Lamotte D'Incamps B


Full name : Lamotte d'Incamps Boris

First name : Boris

Mail : CNRS-Univ. Paris Descartes Paris 75006

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Country : France

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References (10)

Title : Early intrinsic hyperexcitability does not contribute to motoneuron degeneration in amyotrophic lateral sclerosis - Leroy_2014_Elife_3_
Author(s) : Leroy F , Lamotte d'Incamps B , Imhoff-Manuel RD , Zytnicki D
Ref : Elife , 3 : , 2014
Abstract : In amyotrophic lateral sclerosis (ALS) the large motoneurons that innervate the fast-contracting muscle fibers (F-type motoneurons) are vulnerable and degenerate in adulthood. In contrast, the small motoneurons that innervate the slow-contracting fibers (S-type motoneurons) are resistant and do not degenerate. Intrinsic hyperexcitability of F-type motoneurons during early postnatal development has long been hypothesized to contribute to neural degeneration in the adult. Here, we performed a critical test of this hypothesis by recording from identified F- and S-type motoneurons in the superoxide dismutase-1 mutant G93A (mSOD1), a mouse model of ALS at a neonatal age when early pathophysiological changes are observed. Contrary to the standard hypothesis, excitability of F-type motoneurons was unchanged in the mutant mice. Surprisingly, the S-type motoneurons of mSDO1 mice did display intrinsic hyperexcitability (lower rheobase, hyperpolarized spiking threshold). As S-type motoneurons are resistant in ALS, we conclude that early intrinsic hyperexcitability does not contribute to motoneuron degeneration.
ESTHER : Leroy_2014_Elife_3_
PubMedSearch : Leroy_2014_Elife_3_
PubMedID: 25313866

Title : Subunit composition and kinetics of the Renshaw cell heteromeric nicotinic receptors - Lamotte d'Incamps_2013_Biochem.Pharmacol_86(8)_1114
Author(s) : Lamotte d'Incamps B , Ascher P
Ref : Biochemical Pharmacology , 86 :1114 , 2013
Abstract : In Renshaw cells (RCs) of newborn mice, activation of motoneurons elicits a four-component synaptic current (EPSC) mediated by two glutamate receptors and two nicotinic receptors (nAChRs). We have analyzed the nicotinic component of the EPSC which is blocked by dihydro-beta-erythroidine (DHbetaE) with the dual objective of identifying the nAChR subunits involved and of understanding the kinetics of the response. The sensitivity to DHbetaE of the peak of the EPSC was differentially affected by genetic deletion of three specific nAChR subunits: alpha2, beta2 and beta4. The comparison of these effects with published findings on recombinant receptors suggests that, in WT mice, two heteromeric assemblies, alpha4beta2 and alpha2beta4, coexist in variable proportions in a given RC. Some results seem to require, however, the involvement of an additional subunit. The effects of DHbetaE on the decay of the EPSCs were compared in WT mice and in PRiMA(-/-) mice, in which the decay is prolonged by the absence of central acetylcholinesterase. In PRiMA(-/-) mice DHbetaE shortened the decay of the EPSC. In WT mice it did not alter the decay but reduced the amplitude of both components of the EPSC. The results can be interpreted by assuming that the nAChRs exist in two stoichiometries, subsynaptic "low sensitivity" nAChRs and extrasynaptic "high sensitivity" nAChRs activated by spillover.
ESTHER : Lamotte d'Incamps_2013_Biochem.Pharmacol_86(8)_1114
PubMedSearch : Lamotte d'Incamps_2013_Biochem.Pharmacol_86(8)_1114
PubMedID: 23811311

Title : Mechanisms shaping the slow nicotinic synaptic current at the motoneuron-renshaw cell synapse - Lamotte d'Incamps_2012_J.Neurosci_32_8413
Author(s) : Lamotte d'Incamps B , Krejci E , Ascher P
Ref : Journal of Neuroscience , 32 :8413 , 2012
Abstract : In spinal cord slices from newborn mice we have analyzed the kinetics of the EPSCs mediated by heteromeric nicotinic receptors at the motoneuron-Renshaw cell (MN-RC) synapse. The miniature EPSCs decay with a time constant of 13.0 +/- 1.1 ms whereas the decay of the evoked EPSCs (eEPSCs) is biphasic, with time constants of 15.6 +/- 0.8 and 124.8 +/- 9.0 ms. The slow component becomes prominent during a repetitive stimulation, but its time constant is unchanged. It is selectively reduced by the addition of acetylcholinesterase (AChE), and thus appears to involve ACh spillover. The constancy of the slow time constant during a train is best explained by a local spillover activating high-affinity receptors. In many cells a fraction of the eEPSC originates in neighboring RCs and is transmitted by the low-pass filter of the gap junctions. The component transmitted electrically can be eliminated by meclofenamic acid, a blocker of gap junctions. The local spillover produced by a repetitive stimulation was compared with the long-range spillover produced by inactivation of AChE. The pharmacological inactivation of AChE by neostigmine caused the appearance of an ultra-slow (second range) decay component in eEPSCs and also a continuous inward current interpreted as resulting from a continuous ACh presence. In animals lacking functional AChE in the CNS (PRiMA(-/-) mice) the EPSCs resembled those observed in neostigmine but the steady inward current was much smaller, suggesting an adaptation to the absence of AChE.
ESTHER : Lamotte d'Incamps_2012_J.Neurosci_32_8413
PubMedSearch : Lamotte d'Incamps_2012_J.Neurosci_32_8413
PubMedID: 22699921

