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Lieu: CGFB Seminar room

from ICM Paris (team leader / Equipe Inhibition synaptique et auto-modulation des microcircuits du cortex cérébral) will give a presentation entitled 'Long-term Plasticity of Neocortical GABAergic Synapses'

Invitant : Giovanni Marsicano, Neurocentre Magendie

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/alberto-bacci.html

Lieu: Neurocentre Magendie Seminar room

Neurotrophins are essential for the maintenance of neuronal homeostasis and modulation of synaptic plasticity. An impairment in the signaling of different neurotrophins such as Brain-derived Neurotrophic Factor (BDNF), Nerve Growth Factor (NGF) and Transforming-Growth-Factor-ß1 (TGF-ß1) has been demonstrated in Alzheimer’s disease (AD) brain in an early phase of the disease.
ß-amyloid (Aβ) accumulation is an early event in AD pathogenesis which can lead to pro-inflammatory processes even before the onset of cognitive decline (Iulita and Cuello 2014). A strong neurobiological link has been found in AD brain between this early pro-inflammatory process and the deficit of neurotrophic factors such as NGF and TGF-ß1. A dysfunction in the extracellular metabolism of NGF that compromises Pro-NGF maturation and exacerbates its subsequent degradation has been recently proposed as a contributor to cholinergic neuron dysfunction in AD and Down Syndrome (DS), and hence to cognitive decline (Iulita, Caraci & Cuello 2016). However, it is not known whether these CNS alterations are reflected in periphery and finally if a relationship exists between Aβ accumulation, peripheral biomarkers related to inflammation and NGF dysfunction in lymphocytes from DS patients with AD. We are currently examining whether DS lymphocytes from DS individuals can reflect, in the periphery, a deficit of NGF known to occur in DS brain in a preclinical stage of AD (Iulita, Caraci & Cuello 2016).
TGF-β1 is an anti-inflammatory cytokine that exerts neuroprotective effects against Aβ-induced neurodegeneration (Caraci et al. 2008). Recently, we have identified a key role for TGF-ß1 in recognition memory formation demonstrating that this neurotrophic factor is essential for the transition from early to late LTP (Caraci et al. 2015). An impairment of TGF-β1 signaling pathway has been demonstrated to be specific to the AD brain, and particularly to the early phase of the disease. Deficit of TGF-β1 seems also to be a common pathophysiological event both in depression and AD. Depression is a risk factor for the development of AD and the presence of depressive symptoms significantly increases the conversion of Mild Cognitive Impairment (MCI) into AD. Plasma TGF-ß1 levels are reduced in major depressed patients, and, interestingly, different second-generation antidepressant drugs increase circulating TGF-ß1 levels in depressed patients. In addition, it is known that continued long-term antidepressants treatment is associated with a reduction in the rate of AD. Whereas these data identify TGF-β1 signaling as a potential common target for both depression and AD, the potential neuroprotective activity of antidepressant drugs against Aβ-induced neurodegeneration in vitro has been only partially explored.
We have examined the neuroprotective activity of fluoxetine and sertraline both in pure and mixed rat neuronal cultures challenged with synthetic Aß(1-42) oligomers (100nM).We found that fluoxetine and sertraline, at therapeutic concentrations (100nM-1µM), significantly prevented Aβ-induced toxicity in mixed cultures, but not in pure neuronal cultures, via a paracrine mechanism mediated by TGF-ß1. Consistent with a glia-mediated effect, a 24 hr treatment of astrocytes with fluoxetine and sertraline promoted the release of TGF-β1 in the culture media by increasing the conversion of Pro-TGF-ß1 to mature TGF-ß1.
Our data demonstrate that second-generation antidepressants are neuroprotective in vitro against Aß-induced neurodegeneration by rescuing TGF-β1 signaling and also suggest that drugs able to increase the release of active TGF-β1, such as fluoxetine and sertraline, might represent new neuroprotective tools for the treatment of AD.

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/filipo-caraci.html

Lieu: CGFB Seminar room

from Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University's lab will give a presentation entitled 'Synaptic epitranscriptomics and dynamic RNA imaging'

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/dan-othan-wang.html

Lieu: Neurocentre Magendie Seminar room

from Nerve Regeneration Group (Instituto Biologia Molecular e Celular- IBMC and / Instituto de Investigação e Inovação em Saúde, Porto, Portugal)'s lab will give a presentation entitled 'The neuronal and actin commitment: why do neurons need rings?'

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/casper-hoogenraad.html

Lieu: Neurocentre Magendie Seminar room

from Utrecht University's lab will give a presentation entitled 'Cytoskeleton-based mechanisms underlying the biology and diseases of the nervous system'

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/casper-hoogenraad.html

Lieu: Neurocentre Magendie Seminar room

from NIDA (National Institute on Drug Abuse, Bethesda/Maryland/USA)'s lab will give a presentation entitled 'Neuronal mechanisms of incubation of methamphetamine craving after prolonged voluntary abstinence'

Invitant : Serge Ahmed, Team leader: Pathological decison-making in addiction Affiliated with the lab: Neurodegenerative Diseases Institute

Abstract :

Methamphetamine addiction is characterized by high relapse rates often precipitated by exposure to drug-associated cues that provoke drug craving. In rodent studies of drug craving, cue-induced drug seeking is assessed after experimenter-imposed forced abstinence. However, in humans, abstinence is often self-imposed, or voluntary, in favor of other non-addictive alternative rewards. In the present lecture I will present a new choice-based rat model of relapse, along with its first neurobehavioral characterization, in which Meth craving is observed after prolonged voluntary abstinence.

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/daniele-caprioli.html

Lieu: CGFB Seminar room

from ITMO neurosciences's lab will give a presentation entitled 'Unmet therapeutic needs in Parkinson's disease'

Invitant : Gionanni Marsicano, Neurocentre Magendie

Pour plus de détails: www.cgfb.u-bordeaux2.fr/detail-reservation?rid=6233

Lieu: Neurocentre Magendie Seminar room

from Laboratory of Neuropsychology, National Institute of Mental Health's lab will give a presentation entitled "From knowledge to action: the role of the primate orbitofrontal cortex"

Invitant : Etiennne Coutureau, Senior CNRS Researcher Team Leader "Decision and Adaptation, DECAD" Institut de Neurosciences Cognitives et Intégratives d'Aquitaine (INCIA)

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/elizabeth-murray.html

Lieu: Neurocentre Magendie Seminar room

from Sensory Mechanotransduction Werner Reichardt Centre for Integrative Neuroscience (Tübingen, Germany)'s lab will give a presentation entitled "Spinal cord presynaptic modulation of chronic pain"

Invitant : Marc Landry / Team leader/ Central mechanisms of pain sensitization, IINS

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/jing-hu.html

Lieu: CGFB

from Max Plank Florida Institute for Neuroscience's lab will give a presentation entitled 'Local control of spike signaling within unmyelinated axons'

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-fbn-2015/jason-christie.html