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1 e affinity of an alpha(1)-selective agonist (zolpidem).
2 profiles of etomidate and THIP compared with zolpidem.
3 loreclezole and insensitive to diazepam and zolpidem.
4 ere observed during the repeated exposure to zolpidem.
5 smission in a manner similar to diazepam and zolpidem.
6 ir functionally expressed GABAA receptors to zolpidem.
7 ith the ability of single dose detection for zolpidem.
8 when they are treated with the sleeping pill zolpidem.
9 aptic receptors, which were not modulated by zolpidem.
10 itive allosteric modulators, eszopiclone and zolpidem.
11 nsive to diazepam, other benzodiazepines and zolpidem.
12 and frontal brain metabolism in response to zolpidem.
13 is changed to isoleucine are insensitive to zolpidem.
14 neurons, paralleling enhanced sensitivity to zolpidem.
15 eric GABA(A)-R modulators diazepam (DZP) and zolpidem.
16 owed concentration-dependent potentiation by zolpidem (0.03-100 microM), which was substantially blun
17 GABA(A) receptor alpha1 subunits and reduced zolpidem (100 nM) enhancement of GABA-evoked currents.
20 , and alpha5 subunit-containing GABAARs) and zolpidem (a positive modulator mainly at the alpha1 GABA
21 that enhancing phasic GABA signalling using zolpidem, a Food and Drug Administration (FDA)-approved
28 receptors in the frontal cortex by systemic zolpidem administration also reduced sleep latency, but
29 le change in cell survival following chronic zolpidem administration in young versus old animals.
30 ase in Delta sleep, suggesting that repeated zolpidem administration might elicit enduring modificati
31 itecture 24 h after cessation of sub-chronic zolpidem administration revealed a decrease in Delta sle
34 Therefore, sub-chronic administration of zolpidem affected lasting modifications in sleep organiz
35 c BZD flunitrazepam with wild-type affinity, zolpidem affinity is decreased approximately 8-fold.
36 ation of pentobarbital, benzodiazepines, and zolpidem all significantly increased the GABA-evoked res
45 ere relatively insensitive to enhancement by zolpidem and diazepam, and were enhanced by loreclezole
48 lpha- and beta-subunit selective modulators, zolpidem and loreclezole, had different effects on IPSCs
50 azolam and the alpha1GABAA preferential PAMS zolpidem and zaleplon reduced accuracy in both procedure
51 dulation of I(GABA) by positive (flurazepam, zolpidem) and negative [3-carbomethoxy-4-ethyl-6,7-dimet
52 intermediate, and high doses of eszopiclone, zolpidem, and DORA-22 were examined after first defining
54 res; (2) reduced sensitivity to diazepam and zolpidem, and increased sensitivity to Zn2+ indicate tha
56 uring withdrawal from ethanol, diazepam, and zolpidem, and measured consumption of and preference for
57 Treatment of Ndufs4 KO mice with papaverine, zolpidem, and rapamycin-suppressed inflammation, prevent
60 aphy with the alpha(1) selective ligand, [3H]zolpidem, and the non-selective benzodiazepine site liga
61 e accuracy dose-effect curves for triazolam, zolpidem, and zaleplon increased with box number in the
69 Similar to classic benzodiazepines (BZDs), zolpidem binds at the extracellular N-terminal alpha/gam
70 2I77 mice were made selectively sensitive to zolpidem by genetically swapping the gamma2I77 subunits
73 ing that these EEG power-reducing effects of zolpidem do not depend on reduced histamine release.
77 ently stimulated by diazepam (EC(50)=63 nM), zolpidem (EC(50)=85 nM), loreclezole (EC(50)=10.1 microM
78 IC50 = 29 microM), diazepam (EC50 = 158 nM), zolpidem (EC50 = 75 nM), and dimethoxyl-4-ethyl-beta-car
81 pha(1)beta(2)gamma(2) GABA(A)Rs and measured zolpidem, eszopiclone, and BZD-site antagonist binding.
84 sh-language article that examined the use of zolpidem for noninsomnia neurologic disorders in humans
85 showed good semiquantitative correlation to zolpidem hair concentrations obtained from validated rou
87 sket and bistratified cells were enhanced by zolpidem (HW by 18.4 +/- 6.2 % in 10:15 cells tested), d
90 or crossover designs with benzodiazepines or zolpidem in adults younger than 65 years with chronic in
92 epileptic DGCs; and (3) an inverse effect of zolpidem in some epileptic DGCs demonstrates the heterog
93 4, emerge as being important for stabilizing zolpidem in the BZD binding pocket and probably interact
94 The subunit-specific benzodiazepine agonist zolpidem increased the decay time constant of the IPSCs
101 alysis of sorted zolpidem-sensitive (ZS) and zolpidem-insensitive (ZI) subpopulations identified ZS c
102 , we deprived alpha1(H101R) mutant mice with zolpidem-insensitive alpha1-containing GABA(A) receptors
106 fic residue interactions and may explain why zolpidem is highly alpha(1)- and gamma(2)-subunit select
121 tochondrial optic neuropathy, papaverine and zolpidem provided significant protection from multiple p
122 ower of this method in the cerebellum, where zolpidem rapidly induces significant motor deficits when
123 The benzodiazepine type 1 receptor agonist zolpidem reduced hyperexcitability in both silent period
124 actions, suggesting that unlike eszopiclone, zolpidem relies more on shape recognition of the binding
126 ng as a novel therapeutic strategy, indicate zolpidem's potential to improve recovery, and underscore
127 nocytochemical and RT-PCR analysis of sorted zolpidem-sensitive (ZS) and zolpidem-insensitive (ZI) su
128 only synaptic alpha subunit was alpha1, and zolpidem-sensitive mIPSCs had weighted decay time consta
129 When histamine neurons were made selectively zolpidem-sensitive, systemic administration of zolpidem
130 bunit (that is, exchanging Ile77 for Phe77), zolpidem sensitivity can be restored to GABAA receptors
132 creasing mPSC frequency, decay kinetics, and zolpidem sensitivity that were nearly identical to our e
135 lpidem-sensitive, systemic administration of zolpidem shortened sleep latency and increased sleep tim
137 and the benzodiazepine1-selective modulator zolpidem strongly enhanced these IPSPs (45 +/- 28 %, n =
138 e of the gamma-aminobutyric acid A receptor, zolpidem tartrate presents a potential treatment mechani
140 he efficacy of sub-chronic administration of zolpidem to alter sleep architecture was enhanced when t
142 -54 %, 1:1), and the enhancement produced by zolpidem was reduced by flumazenil (-31 +/- 13 %, relati
146 st that DORA-22 differs from eszopiclone and zolpidem whereby DORA-22 promotes somnolence without alt
148 f two distinct BZ-site ligands, diazepam and zolpidem, which is relatively alpha1-subunit selective.
150 reater HICs than LPW mice during ethanol and zolpidem withdrawal, but differed less robustly during d
151 rom pentobarbital also influence ethanol and zolpidem withdrawal, but that diazepam withdrawal may be
152 ct of ethanol on the sensitivity of mPSCs to zolpidem, zinc and 3alpha-hydroxy-5alpha-pregnan-20-one
154 odiazepine receptor agonists (BzRAs) such as zolpidem (ZOL) induce sleep through general inhibition o
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