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Plasticité, métaplasticité synaptique et neuronale dans le cortex somatosensoriel primaire chez le rat dans un modèle de douleur inflammatoire prolongée

Abstract : Chronic neuropathic or inflammatory pain is believed to result from long-lasting synaptic andneuronal changes in pain pathways, including the primary somatosensory cortex (S1) which codes for pain intensity and location. Using ex vivo electrophysiological recordings from S1 layer 2/3 pyramidal neurons, we investigated pain-induced plasticity in a rat model (CFA injection) of chronic facial inflammatory pain. We first establish the relation in basal conditions between synaptic activity and (i) bidirectionalsynaptic plasticity (long-term depression/potentiation; LTD/LTP), (ii) changes in the ability to express synaptic plasticity (metaplasticity), (iii) bidirectional changes in intrinsic neuronal excitability (LTP/LTD-IE); i.e. the rules for synaptic and intrinsic plasticity in S1 layer 2/3pyramidal neurons. We then investigated such plasticity processes in CFA-treated rats exhibiting facial mechanical allodynia, at 1 hour and 3 days post-injection. At 1-hour, mechanical allodynia is associated with (i) LTP of excitatory synaptic transmission, together with (ii) an inhibition to generate further LTP but a facilitation to generate LTD (metaplasticity), consistent with LTP of synaptictransmission, (iii) LTP-IE and (iv) reduced dendritic arbor complexity of S1 layer 2/3 pyramidal neurons. At 3 days, LTP and LTP-IE were still present but metaplasticity and dendritic arbor complexity had returned to control levels.
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Hien Luong Nguyen. Plasticité, métaplasticité synaptique et neuronale dans le cortex somatosensoriel primaire chez le rat dans un modèle de douleur inflammatoire prolongée. Santé. Université Clermont Auvergne, 2018. Français. ⟨NNT : 2018CLFAS027⟩. ⟨tel-02885400⟩

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