Title : Near-complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase - Farar_2012_J.Neurochem_122_1065
Author(s) : Farar V , Mohr F , Legrand M , Lamotte d'Incamps B , Cendelin J , Leroy J , Abitbol M , Bernard V , Baud F , Fournet V , Houze P , Klein J , Plaud B , Tuma J , Zimmermann M , Ascher P , Hrabovska A , Myslivecek J , Krejci E
Ref : Journal of Neurochemistry , 122 :1065 , 2012
Abstract : Acetylcholinesterase AChE rapidly hydrolyzes acetylcholine. At the neuromuscular junction AChE is mainly anchored in the extracellular matrix by the collagen Q whereas in the brain AChE is tethered by the proline-rich membrane anchor PRiMA The AChE-deficient mice in which AChE has been deleted from all tissues have severe handicaps Surprisingly PRiMA KO mice in which AChE is mostly eliminated from the brain show very few deficits. We now report that most of the changes observed in the brain of AChE-deficient mice and in particular the high levels of ambient extracellular acetylcholine and the massive decrease of muscarinic receptors are also observed in the brain of PRiMA KO. However the two groups of mutants differ in their responses to AChE inhibitors. Since PRiMA-KO mice and AChE-deficient mice have similar low AChE concentrations in the brain but differ in the AChE content of the peripheral nervous system these results suggest that peripheral nervous system AChE is a major target of AChE inhibitors and that its absence in AChE deficient mice is the main cause of the slow development and vulnerability of these mice. At the level of the brain the adaptation to the absence of AChE is nearly complete.
ESTHER : Farar_2012_J.Neurochem_122_1065
PubMedSearch : Farar_2012_J.Neurochem_122_1065
PubMedID: 22747514

Title : Four excitatory postsynaptic ionotropic receptors coactivated at the motoneuron-Renshaw cell synapse - Lamotte d'Incamps_2008_J.Neurosci_28_14121
Author(s) : Lamotte d'Incamps B , Ascher P
Ref : Journal of Neuroscience , 28 :14121 , 2008
Abstract : Renshaw cells (RCs) are spinal interneurons excited by collaterals of the axons of motoneurons (MNs). They respond to a single motoneuronal volley by a surprisingly long (tens of milliseconds) train of action potentials. We have analyzed this synaptic response in spinal cord slices of neonatal mice in light of recent observations suggesting that the MN axons release both acetylcholine and glutamate. We found that the RC synaptic current involves four components of similar amplitudes mediated by two nicotinic receptors (nAChRs, tentatively identified as alpha(7) homomers and alpha(4)beta(2) heteromers) and two glutamate receptors (AMPARs and NMDARs). The decay time constants of the four components cover a wide range: from 3.6 +/- 2.2 ms (alpha(7) nAChRs) to 54.6 +/- 19.5 ms (NMDARs, at -45 mV). The RC discharge can be separated into an initial doublet of high-frequency action potentials followed by later spikes with a variable latency and longer interspike intervals. The initial doublet involves the four ionotropic receptors as well as endogenous voltage-dependent conductances. The late discharge depends on NMDARs, but these receptors must be primed by the initial depolarization. The activation of the NMDARs is prolonged by the fact that their slow deactivation is further slowed by depolarization. The formation of the initial doublet is favored by hyperpolarization, whereas the late discharge is favored by depolarization. This suggests that in physiological conditions the pattern of discharge of the RC in response to a MN input may alternate between a phasic and a tonic response.
ESTHER : Lamotte d'Incamps_2008_J.Neurosci_28_14121
PubMedSearch : Lamotte d'Incamps_2008_J.Neurosci_28_14121
PubMedID: 19109494

