View and buy high purity Diazepam from Tocris Bioscience. Acts at the benzodiazepine modulatory site. Cited in 7 publications.
Huang et al (2010) A refractory period for rejuvenating GABAergic synaptic transmission and ocular dominance plasticity with dark exposure. J Neurosci 30 16636 PMID:.
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Zhu (2018) Structure of a human synaptic GABAA receptor. Nature 559 67 PMID:.
Written by Ian Martin, Norman Bowery and Susan Dunn, this review provides a history of the GABA receptor, as well as discussing the structure and function of the various subtypes and the clinical potential of receptor modulators; compounds available from Tocris are listed.
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Diazepam; CAS Number: ; EC Number: ; Synonym: 7-Chloro-1-methyl-5-phenyl-3H-1,4-benzodiazepin-2(1H)-one, Ro 5-2807; Linear.
Benzodiazepine anxiolytic; prototype ligand for the GABA A receptor benzodiazepine modulatory site.
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Synonym: 7- Chloro- 1- methyl- 5- phenyl- 3H- 1,4- benzodiazepin- 2(1H) - one, Ro 5-2807 CAS Number.
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To browse other handbook pages, click here. This compound is featured on the GABAA Receptors page of the Handbook of Receptor Classification and Signal Transduction.
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D0899 - Diazepam.
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Keywords: Bioactive small molecules, Central Nervous System, Diseases, Metabolism, Neurodegenerative Diseases, Neuroscience, Neurotransmission, Neurotransmitters. The nervous system, comprised of the brain and spinal cord (central nervous system, or CNS) and network of nerves that connects the CNS to the rest of the body (peripheral nervous system, or PNS) is.
Empirical Formula (Hill Notation) C 16 H 13 ClN 2 O Molecular Weight 284.74 EC Number MDL number MFCD.
Diazepam for treating tetanus. Okoromah CN(1), Lesi FE. Author information: (1)Paediatrics and Child Health, College of Medicine of the University of Lagos.
We searched the Cochrane Neonatal Group trials register (October 2003), Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 3, 2003), MEDLINE (1966 to October 2003), EMBASE (1980 to October 2003), LILACS (2003), CINAHL (October 2003), Science Citation Index, African Index Medicus, conference abstracts and reference lists of articles. We contacted researchers, experts and organizations working in the field and used personal communication.
Diazepam compared to other drugs (eg phenobarbitone and chlorpromazine) may have advantages because of combined anticonvulsant, muscle relaxant, sedative and anxiolytic effects.
Chronobiol Int. 2005;22(6):975-85. Diazepam affects both level and amplitude of rat locomotor activity rhythm but has no effect on core body temperature.
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Diazepam lacked effect on body core temperature even on the first day of administration, thereby ruling out the possibility of drug tolerance development. Diazepam exerted no effects on the length of the period and did not affect the phase of the locomotor activity rhythm. Diazepam was administered subcutaneously for 3 wks in a dosage of 3 mg/kg body weight/day, 1 h before the onset of darkness. The fact that diazepam affects locomotor activity, but not core body temperature, suggests that different mechanisms mediate the actions of diazepam on locomotor activity and on core body temperature. The present study investigates the effects of a chronic administration of diazepam, a benzodiazepine widely used as an anxiolytic, on locomotor activity and body core temperature rhythms in male Wistar rats housed under 12 : 12 light : dark (LD) cycle conditions. The body temperature rhythm of rats was affected neither by short-term (a single injection) nor by long-term (every day for 3 wks) diazepam treatment. Diazepam increased the level of locomotor activity from the first day until the end of treatment, and also increased the amplitude of the activity circadian rhythm, but only on the third wk of treatment.
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Br J Pharmacol. 1998 Mar;123(6):1047-54. Functional and biochemical evidence for diazepam as a cyclic nucleotide phosphodiesterase type 4 inhibitor.
This effect of diazepam was not gamma-aminobutyric acid (GABA)-dependent, since it was neither mimicked nor potentiated by GABA, and was not affected by either a high concentration (5 microM) of the antagonists of the benzodiazepine/GABA/channel chloride receptor complex, picrotoxin, flumazenil and beta-carboline-3-carboxylic acid methyl ester (betaCCMe), or by the inverse agonists, beta-carboline-3-carboxylic acid N-methylamide (betaCCMa) and methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM, 0.1 microM).