Detail of "65474-79-5"

Reference

Animal behavioral analysis of putative endogenous ligands

Animal behavioral analysis of putative endogenous ligands. Crawley, J. N. (Cent. Res. Dev. Dep., E I DuPont de Nemours and Co., Glenolden, PA 19036, USA). Pharmacol. Benzodiazepines, Proc. Conf., Meeting Date 1982, 549-59. Edited by: Usdin, Earl. Verlag Chem.: Weinheim, Fed. Rep. Ger. (English) 1983. CODEN: 52AKA7. DOCUMENT TYPE: Conference CA Section: 1 (Pharmacology) In order to detect the anxiolytic or anxiogenic properties of proposed endogenous ligands for the benzodiazepine receptor, the actions of purines, nicotinamide [98-92-0], and b-carbolines on anxiety-related behaviors in mice was detd. Several purines and 3-hydroxymethyl-b-carboline [65474-79-5] blocked the anxiolytic actions of diazepam [439-14-5] in an exploratory model for anxiety-related behaviors in mice. None of these proposed endogenous ligands for the benzodiazepine binding site mimicked the anxiolytic effects of diazepam in this system, although analogous sedative effects were seen at higher doses. This model system may be one useful technique for detg. the anxiolytic properties of naturally-occurring agonists and antagonists for the brain benzodiazepine receptor.

Electrophysiological studies of benzodiazepine actions

Electrophysiological studies of benzodiazepine actions. Geller, H. M.; Krespan, B.; Baldino, F., Jr.; Springfield, S. (Rutgers Med. Sch., UMDNJ, Piscataway, NJ 08854, USA). Pharmacol. Benzodiazepines, Proc. Conf., Meeting Date 1982, 465-72. Edited by: Usdin, Earl. Verlag Chem.: Weinheim, Fed. Rep. Ger. (English) 1983. CODEN: 52AKA7. DOCUMENT TYPE: Conference CA Section: 1 (Pharmacology) Section cross-reference(s): 2 In tissue culture of hypothalamic neurons, GABA [56-12-2] applied in the vicinity of the neuron by iontophoresis depressed neuronal activity. There was a slight redn. in the efficacy of GABA during perfusion of the benzodiazepine antagonist 3-hydroxymethyl-b-carboline [65474-79-5], whereas another antagonist Ro 14-7437 [78756-03-3] induced a decrease in GABA efficacy in a majority of cells and a potentiation of GABA efficacy in a minority of cells. Spontaneous neuron activity was not affected by antagonist perfusion. Apparently, GABAergic transmission does not require occupancy of the benzodiazepine receptor to be efficacious. The role of benzodiazepines thus seems to be a permissive one in facilitation of GABAergic neurotransmission. Moreover, an endogenous ligand would not appear to have an obligatory role in GABAergic neurotransmission. In rat cerebral cortex neurons, the anticonvulsant valproate [99-66-1] increased the efficacy of iontophoretically applied GABA. The expts. on the interactions of anticonvulsants and GABA suggest a model with at least 3 major components involved in regulating the permeability of the Cl- ionophore: the GABA receptor, the benzodiazepine receptor, and the Cl- ionophore itself. The primary regulator of Cl- channel conductance appears to be GABA.