Title : Postnatal electrical and morphological abnormalities in lumbar motoneurons from transgenic mouse models of amyotrophic lateral sclerosis - Amendola_2007_Arch.Ital.Biol_145_311
Author(s) : Amendola J , Gueritaud JP , Lamotte d'Incamps B , Bories C , Liabeuf S , Allene C , Pambo-Pambo A , Durand J
Ref : Archives Italiennes de Biologie , 145 :311 , 2007
Abstract : Antidromically identified lumbar motoneurons intracellularly recorded in the entire brainstem/spinal cord preparation isolated from SOD1(G85R) postnatal mice (P3-P10) were labelled with neurobiotin and fully reconstructed in 3D from serial sections in order to analyse their morphology. This staining procedure revealed differences between WT and SOD1(G85R) dendritic trees for most metric and topologic parameters analyzed. A highly complex morphology of SOD1(G85R) motoneurons dendrites (increased number of branching points and terminations) was found and the dendritic trees were longer compared to the WT motoneurons. These morphological changes observed in P8-P9 motoneurons mice occurred concomitantly with a decrease in the input resistance and gain. During electrophysiological recordings, four patterns of discharge were observed in response to ramp stimulations, that were equally distributed in WT and SOD1(G85R) motoneurons. In slice preparation, whole cell patch-clamp recordings made from developing motoneurons in SOD1(G85R) and double transgenic SOD1(G93A)/Hb9-eGFP mice showed that Riluzole, a blocker of persistent inward sodium conductance, altered the repetitive firing in a similar way for the 2 strains. These results show that the SOD1 mutations linked to familial ALS alter the development of the electrical and morphological properties of lumbar motoneurons.
ESTHER : Amendola_2007_Arch.Ital.Biol_145_311
PubMedSearch : Amendola_2007_Arch.Ital.Biol_145_311
PubMedID: 18075124

Title : Early abnormalities in transgenic mouse models of amyotrophic lateral sclerosis - Durand_2006_J.Physiol.Paris_99_211
Author(s) : Durand J , Amendola J , Bories C , Lamotte d'Incamps B
Ref : Journal de Physiologie (Paris) , 99 :211 , 2006
Abstract : Amyotrophic lateral sclerosis (ALS) is a neurodegenerative and fatal human disorder characterized by progressive loss of motor neurons. Transgenic mouse models of ALS are very useful to study the initial mechanisms underlying this neurodegenerative disease. We will focus here on the earlier abnormalities observed in superoxide dismutase 1 (SOD1) mutant mice. Several hypotheses have been advanced to explain the selective loss of motor neurons such as apoptosis, neurofilament disorganisation, oxidative stress, mitochondrial dysfunction, astrogliosis and excitotoxicity. Although disease onset appears at adulthood, recent studies have detected abnormalities during embryonic and postnatal maturation in animal models of ALS. We reported that SOD1G85R mutant mice exhibit specific delays in acquiring sensory-motor skills during the first week after birth. In addition, physiological measurements on in vitro spinal cord preparations reveal defects in evoking rhythmic activity with N-methyl-dl-aspartate and serotonin at lumbar, but not sacral roots. This is potentially significant, as functions involving sacral roots are spared at late stages of the disease. Moreover, electrical properties of SOD1 lumbar motoneurons are altered as early as the second postnatal week when mice begin to walk. Alterations concern the input resistance and the gain of SOD1 motoneurons which are lower than in control motoneurons. Whether or not the early changes in discharge firing are responsible for the uncoupling between motor axon terminals and muscles is still an open question. A link between these early electrical abnormalities and the late degeneration of motoneurons is proposed in this short review. Our data suggest that ALS, as other neurodegenerative diseases, could be a consequence of an abnormal development of neurons and network properties. We hypothesize that the SOD1 mutation could induce early changes during the period of maturation of motor systems and that compensatory mechanismslinked to developmental spinal plasticitymight explain the late onset of the disease.
ESTHER : Durand_2006_J.Physiol.Paris_99_211
PubMedSearch : Durand_2006_J.Physiol.Paris_99_211
PubMedID: 16448809

