Mediterranean Institute of Neurobiology

Marseille, France

Mediterranean Institute of Neurobiology

Marseille, France
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Otsmane B.,Mediterranean Institute of Neurobiology | Moumen A.,Mediterranean Institute of Neurobiology | Aebischer J.,Mediterranean Institute of Neurobiology | Aebischer J.,Ecole Polytechnique Federale de Lausanne | And 9 more authors.
EMBO Reports | Year: 2014

A receptor-ligand interaction can evoke a broad range of biological activities in different cell types depending on receptor identity and cell type-specific post-receptor signaling intermediates. Here, we show that the TNF family member LIGHT, known to act as a death-triggering factor in motoneurons through LT-βR, can also promote axon outgrowth and branching in motoneurons through the same receptor. LIGHT-induced axonal elongation and branching require ERK and caspase-9 pathways. This distinct response involves a compartment-specific activation of LIGHT signals, with somatic activation-inducing death, while axonal stimulation promotes axon elongation and branching in motoneurons. Following peripheral nerve damage, LIGHT increases at the lesion site through expression by invading B lymphocytes, and genetic deletion of Light significantly delays functional recovery. We propose that a central and peripheral activation of the LIGHT pathway elicits different functional responses in motoneurons. Synopsis Activation of the LIGHT receptor LT-βR in the somatic compartment of motoneurons elicits death, while activation in the axonal compartment stimulates axon outgrowth and branching. LIGHT also promotes functional recovery following peripheral nerve lesion. Somatic activation of LIGHT-LT-βR signaling triggers motoneuron death, while axonal activation increases motoneuron axon length and branching. LIGHT-induced axon outgrowth and branching depend on ERK and caspase-9 pathways Following peripheral nerve injury, LIGHT is required for reinnervation and functional recovery. Activation of the LIGHT receptor LT-βR in the somatic compartment of motoneurons elicits death, while activation in the axonal compartment stimulates axon outgrowth and branching. LIGHT also promotes functional recovery following peripheral nerve lesion. © 2014 The Authors.


News Article | November 14, 2016
Site: www.eurekalert.org

A newborn rat's brain development stage is close to that of a human embryo in the second half of pregnancy, so this discovery allows to hypothesize that the same movement patterns can help neuron development in humans. The research was published in Nature Communications on October 7th. This work has been going on for four years under the helm of Rustem Khazipov and his overseas colleagues, including Ana Rita Lourenco Inacio (Mediterranean Institute of Neurobiology). The KFU Neurobiology Lab was established to study developing brain thanks to a megagrant from the Russian government. Physiological movement has been studied by observing both the brain and the spinal cord. Thus new information has been obtained about the spinal cord activation in rats. Azat Nasretdinov, Junior Research Associate at the Neurobiology Lab and a co-author of the latest paper, explains, "We had to find out how spinal neurons communicate during spontaneous limb movements. We simultaneously registered hind limb movements and electric activity in the spinal cord. Our main takeaway is that the activation of motor and sensor zones of the spinal cord resulting from short twitches and long complex movements is carried out through sensory feedback (activities of the movement zones of the spinal cord lead to limb movements and thus to sensor zone activation), so we think these spontaneous movements are the main instrument of sensorimotor synchronization. One of the proofs is that spinal cord activity diminished when sensory signals from the limbs were disconnected. The final confirmation came during in vitro experiments on spinal cords - sensory and motor zones both demonstrated bursts of activity, but with little correlation because isolated spinal cord preparations had no anatomical feedback".

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