5-HT inhibits N-type but not L-type Ca2+ channels via 5-HT1A receptors in lamprey spinal neurons
Hill, RH;Svensson, E;Dewael, Y;Grillner, S
(2003) European Journal of Neuroscience — Vol. 18, n° 11, p. 2919-2924 (2003)
Files
No attached file found for this publication.
Details
Authors
Hill, RH
Author
Svensson, E
Author
Dewael, Y
Author
Grillner, S
Author
Abstract
5-HT is a potent modulator of locomotor activity in vertebrates. In the lamprey, 5-HT dramatically slows fictive swimming. At the neuronal level it reduces the postspike slow afterhyperpolarization (sAHP), which is due to apamin-sensitive Ca2+-dependent K+ channels (K-Ca). Indirect evidence in early experiments suggested that the sAHP reduction results from a direct action of 5-HT on K-Ca channels rather than an effect on the Ca2+ entry during the action potential [Wallen et al., (1989) J. Neurophysiol., 61, 759-768]. In view of the characterization of different subtypes of Ca2+ channels with very different properties, we now reinvestigate if there is a selective action of 5-HT on a Ca2+ channel subtype in dissociated spinal neurons in culture. 5-HT reduced Ca2+ currents from high voltage activated channels. N-type, but not L-type, Ca2+ channel blockers abolished this 5-HT-induced reduction. It was also confirmed that 5-HT depresses Ca2+ currents in neurons, including motoneurons, in the intact spinal cord. 8-OH-DPAT, a 5-HT1A receptor agonist, also inhibited Ca2+ currents in dissociated neurons. After incubation in pertussis toxin, to block G(i/o) proteins, 5-HT did not reduce Ca2+ currents, further indicating that the effect is caused by an activation of 5-HT1A receptors. As N-type, but not L-type, Ca2+ channels are known to mediate the activation of K-Ca channels and presynaptic transmitter release at lamprey synapses, the effects of 5-HT reported here can contribute to a reduction in both actions.
Hill, R., Svensson, E., Dewael, Y., & Grillner, S. (2003). 5-HT inhibits N-type but not L-type Ca2+ channels via 5-HT1A receptors in lamprey spinal neurons. European Journal of Neuroscience, 18(11), 2919-2924. https://doi.org/10.1046/j.1460-9568.2003.03051.x (Original work published 2003)