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J Neurophysiol (August 16, 2006). doi:10.1152/jn.00352.2006
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Submitted on April 5, 2006
Accepted on August 9, 2006

Emergence of intrinsic bursting in trigeminal sensory neurons parallels the acquisition of mastication in weanling rats

Frédéric Brocard1, Dorly Verdier2, Isabel Arsenault2, James P. Lund3, and Arlette Kolta4*

1 Centre de Recherche en Sciences Neurologiques, Université de Montréal, Montreal, Canada; Laboratoire Plasticité et Physio-Pathologie de la Motricité, Université de la Méditerranée, Marseille, France
2 Centre de Recherche en Sciences Neurologiques, Université de Montréal, Montreal, Canada
3 Centre de Recherche en Sciences Neurologiques, Université de Montréal, Montreal, Canada; Faculty of dentistry, McGill University, Montreal, Canada
4 Centre de Recherche en Sciences Neurologiques, Université de Montréal, Montreal, Canada; Faculté de Médecine dentaire, Université de Montréal, Montreal, Canada; Faculty of dentistry, McGill University, Montreal, Canada

* To whom correspondence should be addressed. E-mail: arlette.kolta{at}umontreal.ca.

There is increasing evidence that a subpopulation of neurons in the dorsal principal sensory trigeminal nucleus are not simple sensory relays to the thalamus, but may form the core of the central pattern generating circuits responsible for mastication. In this paper, we used whole-cell patch recordings in brainstem slices of young rats to show that these neurons have intrinsic bursting abilities that persist in absence of extracellular Ca++. Application of different K+ channel blockers affected duration and firing rate of bursts, but left bursting ability intact. Bursting was voltage-dependent, and was abolished by low concentrations of Na+ channel blockers. The proportion of bursting neurons increased dramatically in the second postnatal week, in parallel with profound changes in several electrophysiological properties. This is the period in which masticatory movements appear and mature. Bursting was associated with the development of an after-depolarization that depend on maturation of a persistent sodium conductance (INaP). An interesting finding was that the occurrence of bursting and the magnitude of INaP were both modulated by the extracellular concentration of Ca++. Lowering extracellular [Ca++] increased both INaP and probability of bursting. We suggest that these mechanisms underlie burst generation in mastication and that similar processes may be found in other motor pattern generators.




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