Augmenting Effect of Serotonin on the Voltage-Dependent Ca'2+' Current and Subsequently Activated K'+' Current in Aplysia Neurons
|
Accession number;07A0040439
|
| Title;Augmenting Effect of Serotonin on the Voltage-Dependent Ca'2+' Current and Subsequently Activated K'+' Current in Aplysia Neurons |
| Author;
KAWASAKI SATOSHI
(Department of Physiology, School of Medicine, Iwate Medical University)
KIMURA SHINGO
(Department of Physiology, School of Medicine, Iwate Medical University)
WATANABE SHUJI
(Department of Physiology, School of Medicine, Iwate Medical University)
FUJITA REIKO
(Department of Chemistry, School of Liberal Arts and Sciences, Iwate Medical University)
MATSUMOTO MITSUHIKO
(Department of Occupational Therapy, School of Health Sciences, Hirosaki University)
SASAKI KAZUHIKO
(Department of Physiology, School of Medicine, Iwate Medical University)
|
Journal Title;Tohoku J Exp Med
|
Journal Code:G0649A
|
ISSN:0040-8727
|
|
VOL.211;NO.1;PAGE.31-41 (J-STAGE)(2007)
|
| Figure&Table&Reference;FIG.6, REF.24 |
| Pub. Country;Japan |
| Language;English |
| Abstract;Receptor-induced activation of protein kinase C (PKC) plays an important role in modulation of various types of ionic channels in neurons. For example, PKC causes facilitation or long-lasting activation of certain ionic channels involved in spike firing after the receptor stimulation. We investigated the effect of serotonin (5-HT) on the voltage-dependent Ca'2+' channels in RB and RC neurons of Aplysia ganglia under voltage clamp. An outward current response was induced by voltage change of the cell membrane from -60 mV to +10 mV. Application of 5-HT significantly augmented the outward current response to the voltage change. Both the outward current and the augmenting effect of 5-HT markedly decreased when examined in either Ca'2+'-free, 10 mM tetraethylammonium, or 0.3 mM Cd'2+'-solution, indicating the current to be Ca'2+'-activated K'+' current produced by Ca'2+' entry. Intracellular application of either guanosine 5'-O-(2-thiodiphosphate) or cholera toxin (CTX), reagents for G-proteins, irreversibly blocked the augmenting effect of 5-HT. Application of phorbol dibutylate (PDBu), an activator of PKC, augmented the outward current and the effect of 5-HT was occluded after PDBu application. Staurosporine, a specific inhibitor of PKC, markedly suppressed the augmenting effects of both 5-HT and PDBu on the outward current. However, either 5-HT or PDBu did not augment the Ca'2+'-activated K'+' current induced by intracellular injection of Ca'2+' but rather depressed it. These results suggest that stimulation of 5-HT receptor may activate a novel type of CTX-sensitive G-protein and subsequent PKC, and that phosphorylation of voltage-dependent Ca'2+' channels may result in the increase in Ca'2+' entry and subsequent Ca'2+'-activated K'+' current. The mechanism may contribute to retain the long-lasting activation without broadening of the spike width during the excitatory response to 5-HT in these neurons. (Author abst.) |
|
|
|
Related Articles;
|
|
|
