In the intact rat adrenal gland perfused with an oxygenated Krebs-bicarbonate solution at 37 degrees C, the electrical field stimulation of splanchnic nerves (100 V, 0.5 ms duration, 10 Hz during 10 s) produced transient catecholamine release peaks that were reproduced in subsequent stimuli, applied at 8-min intervals. Omega-Conotoxin GVIA (0.3 microM) caused only a modest inhibition of the secretory response, suggesting that the N-subtype of voltage-dependent Ca2+ channels are scarcely involved in such a response. Both omega-conotoxin MVIIC (1 microM) and furnidipine (1 microM) halved the secretion, suggesting that the L- and P/Q-types of Ca2+ channels were involved. N-type Ca2+ channels appear to be involved in the maintenance of secretion in response to sustained stimulus since omega-conotoxin GVIA (0.3 microM) reduced the catecholamine output to 28%. When secretion was elicited by acetylcholine (10 microM), furnidipine reduced the catecholamine release by 50% and omega-conotoxin MVIIC by 40%, whereas omega-conotoxin GVIA did not modify the response. The K+-induced secretory responses (23.6 mM K+, 15 s) were reduced 75% by furnidipine and 45% by omega-conotoxin MVIIC, indicating that this type of stimulation preferentially recruited L-type channels. These data show that electrical stimulation recruits Ca2+ channel subtypes different from those recruited by direct depolarization of chromaffin cells.
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http://dx.doi.org/10.1007/s002109900041 | DOI Listing |
BMC Complement Med Ther
December 2024
Department of Pediatrics, E-Da Hospital, I-Shou University, No. 1, Yi-Da Road, Yan-Chao District, Kaohsiung City, 82445, Taiwan, R.O.C..
J Physiol
September 2024
Department of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, USA.
The subiculum is a key region of the brain involved in the initiation of pathological activity in temporal lobe epilepsy, and local GABAergic inhibition is essential to prevent subicular-originated epileptiform discharges. Subicular pyramidal cells may be easily distinguished into two classes based on their different firing patterns. Here, we have compared the strength of the GABAa receptor-mediated inhibitory postsynaptic currents received by regular- vs.
View Article and Find Full Text PDFEur J Pharmacol
June 2024
Universitat Autònoma de Barcelona, Department of Cell Biology, Physiology and Immunology, Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain. Electronic address:
Introduction: Hyoscine butylbromide (HBB) is one of the most used antispasmodics in clinical practice. Recent translational consensus has demonstrated a similarity between human colonic motor patterns studied ex vivo and in vivo, suggesting ex vivo can predict in vivo results. It is unclear whether the mechanism of action of antispasmodics can predict different use in clinical practice.
View Article and Find Full Text PDFEur J Pharmacol
January 2024
School of Medicine, Fu Jen Catholic University, No.510, Zhongzheng Rd., Xinzhuang Dist, New Taipei City, 24205, Taiwan; Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, 33303, Taiwan. Electronic address:
The present study evaluated the effect of ursolic acid, a natural pentacyclic triterpenoid, on glutamate release in rat cortical nerve terminals (synaptosomes) and its neuroprotection in a kainic acid-induced excitotoxicity rat model. In cortical synaptosomes, ursolic acid produced a concentration-dependent inhibition of evoked glutamate release with a half-maximum inhibition of release value of 9.5 μM, and calcium-free medium and the P/Q -type Ca channel blocker, ω-agatoxin IVA, but not ω-conotoxin GVIA, an N-type Ca channel blocker, prevented the ursoloic acid effect.
View Article and Find Full Text PDFMol Neurobiol
April 2024
Department of Biophysics, Meram Faculty of Medicine, University of Konya-NE, Konya, Turkey.
High-voltage-gated calcium channels have pivot role in the cellular and molecular mechanisms of various neurological disorders, including epilepsy. Similar to other calcium channels, P/Q-type calcium channels (Ca2.1) are also responsible for vesicle release at synaptic terminals.
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