Effects of ginkgolide B on neuronal discharges in paraventricular nucleus of rat hypothalamic slices.
- Author:
Yue LIN
1
;
Ru WANG
;
Xin WANG
;
Rui-Rong HE
;
Yu-Ming WU
Author Information
- Publication Type:Journal Article
- MeSH: 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; pharmacology; Action Potentials; drug effects; Analysis of Variance; Animals; Animals, Newborn; Calcium Channel Agonists; pharmacology; Dose-Response Relationship, Drug; Drug Interactions; Fibrinolytic Agents; pharmacology; Ginkgolides; pharmacology; Glutamic Acid; pharmacology; In Vitro Techniques; Lactones; pharmacology; Neural Inhibition; drug effects; Neurons; drug effects; Paraventricular Hypothalamic Nucleus; cytology; Potassium Channel Blockers; pharmacology; Rats; Rats, Sprague-Dawley; Tetraethylammonium; pharmacology
- From: Neuroscience Bulletin 2008;24(6):345-350
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study the central role of ginkgolide B (BN52021) in regulating cardiovascular function of nerve center by examining the effects of ginkgolide B on the electrical activity of rat paraventricular nucleus (PVN) neurons in hypothalamic slice preparation and to elucidate the mechanism involved.
METHODSExtracellular single-unit discharge recording technique.
RESULTS(1) In response to the application of ginkgolide B (0.1, 1, 10 micromol/L; n = 27) into the perfusate for 2 min, the spontaneous discharge rates (SDR) of 26 (26/27, 96.30%) neurons were significantly decreased in a dose-dependent manner. (2) Pretreatment with L-glutamate (L-Glu, 0.2 mmol/L) led to a marked increase in the SDR of all 8 (100%) neurons in an epileptiform pattern. The increased discharges were suppressed significantly after ginkgolide B (1 micromol/L) was applied into the perfusate for 2 min. (3) In 8 neurons, perfusion of the selective L-type calcium channel agonist, Bay K 8644 (0.1 micromol/L), induced a significant increase in the discharge rates of 8 (8/8, 100%) neurons, while ginkgolide B (1 micromol/L) applied into the perfusate, could inhibit the discharges of 8 (100%) neurons. (4) In 8 neurons, the broad potassium channels blocker, tetraethylammonium (TEA, 1 mmol/L) completely blocked the inhibitory effect of ginkgolide B (1 micromol/L).
CONCLUSIONThese results suggest that ginkgolide B can inhibit the electrical activity of paraventricular neurons. The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and potentially concerned with delayed rectifier potassium channel (K(DR)).
