type I benzodiazepine recognition site, on the function of the GABAA/ionophore receptor complex was studied in vitro. Zolpidem, mimicking the action of diazepam, increased [3H]GABA binding, enhanced muscimol-stimulated 36Cl- uptake and reduced [35S]TBPS binding in rat cortical membrane preparations. Zolpidem was less effective than diazepam on the above parameters. Zolpidem induced a lower increase of [3H]GABA binding (23 vs. 35%) and muscimol-stimulated 36Cl- uptake (22 vs. 40%) and a smaller decrease of [35S]TBPS binding (47 vs. 77%) than diazepam. The finding that zolpidem enhanced the function of GABAergic synapses with an efficacy qualitatively and quantitatively different from that of diazepam suggests that this compound is a partial agonist at the benzodiazepine recognition site. Thus, our results are consistent with the view that the biochemical and pharmacological profile of a benzodiazepine recognition site ligand reflects its efficacy to enhance GABAergic transmission. Whether the preferential affinity of zolpidem at the type I site is involved in its atypical biochemical and pharmacological profile remains to be clarified.
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Pharmacol Biochem Behav. 1989 Jun;33(2):303-7.
Novel benzodiazepine receptor ligands: palatable food intake following zolpidem, CGS 17867A, or Ro23-0364, in the rat.
Yerbury RE, Cooper SJ.
School of Psychology, University of Birmingham, United Kingdom.
The potent imidazopyridine hypnotic, zolpidem, binds to central benzodiazepine receptors and has predominantly sedative properties, as determine in animal models. In tests of palatable food consumption in nondeprived male rats, the present results indicate that zolpidem (0.3-3.0 mg/kg) had no effect on food intake. Its lack of effect contrasts sharply with other benzodiazepine agonists which strongly stimulate palatable food intake. Two other novel compounds, both of which bind to benzodiazepine receptors, and which have reduced propensity to induce sedative effects, increased palatable food consumption, although in differing ways. The imidazobenzodiazepine Ro23-0364 (0.3-10.0 mg/kg) dose-dependently increased feeding in the standard procedure, but failed to stimulate food intake in presatiated animals. The pyrazoloquinoline CGS 17867A (1.0-30.0 mg/kg) increased food intake in both test procedures, although the dose-effect relationship was nonmonotonic. Taken together, the data indicate a probable separation between hyperphagic and sedating effects of benzodiazepine receptor agonists. If zolpidem's sedative effect is linked to an action at a receptor subtype (benzodiazepine Type 1 or omega 1), then the hyperphagic effect of benzodiazepines may depend more on the alternative subtype.
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