Title : Cooperation of muscle and cutaneous afferents in the feedback of contraction to peroneal motoneurons - Perrier_2000_J.Neurophysiol_83_3201
Author(s) : Perrier JF , Lamotte d'Incamps B , Kouchtir-Devanne N , Jami L , Zytnicki D
Ref : Journal of Neurophysiology , 83 :3201 , 2000
Abstract : Peroneal motoneurons were recorded intracellularly in anesthetized cats during sustained submaximal contractions of peroneus brevis muscle (PB) elicited by repetitive electrical stimulation of motor axons in the distal portion of cut ventral root filaments. Mechanical stimulation of the territory innervated by the superficial peroneal nerve (SP) was applied during contraction to assess the influence of afferents from this territory on the contraction-induced excitation of motoneurons. In 21 peroneal motoneurons in which PB contraction evoked excitatory potentials, a stimulation engaging mechanoreceptors located in the skin around toes was found to either enhance (in 12 motoneurons) or reduce (in 9 motoneurons) the contraction-induced excitatory potentials. Among positive effects, six showed simple summation of the responses to each individual stimulus, suggesting a convergence of afferent pathways on motoneurons. In six other motoneurons, complex interactions were observed, as may result from convergence at a premotoneuronal level. Among negative effects, a single instance was observed of inhibitory facilitation, as may result from convergence of cutaneous and muscular, possibly Ib, afferents on inhibitory interneurons. Several pathways, mediating either facilitory or inhibitory influences, are available for cooperation of muscle and cutaneous input, allowing flexibility of motoneuron activation in different tasks.
ESTHER : Perrier_2000_J.Neurophysiol_83_3201
PubMedSearch : Perrier_2000_J.Neurophysiol_83_3201
PubMedID: 10848540

Title : Effects on peroneal motoneurons of cutaneous afferents activated by mechanical or electrical stimulations - Perrier_2000_J.Neurophysiol_83_3209
Author(s) : Perrier JF , Lamotte d'Incamps B , Kouchtir-Devanne N , Jami L , Zytnicki D
Ref : Journal of Neurophysiology , 83 :3209 , 2000
Abstract : The postsynaptic potentials elicited in peroneal motoneurons by either mechanical stimulation of cutaneous areas innervated by the superficial peroneal nerve (SP) or repetitive electrical stimulation of SP were compared in anesthetized cats. After denervation of the foot sparing only the territory of SP terminal branches, reproducible mechanical stimulations were applied by pressure on the plantar surface of the toes via a plastic disk attached to a servo-length device, causing a mild compression of toes. This stimulus evoked small but consistent postsynaptic potentials in every peroneal motoneuron. Weak stimuli elicited only excitatory postsynaptic potentials (EPSPs), whereas increase in stimulation strength allowed distinction of three patterns of response. In about one half of the sample, mechanical stimulation or trains of 20/s electric pulses at strengths up to six times the threshold of the most excitable fibers in the nerve evoked only EPSPs. Responses to electrical stimulation appeared with 3-7 ms central latencies, suggesting oligosynaptic pathways. In another, smaller fraction of the sample, inhibitory postsynaptic potentials (IPSPs) appeared with an increase of stimulation strength, and the last fraction showed a mixed pattern of excitation and inhibition. In 24 of 32 motoneurons where electrical and mechanical effects could be compared, the responses were similar, and in 6 others, they changed from pure excitation on mechanical stimulation to mixed on electrical stimulation. With both kinds of stimulation, stronger stimulations were required to evoke inhibitory postsynaptic potentials (IPSPs), which appeared at longer central latencies than EPSPs, indicating longer interneuronal pathways. The similarity of responses to mechanical and electrical stimulation in a majority of peroneal motoneurons suggests that the effects of commonly used electrical stimulation are good predictors of the responses of peroneal motoneurons to natural skin stimulation. The different types of responses to cutaneous afferents from SP territory reflect a complex connectivity allowing modulations of cutaneous reflex responses in various postures and gaits.
ESTHER : Perrier_2000_J.Neurophysiol_83_3209
PubMedSearch : Perrier_2000_J.Neurophysiol_83_3209
PubMedID: 10848541

Title : Reduction of presynaptic action potentials by PAD: model and experimental study - Lamotte d'Incamps_1998_J.Comput.Neurosci_5_141
Author(s) : Lamotte d'Incamps B , Meunier C , Monnet ML , Jami L , Zytnicki D
Ref : J Comput Neurosci , 5 :141 , 1998
Abstract : A compartmental model of myelinated nerve fiber was used to show that primary afferent depolarization (PAD), as elicited by axo-axonic synapses, reduces the amplitude of propagating action potentials primarily by interfering with ionic current responsible for the spike regeneration. This reduction adds to the effect of the synaptic shunt, increases with the PAD amplitude, and occurs at significant distances from the synaptic zone. PAD transiently enhances the sodium current activation, which partly accounts for the PAD-induced fiber hyperexcitability, and enhances sodium inactivation on a slower time course, thus reducing the amplitude of action potentials. In vivo, intraaxonal recordings from the intraspinal portion of group I afferent fibers were carried out to verify that depolarizations reduced the amplitude of propagating action potentials as predicted by the model. This article suggests PAD might play a major role in presynaptic inhibition.
ESTHER : Lamotte d'Incamps_1998_J.Comput.Neurosci_5_141
PubMedSearch : Lamotte d'Incamps_1998_J.Comput.Neurosci_5_141
PubMedID: 9617664