|Boris Lamotte d'Incamps
Tel: +33 1 42 86 38 12
Fax: +33 1 49 27 90 62
| My research
activity is focussed on the physiology of normal and pathological
spinal motor neurons. This includes their intrinsic properties as
well as the spinal circuits which control their activity.
Currently, I am working on the recurrent inhibition of spinal motoneurons (the neurons responsible for muscle contraction). This di-synaptic pathway involves i) the synapse of the recurrent collateral of the motoneuron axons that excites the Renshaw cells, and ii) the inhibitory synappse between the Renshaw cells and the motoneurons (see Figure). Although this was the first inhibitory circuit to be studied in the vertebrate central nervous system (Renshaw 1941, 1946, Eccles et al. 1954), we still do not understand its function (for reviews see Windhorst 1996, Alvarez and Fyffe 2007). In collaboration with P. Ascher (CNRS UMR 8118, Paris), we studied the pharmacological properties of the synapse between the recurrent axonal collateral of motoneurons and Renshaw cells. We demonstrated that the recurrent synapse activates at least four types of ionotropic receptors, in particular, acetylcholine α7 receptors and glutamate NMDA receptors. The characteristics of these synaptic currents led us to propose that the Renshaw cell response may switch between a short high frequency burst and a longer tonic discharge (Lamotte d'Incamps and Ascher 2008). We are now investigating the spillover of acetylcholine at this synapse and the efficiency of its control by the enzymatic degradation of the neurotransmitter.
Recently, in a theoretical study with Claude Meunier, we have extended the cable theory to allow the description of heterogeneities along the dendrites (or axons) of neurons. This work allowed us to link the influence of heterogeneities of the morphological and electrical properties of neurons to their integrative properties (Meunier and Lamotte d'Incamps 2008).
In collaboration with J. Durand (CNRS UMR 6196, Marseille, France) we have compared the electrical properties of lumbar motoneurons from mice transfected with the human mutated gene SOD1, considered as a model of Amyotrophic Lateral sclerosis (ALS), with the motoneuron properties of control mice (Bories et al. 2007).