Ambien online research references
J Pharm Pharmacol. 1994 Jul;46(7):611-3.
Pharmacokinetics and brain distribution of zolpidem in the rat after acute and chronic administration.
Trenque T, Bustany P, Lamiable D, Legros S, Choisy H.
Laboratoire de Pharmacologie, Hopital Maison Blanche, Reims, France.
The pharmacokinetics of zolpidem were studied after single dose, administered for either 7 or 28 days to rats. Thirty minutes after the last dose, animals were killed and the brain removed. The highest concentrations in plasma, which were observed at the first sampling time (0.5 h) were 2341 +/- 540 (day 0), 1956 +/- 325 (day 7) and 2908 +/- 1369 ng mL-1 (day 28). Corresponding AUC values of 1742 +/- 488, 1583 +/- 422 and 2683 +/- 1249 ng mL-1 h were found. MRT increased significantly from 0.46 +/- 0.06 h on day 0 to 0.67 +/- 0.02 h on day 28. The cerebral levels showed no significant change during the chronic administration (766 +/- 285, 685 +/- 171 and 887 +/- 264 ng g-1, respectively). No modification of the principal kinetic parameters was detected up to the 28th day of treatment.
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J Pharmacol Exp Ther. 1999 Dec;291(3):1233-41.
Discriminative stimulus effects of zolpidem in squirrel monkeys: comparison with conventional benzodiazepines and sedative-hypnotics.
Rowlett JK, Spealman RD, Lelas S.
Harvard Medical School, New England Regional Primate Research Center, Southborough, Massachusetts 01772-9102, USA.
The present study examined whether zolpidem, an imidazopyridine with selectivity for benzodiazepine (BZ)/gamma-aminobutyric acid(A) receptors containing the alpha1-subunit, had discriminative stimulus effects similar to typical BZs and other sedative/hypnotic drugs in primates. Squirrel monkeys (Saimiri sciureus) were trained to discriminate zolpidem (1.0 mg/kg i.v.) from vehicle under a 10-response fixed-ratio schedule of food delivery. Under test conditions, zolpidem (0.1-3.0 mg/kg) increased responding on the drug lever to an average maximum of 90% of total responding. When pretreatment times were varied from 5 to 50 min, the discriminative stimulus effects of zolpidem were maximal at 5 min and near control levels 35 min after administration. Flumazenil antagonized both the discriminative stimulus and rate-decreasing effects of zolpidem in a dose-dependent and surmountable fashion (in vivo apparent pA(2) values of 7.3 and 6.6 for the discriminative stimulus and rate-suppressing effects, respectively). The BZs triazolam, midazolam, diazepam, and N-desmethyldiazepam engendered dose-related increases in drug-lever responding that reached zolpidem-like levels (90%) in the majority of monkeys tested. In contrast, lorazepam, chlordiazepoxide, and oxazepam engendered average maximums of 70% or less and substituted fully for zolpidem in one or two monkeys only. Representative barbiturates as well as drugs that bind to non-BZ sites (muscimol, baclofen, buspirone, cyproheptadine, diphenhydramine) engendered 0 to 45% of responses on the drug lever up to doses that markedly reduced response rate. These results support the view that zolpidem's selectivity for the alpha1-subunit of the BZ/gamma-aminobutyric acid(A) receptor complex confers a distinctive profile of interoceptive effects that overlaps partially with those of typical BZs but not with those of barbiturates.
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Eur J Pharmacol. 1994 Apr 15;267(2):243-7.
Effects of chronic ethanol administration on [3H]zolpidem binding in rat brain.
Devaud LL, Morrow AL.
Department of Psychiatry and Center for Alcohol Studies, University of North Carolina School of Medicine, Chapel Hill 27599-7175.
The effect of chronic ethanol administration on [3H]zolpidem binding was measured in rat brain. [3H]Zolpidem selectively labels gamma-aminobutyric acidA-benzodiazepine type 1 receptors, which are highly correlated with ethanol-sensitive gamma-aminobutyric acid (GABA) responses in brain. Recombinant expression studies have suggested that this GABAA receptor subtype requires the expression of alpha 1 subunits and is not selectively labeled by classic GABAergic ligands. Since chronic ethanol administration reduces alpha 1 subunit mRNA and polypeptide levels, we investigated whether alterations in [3H]zolpidem binding would also be detected. Chronic ethanol administration did not reduce [3H]zolpidem binding. Instead small, but reproducible, increases in [3H]zolpidem binding density were detected in cortex and cerebellum with no change in affinity. No alterations in [3H]zolpidem binding to striatum and hippocampus were observed. These findings suggest that chronic ethanol administration may have differential effects on [3H]zolpidem binding sites and alpha 1 subunit expression. Alterations in alpha 1 subunit expression following chronic ethanol administration may involve other GABAA receptor subtypes or high affinity [3H]zolpidem binding may be dependent on the expression of additional GABAA receptor subunits.
