Serotonin modulates the properties of ascending commissural interneurons in the neonatal mouse spinal cord.
Enviado por Manuel Esteban Diaz-Rios el
Título | Serotonin modulates the properties of ascending commissural interneurons in the neonatal mouse spinal cord. |
Publication Type | Journal Article |
Year of Publication | 2006 |
Autores | Zhong, G, Díaz-Ríos, M, Harris-Warrick, RM |
Journal | J Neurophysiol |
Volume | 95 |
Issue | 3 |
Pagination | 1545-55 |
Date Published | 2006 Mar |
ISSN | 0022-3077 |
Palabras clave | Action Potentials, Animals, Animals, Newborn, Biological Clocks, Dose-Response Relationship, Drug, In Vitro Techniques, Interneurons, Locomotion, Lumbar Vertebrae, Mice, Mice, Inbred ICR, Neural Pathways, Serotonin, Spinal Cord |
Abstract | The interneuron populations that constitute the central pattern generator (CPG) for locomotion in the mammalian spinal cord are not well understood. We studied the properties of a set of commissural interneurons whose axons cross and ascend in the contralateral cord (aCINs) in the neonatal mouse. During N-methyl-D-aspartate (NMDA) and 5-HT-induced fictive locomotion, a majority of lumbar (L2) aCINs examined were rhythmically active; most of them fired in phase with the ipsilateral motoneuron pool, but some fired in phase with contralateral motoneurons. 5-HT plays a critical role in enabling the locomotor CPG to function. We found that 5-HT increased the excitability of aCINs by depolarizing the membrane potential, reducing the postspike afterhyperpolarization amplitude, broadening the action potential, and decreasing the action potential threshold. Serotonin had no significant effect on the input resistance and sag amplitude of aCINs. These results support the hypothesis that aCINs play important roles in coordinating left-right movements during fictive locomotion and thus may be component neurons in the locomotor CPG in neonatal mice. |
DOI | 10.1152/jn.01103.2005 |
Alternate Journal | J. Neurophysiol. |
PubMed ID | 16338993 |
Grant List | R01-NS-35631 / NS / NINDS NIH HHS / United States R01-NS-50943 / NS / NINDS NIH HHS / United States |