Ambien online research references
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The dentate gyrus (DG) normally functions as a filter, preventing propagation of synchronized activity into the seizure-prone hippocampus. This filter or 'gatekeeper' attribute of the DG is compromised in various pathological states, including temporal lobe epilepsy (TLE). This study examines the role that altered inhibition may play in the deterioration of this crucial DG function. Using the pilocarpine animal model of TLE, we demonstrate that inhibitory synaptic function is altered in principal cells of the DG. Spontaneous miniature inhibitory postsynaptic currents (mIPSCs) recorded in dentate granule cells (DGCs) from epileptic animals were larger, more sensitive to blockade by zinc and less sensitive to augmentation by the benzodiazepine type site 1 modulator zolpidem. Furthermore, mIPSCs examined during a quiescent period following injury but preceding onset of epilepsy were significantly smaller than those present either in control or in TLE DGCs, and had already acquired sensitivity to blockade by zinc prior to the onset of spontaneous seizures. Rapid agonist application experiments demonstrated that prolonged (>35 ms) exposure to zinc is required to block GABAA receptors (GABAARs) in patches pulled from epileptic DGCs. Therefore, zinc must be tonically present to block DGC GABAARs and alter DG function. This would occur only during repetitive activation of mossy fibres. Thus, in the pilocarpine animal model of TLE, an early, de novo, expression of zinc-sensitive GABAARs is coupled with delayed, epilepsy-induced development of a zinc delivery system provided by aberrant sprouting of zinc-containing mossy fibre recurrent collaterals. The temporal and spatial juxtaposition of these pathophysiological alterations may compromise normal 'gatekeeper' function of the DG through dynamic zinc-induced failure of inhibition, predisposing the hippocampal circuit to generate seizures.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12752378&dopt=Abstract
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Am J Drug Alcohol Abuse. 2003 May;29(2):281-99.
Differential effects in humans after repeated administrations of zolpidem and triazolam.
Stoops WW, Rush CR.
Department of Behavioral Science, College of Medicine, University of Kentucky, Lexington, Kentucky 40536-0086, USA.
Zolpidem, a commonly prescribed hypnotic, is an imidazopyridine that purportedly has a unique benzodiazepine-receptor binding profile. Despite its unique binding profile, human laboratory experiments have generally failed to demonstrate meaningful behavioral pharmacological differences between zolpidem and classic benzodiazepine-receptor agonists like triazolam. In this article, two groups of nondrug-abusing volunteers received 15 mg zolpidem (N = 11) or 0.375 mg zolpidem (N = 15) on four separate occasions and placebo on two other occasions. In both groups, the order of drug administration was quasi-random. Drug effects were assessed with a battery of laboratory performance tasks and subject-rated drug-effect questionnaires. Zolpidem and triazolam produced prototypical sedative-like effects (e.g., impaired performance, increased subject-ratings of sedation). The performance-impairing effects of triazolam, but not zolpidem, were significantly less after the final administration relative to the initial administration. The subject-rated effects of both zolpidem and triazolam were significantly less after the final administration relative to the initial administration. The results of this experiment suggest that zolpidem and triazolam differ in terms of tolerance-producing effects. Future studies should assess the tolerance-producing effects of zolpidem across a range of doses, as well as other novel sedatives such as zaleplon.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12765207&dopt=Abstract
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Nucl Med Biol. 2003 May;30(4):435-9.
Synthesis and in vivo evaluation of [11C]zolpidem, an imidazopyridine with agonist properties at central benzodiazepine receptors.
Dumont F, Waterhouse RN, Montoya JA, Mattner F, Katsifis A, Kegeles LS, Laruelle M.
Department of Psychiatry, Columbia University, 1051 Riverside Drive, New York, New York 10032, USA.
The synthesis and evaluation of [(11)C]zolpidem, an imidazopyridine with agonist properties at central benzodiazepine receptors, is reported herein. The reaction of desmethylzolpidem with [(11)C] methyl iodide afforded the title compound [(11)C]zolpidem in a yield of 19.19 +/- 3.23% in 41 +/- 2 min in specific activities of 0.995-1.19 Ci/micromol (1.115 +/- 0.105 Ci/micromol) (n = 3; decay corrected, EOB). The amount of radioactivity in the brain after tail vein injection in male Wistar rats was low, and the regional distribution was homogeneous and not consistent with the known distribution of the central benzodiazepine receptors. The frontal cortex/cerebellum ratio was not significantly greater than one (1.007 +/- 0.266 at 5 min) and did not increase from 5 to 40 min post-injection. A PET brain imaging study in one baboon confirmed the results obtained in rats. Therefore, it can be concluded that [(11)C]zolpidem is not a suitable tracer for in vivo visualization of central benzodiazepine receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12767401&dopt=Abstract
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Pharmacol Biochem Behav. 2003 May;75(2):435-45.
Selectivity in generalization to GABAergic drugs in midazolam-trained baboons.
Ator NA.
Department of Psychiatry and Behavioral Sciences, Behavioral Biology Research Center, Johns Hopkins University School of Medicine, 5510 Nathan Shock Drive, Suite 3000, Johns Hopkins Bayview Campus, Baltimore, MD 21224, USA. ator
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jhmi.edu
When barbiturates have been tested in animals trained to discriminate the intravenous benzodiazepine (Bz) anesthetic midazolam, squirrel monkeys and pigeons did not reliably generalize to barbiturates but rats did. To explore this unexpected phenomenon in another species and to extend the midazolam generalization profile to GABAergic compounds not previously tested, five baboons were trained to discriminate midazolam maleate (0.32 mg/kg i.v.) from saline under a two-lever procedure. In tests 10 min after dose delivery, the partial agonist imidazenil, the full agonist chlordiazepoxide, and the receptor-subtype-selective hypnotic zolpidem fully shared discriminative effects with midazolam. The barbiturate pentobarbital did so in only one of five baboons, and the intravenous anesthetic propofol failed to do so in the three baboons tested. Testing 1 min after dose delivery shifted midazolam and zolpidem curves to the left and increased generalization to propofol but not pentobarbital. Taken together with previous published data, partial or full agonism at the Bz binding site appears sufficient for midazolam-like discriminative effects in nonhuman primates, pigeons, and rodents, and modulation through the anesthetic site is sufficient in baboons. However, to date, positive modulation of GABA through the barbiturate site is not generally sufficient for this effect in nonhuman primates and pigeons although it is in rodents.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12873636&dopt=Abstract
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