Ionic Basis for Serotonin-Induced Bistable Membrane Properties in Guinea Pig Trigeminal Motoneurons

• Published in: Journal of neurophysiology 1998-06, Vol.79 (6), p.2847-2856
• Main Authors: Hsiao, Chie-Fang, Negro, Christopher A. Del, Trueblood, Peggy R, Chandler, Scott H
• Format: Article
• Language: English
• Subjects: 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology; Animals; Calcium Channel Agonists - pharmacology; Calcium Channel Blockers - pharmacology; Cesium - pharmacology; Electrophysiology; Guinea Pigs; In Vitro Techniques; Ion Channels - physiology; Membrane Potentials - drug effects; Membrane Potentials - physiology; Membranes - chemistry; Membranes - drug effects; Membranes - physiology; Motor Neurons - chemistry; Motor Neurons - drug effects; Motor Neurons - physiology; Nifedipine - pharmacology; Serotonin - chemistry; Serotonin - pharmacology; Sodium Channels - drug effects; Sodium Channels - metabolism; Trigeminal Nerve - chemistry; Trigeminal Nerve - cytology; Trigeminal Nerve - physiology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.1998.79.6.2847

Chie-Fang Hsiao 1 , Christopher A. Del Negro 1 , Peggy R. Trueblood 2 , and Scott H. Chandler 1 1  Department of Physiological Science, University of California at Los Angeles, Los Angeles, 90095-1568; and 2  Department of Physical Therapy, California State University at Fresno, Fresno, California 93740 Hsiao, Chie-Fang, Christopher A. Del Negro, Peggy R. Trueblood, and Scott H. Chandler. Ionic basis for serotonin-induced bistable membrane properties in guinea pig trigeminal motoneurons. J. Neurophysiol. 79: 2847-2856, 1998. Intracellular recordings and pharmacological manipulations were employed to investigate the ionic basis for serotonin-induced bistable membrane behaviors in guinea pig trigeminal motoneurons (TMNs). In voltage clamp, 10 µM serotonin (5-HT) induced a region of negative slope resistance (NSR) in the steady-state current-voltage ( I-V ) relationship at potentials less negative than 58 mV, creating the necessary conditions for membrane bistability. The contributions of sustained Na + and Ca 2+ currents to the generation of the NSR were investigated using specific ion channel antagonists and agonists. The NSR was eliminated by the L-type Ca 2+ channel antagonist nifedipine (5-10 µM), indicating the contribution of L channels. In nifedipine, inward rectification was present in the I-V relationship in a similar voltage range (greater than 58 mV). This region was subsequently linearized by tetrodotoxin (TTX), indicating the presence of a persistent Na + current. When the 5-HT-induced NSR was eliminated by perfusion in low Ca 2+ solution (0.4 mM), it was restored by the Na + channel agonist veratridine (10 µM). Commensurate with bistability, in current clamp during bath application of 5-HT, plateau potentials were elicited by transient depolarizing or hyperpolarizing stimuli. Plateau potentials evoked by depolarization were observed under control and TTX conditions, but were blocked by nifedipine, suggesting the participation of an L-type Ca 2+ current. Plateau potentials initiated after release from hyperpolarization (anode break) were blocked by 300 µM Ni 2+ , suggesting the responses relied on deinactivation of a T-type Ca 2+ current. Conditional bursting was also observed in 5-HT. Nifedipine or low Ca 2+ solutions blocked bursting, and the L-channel agonist Bay K 8644 (10 µM) extended the duration of individual bursts, demonstrating the role of L-type Ca 2+ currents. Interestingly, when bursting was blocked by nifedipine or low Ca 2+ , it c