A new benzodiazepine pharmacology.
By H. Möhler, J. Fritschy, U. Rudolph. Journal of Pharmacology and Experimental Therapeutics, 2002
706 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1036f5b505aa93936afa5440472bdf4eef37ca29
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- Michael M. Merzenich
- T. Steimer
- Craig Lindsley
- John L. Rubenstein
- Arthur Christopoulos
- D. Schoepp
- G. Homanics
- Takao K. Hensch
In Cognitive Neuroscience
In Molecular Biology
- Craig Lindsley
- P. Conn
- P. Gentry
- Thomas P Mathews
- Cody J. Wenthur
- John L. Rubenstein
- Michael M. Merzenich
- Arthur Christopoulos
Citations in the corpus
- The endocannabinoid system controls key epileptogenic circuits in the hippocampus. (2006, neutral): “Benzodiazepines are allosteric modulators of GABA-A receptors that act as potent anticonvulsants by enhancing the inhibitory effects of GABAergic transmission (Möhler et al., 2002).”
- Compensatory alteration of inhibitory synaptic circuits in cerebellum and thalamus of γ‐aminobutyric acid type A receptor α1 subunit knockout mice (2006, background): “…postsynaptic clustering -Aminobutyric acid type A (GABAA) receptors mediate the majority of inhibitory neurotransmission in the brain and represent major drug targets for the treatment of anxiety, sleep disorders, epilepsy, and muscle spasms (Mohler et al., 2002; Sieghart and Sperk, 2002).”
- Model of autism: increased ratio of excitation/inhibition in key neural systems (2003, background): “Ongoing efforts are aimed at identifying novel benzodiazapines that can selectively activate distinct GABA A receptors, and therefore affect specific symptoms (Mohler et al. 2002).”
- The biology of fear- and anxiety-related behaviors (2002, background): “Several GABAA receptor subtypes have been described.(96,97) The diazepam-sensitive α2-GABAA subtype appears to be specifically involved in anxiolysis.”
- Expression of Distinct α Subunits of GABAA Receptor Regulates Inhibitory Synaptic Strength (2004, positive): “Given that the presence of 2 and 6 subunits has opposite actions on benzodiazepine sensitivity (Mohler et al. 2002; Olsen and MacDonald 2002), our data suggest that a developmental increase in the expression of both subunits but in different receptor subtypes occurs at CGC’s inhibitory synapses.”
- Metabotropic glutamate receptors as novel targets for anxiety and stress disorders (2005, background): “Recent advances in the molecular biology of the GABA A receptor complex have indicated that the sedation and memory impairment linked to benzodiazepine treatment are attributable to actions on α 1 -containing GABA receptor complexe”
- Molecular and neuronal substrates for general anaesthetics (2004, neutral): “The subunit combinations α4β2γ/α4βnδ, α5β1/3γ2, α6β2/3γ2 and α6βnδ each represent less than 5% of all receptors in the brai”
- Drugs for allosteric sites on receptors. (2014, background): “In addition to PAMs and NAMs, silent allosteric modulators (SAMs; also known as neutral allosteric ligands) bind at allosteric sites and can block the activity of PAMs and NAMs, yet they have no effect on orthosteric ligand responses (1-14).”
- Allosteric modulators of GPCRs: a novel approach for the treatment of CNS disorders (2009, background): “Benzodiazepines provide an effective and safe approach to the treatment of anxiety and sleep disorders without inducing the potentially lethal effects of direct-acting GABA receptor agonist”