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J Toxicol Clin Toxicol. 1994;32(4):391-404.
Acute zolpidem poisoning--analysis of 344 cases.
Garnier R, Guerault E, Muzard D, Azoyan P, Chaumet-Riffaud AE, Efthymiou ML.
Paris Poison Center, Hopital Fernand-Widal, France.
Zolpidem is a new short acting hypnotic agent, first launched in France in 1988. Three hundred forty-four cases of intentional acute overdoses are reviewed retrospectively. Patients were predominantly female (70%) in their third or fourth decade. Ingested doses of zolpidem ranged between 10 and 1400 mg (one pack or less in 80%). Half of the patients ingested other substances (psychotropic drugs and alcohol) concomitantly. Signs of intoxication were observed in two thirds of the population but could be attributed to zolpidem in only 105 cases: drowsiness (N = 89) occurred at doses of 140 to 440 mg; coma (N = 4) or respiratory failure (N = 1). Other symptoms were rare (excepted vomiting, N = 7). Of the rare electrocardiographic or biological abnormalities, none appeared to be directly related to zolpidem. Therapy for intoxication was usually limited to supportive measures and/or gastric lavage. Symptoms of intoxication rapidly remitted in 91% of cases. Three percent of patients with multiple drug ingestion recovered despite severe complications during intensive care. Fatalities were reported for 6% but could not be directly linked to zolpidem. Previous published reports are confirmed: zolpidem acute overdose is generally benign and requires no specific therapeutic measures.
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Brain Res. 1993 Feb 26;604(1-2):240-50.
Comparative autoradiographic distribution of central omega (benzodiazepine) modulatory site subtypes with high, intermediate and low affinity for zolpidem and alpidem.
Benavides J, Peny B, Ruano D, Vitorica J, Scatton B.
Department of Biology, Synthelabo Recherche--LERS, Bagneux, France.
Pharmacological characterization of [3H]benzodiazepine binding to membrane preparations of adult rat hippocampus and neonatal rat brain have demonstrated, in addition to the omega 1 and omega 2 populations of central omega benzodiazepine binding sites associated with GABAA receptors, the existence of binding sites with microM affinity for the imidazopyridines zolpidem and alpidem. In the present study we have investigated their comparative autoradiographic distribution using [3H]flumazenil as a ligand. In the neonatal rat CNS, the imidazopyridine derivatives zolpidem and alpidem were found to discriminate two [3H]flumazenil binding site populations with an IC50 value ratio of more than 200-fold. In the different regions investigated (spinal cord, striatum, neocortex and inferior colliculus) the low affinity component had IC50 values of 20-40 microM (zolpidem) and 5-15 microM (alpidem) and accounted for ca. 50% of the total binding site population. In the adult rat, these imidazopyridine derivatives displayed a greater displacing potency in the cerebellum (IC50 = 6 and 36 nM, respectively) than in the hippocampus (IC50 = 37 and 403 nM, respectively). In the cerebellum, [3H]flumazenil binding was fully displaced by 1 microM of either compound and Hill coefficients of displacement curves were close to unity. In the hippocampus, 25% of [3H]flumazenil binding were resistant to 3 microM zolpidem or 1 microM alpidem, but were displaced by 100 microM of either compound. CL 218,872 also displayed a greater displacing potency in the cerebellum (IC50 = 83 nM) than in the hippocampus (IC50 = 711 nM) but [3H]flumazenil binding in the hippocampus was fully displaced by 10 microM of this compound. In adult rat hippocampus, zolpidem and alpidem were found to discriminate between three central omega site subtypes which display high (IC50 = 31 and 6.1 nM, for these imidazopyridine derivatives. In contrast, CL 218,872 discriminated between omega 1 and omega 2 sites but not between two omega 2 receptor subpopulations. omega 1 sites were mainly localized in layer IV of the sensorimotor cortex, cerebellum, substantia nigra, olfactory bulb and inferior colliculus. omega 2I sites were present in the cortical mantle (with higher levels in the cingulate and olfactory than in the sensorimotor cortex) and in subcortical (hippocampus, hypothalamus and nucleus accumbens) limbic structures. In the hippocampus, hypothalamus, spinal cord and nucleus accumbens, omega 2L sites accounted for more than 25% of the specific [3H]flumazenil binding; the density of these sites was minor in the cortex and in most pyramidal and extrapyramidal system structures.(ABSTRACT TRUNCATED AT 400 WORDS)
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