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J Neurophysiol 89: 954-959, 2003. First published October 23, 2002; doi:10.1152/jn.00753.2002
0022-3077/03 $5.00
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J Neurophysiol (February 1, 2003). 10.1152/jn.00753.2002
Submitted on Submitted 3 September 2002; accepted in final form 19 October 2002

5-HT2 Receptors Promote Plateau Potentials in Turtle Spinal Motoneurons by Facilitating an L-Type Calcium Current

Jean-François Perrier and Jørn Hounsgaard

Department of Medical Physiology, Panum Institute, University of Copenhagen, DK 2200 Copenhagen N, Denmark

Perrier, Jean-François and Jørn Hounsgaard. 5-HT2 Receptors Promote Plateau Potentials in Turtle Spinal Motoneurons by Facilitating an L-Type Calcium Current. J. Neurophysiol. 89: 954-959, 2003. The effects of serotonin (5-HT) on intrinsic properties of spinal motoneurons were investigated with intracellular recordings in a slice preparation from adult turtles. In 55% of the cells that were recorded, addition of 5-HT to the extracellular medium promoted plateau potentials as revealed by the response to depolarizing current pulses applied through the intracellular electrode. In the remaining 45% of cells, 5-HT had an inhibitory effect. However, when tested with an applied electric field that preferentially polarizes distal dendrites, 5-HT facilitated plateau potentials in 100% of the cells. Plateau potentials were also promoted by 5-HT focally applied on a dendrite by iontophoresis. Applied near the soma, 5-HT either promoted plateau potentials or inhibited spike generation. The latter effect was accompanied by a decrease in input resistance. Voltage-clamp recordings showed that the facilitation of plateau potentials mediated by L-type Ca2+ channels was due to activation of 5-HT2 receptors. These findings show that 5-HT regulates intrinsic properties of motoneurons in opposite ways: activation of 5-HT receptors in the soma region inhibits spike generation and plateau potentials, while activation of 5-HT2 receptors in the dendrites and the soma region promotes spiking by facilitation of plateau potentials mediated by L-type Ca2+ channels.




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