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[Effect of GABA-positive drugs on the background and superior sagittalis sinus-electrostimulated activity of neurons in the nucleus trigeminalis caudalis of rats].

Abstract
There is extensive clinical evidence for the high efficacy of GABA-ergic drugs in prophylactic and abortive treatment of migraine and cluster headache, while the mechanisms of anticephalgic drugs action are not clear, in particular, because of insufficient number of investigations on experimental headache models. In this study, the influence of baclofen (i.v.) in doses 2.5, 5, 10, and 15 mg/kg and valproate (i.v.) in doses 25, 50, 100, and 200 mg/kg on the background activity of the trigeminal nucleus caudalis neurons and that evoked by electrical stimulation of the superior sagittalis sinus was investigated in series of acute experiments on rats. It is established, that baclofen and valproate reduce both the background and evoked activity of trigeminal complex neurons in dose-dependent manner, thus determining the role of GABA-A and GABA-B receptors in realization of this effect. These results provide experimental basis for explanation of the clinical efficacy of the GABA-positive drugs in vascular headaches.
AuthorsA Iu Sokolov, A V Amelin, Iu D Ignatov, S S Panteleev
JournalEksperimental'naia i klinicheskaia farmakologiia (Eksp Klin Farmakol) 2008 Sep-Oct Vol. 71 Issue 5 Pg. 3-7 ISSN: 0869-2092 [Print] Russia (Federation)
PMID19093363 (Publication Type: English Abstract, Journal Article)
Chemical References
  • GABA Agonists
  • Receptors, GABA-A
  • Receptors, GABA-B
  • gamma-Aminobutyric Acid
  • Valproic Acid
  • Baclofen
Topics
  • Animals
  • Baclofen (pharmacology)
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Electric Stimulation
  • GABA Agonists (pharmacology)
  • Headache (drug therapy, metabolism, physiopathology)
  • Neurons (metabolism)
  • Rats
  • Rats, Wistar
  • Receptors, GABA-A (metabolism)
  • Receptors, GABA-B (metabolism)
  • Superior Sagittal Sinus (metabolism, physiopathology)
  • Valproic Acid (pharmacology)
  • gamma-Aminobutyric Acid (metabolism)

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