CNS Drug Reviews
CNS Drug Reviews focuses on extensive reviews on the pharmacology, pharmacokinetics, toxicology and clinical trials of new drugs affecting the central nervous system. These peer reviewed articles are written by industrial or academic scientists who participated in the development of a particular drug. The Editorial Board is composed of eminent and highly reputable scientists.
- Impact factor4.92
- 5-year impact5.44
- Cited half-life4.60
- Immediacy index0.00
- Article influence1.51
- WebsiteCNS Drug Reviews website
- Other titlesCNS drug reviews (Online), CNS drug reviews
- Material typeDocument, Periodical, Internet resource
- Document typeInternet Resource, Computer File, Journal / Magazine / Newspaper
- Author can archive a pre-print version
- Author cannot archive a post-print version
- Some journals impose embargoes typically of 6 or 12 months, occasionally of 24 months
- no listing of affected journals available as yet
- See Wiley-Blackwell entry for articles after February 2007
- Publisher version cannot be used
- On author or institutional or subject-based server
- Server must be non-commercial
- Publisher copyright and source must be acknowledged with set statement ("The definitive version is available at www.blackwell-synergy.com ")
- Articles in some journals can be made Open Access on payment of additional charge
- 'Blackwell Publishing' is an imprint of 'Wiley-Blackwell'
- Classification yellow
Publications in this journal
- SourceAvailable from: onlinelibrary.wiley.com[Show abstract] [Hide abstract]
ABSTRACT: Given the well-established role of benzodiazepines in treating anxiety disorders, β-carbolines, spanning a spectrum from full agonists to full inverse agonists at the benzodiazepine allosteric site for the GABAA receptor, can provide valuable insight into the neural mechanisms underlying anxiety-related physiology and behavior. FG-7142 is a partial inverse agonist at the benzodiazepine allosteric site with its highest affinity for the α1 subunit-containing GABAA receptor, although it is not selective. FG-7142 also has its highest efficacy for modulation of GABA-induced chloride flux mediated at the α1 subunit-containing GABAA receptor. FG-7142 activates a recognized anxiety-related neural network and interacts with serotonergic, dopaminergic, cholinergic, and noradrenergic modulatory systems within that network. FG-7142 has been shown to induce anxiety-related behavioral and physiological responses in a variety of experimental paradigms across numerous mammalian and non-mammalian species, including humans. FG-7142 has proconflict actions across anxiety-related behavioral paradigms, modulates attentional processes, and increases cardioacceleratory sympathetic reactivity and neuroendocrine reactivity. Both acute and chronic FG-7142 treatment are proconvulsive, upregulate cortical adrenoreceptors, decrease subsequent actions of GABA and β-carboline agonists, and increase the effectiveness of subsequent GABAA receptor antagonists and β-carboline inverse agonists. FG-7142, as a partial inverse agonist, can help to elucidate individual components of full agonism of benzodiazepine binding sites and may serve to identify the specific GABAA receptor subtypes involved in specific behavioral and physiological responses.CNS Drug Reviews 12/2007; 13(4):475 - 501.
- CNS Drug Reviews 09/2006; 1(2):204 - 226.
- CNS Drug Reviews 09/2006; 3(1):24 - 33.
- CNS Drug Reviews 09/2006; 2(2):175 - 194.
- CNS Drug Reviews 09/2006; 3(3):260 - 277.
Article: RiluzoleCNS Drug Reviews 09/2006; 2(1):40 - 51.
- CNS Drug Reviews 09/2006; 2(2):214 - 225.
- CNS Drug Reviews 09/2006; 1(1):107 - 128.
- CNS Drug Reviews 09/2006; 2(4):363 - 383.
- CNS Drug Reviews 09/2006; 1(1):27 - 49.
- CNS Drug Reviews 09/2006; 3(4):325 - 345.
- CNS Drug Reviews 09/2006; 1(2):129 - 148.
- CNS Drug Reviews 09/2006; 3(2):103 - 119.
- [Show abstract] [Hide abstract]
ABSTRACT: Zaleplon (N-[3-(3-cyanopyrazolo[l,5-a]pyrimidin-7-y l)phenyl)]-N-ethylacetamide) is a non-benzodiazepine sedative-hypnotic with benzodiazepine-like sedative effects, but with less apparent liability for accompanying undesirable side effects. Zaleplon displaces [3H]flunitrazepam from rat cortical membranes with an IC50 value of 200 nM and enhances t-butylbicyclophosphorothionate [35S]TBPS binding by 73%, suggesting pharmacological activity mediated by the GABAA benzodiazepine receptor complex. In various preclinical procedures such as motor activity, muscle relaxation, EEG, anticonvulsant activity, and vigilance, zaleplon produced effects similar to those of other sedative-hypnotic compounds such as triazolam and flurazepam; furthermore, these effects, when evaluated, were reversed by the benzodiazepine receptor antagonist flumazenil. Zaleplon increased punished (conflict) responding in squirrel monkeys and rats and these effects were also antagonized by flumazenil. When established as a discriminative stimulus in rats at 3.0mg/kg i.p., zaleplon showed a dose-related increase in drug-appropriate responding up to the training dose and a correlated decrease in response rate. Triazolam (0.1 to 1.0 mg/kg), the benzodiazepine partial agonist Ro 17-1812 (0.3 to 3.0mg/kg), and the triazolopyridine CL 218,872 (1.0 to 3.0 mg/kg) substituted consistently for zaleplon in all rats, whereas the imidazo-pyridines zolpidem (3.0 to 10 mg/kg) and alpidem (10 to 30 mg/kg), the benzodiazepine partial agonist bretazenil (0.03 to 10 mg/kg) and the novel putative anxio-lytic CL 273,547 (10 to 56 mg/kg) did not result in consistent drug-appropriate responding in all rats. These results suggest that the effects of zaleplon are similar in many respects to other compounds acting at the benzodiazepine receptor complex but differ as well from both benzodiazepine and non- benzodiazepine drugs. This profile of activity, coupled with additional information in ancillary procedures, yields a pre-clinical profile of a short-acting sedative-hypnotic non-benzodiazepine that is currently in Phase III development for the treatment of sleep disturbances.CNS Drug Reviews 09/2006; 3(3):207 - 224.
- CNS Drug Reviews 09/2006; 3(4):346 - 362.
- CNS Drug Reviews 09/2006; 2(2):226 - 237.
- CNS Drug Reviews 09/2006; 2(1):91 - 126.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.