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ANNEE : 2003

Brain plasticity and ion channels.

AUTEURS : Debanne D, Daoudal G, Sourdet V, Russier M.

REVUE : Journal of Physiology (Paris)
It is generally believed that spatio-temporal configurations of distributed activity in the brain contribute to the coding of neuronal information and that synaptic contacts between nerve cells could play a central role in the formation of privileged pathways of activity. Synaptic plasticity is not the only mode of regulation of information processing in the brain and persistent regulations of ionic conductances in some specialized neuronal areas such as the dendrites, the cell body and the axon could also modulate, in the short- and the long-term, the propagation of information in the brain. Persistent changes in intrinsic excitability have been reported in several brain areas in which activity is modified during a classical conditioning. The role of synaptic activity seems to be determinant in the induction but the learning rules and the underlying mechanisms remain to be defined. This review discusses the role of neuronal activity in the induction of intrinsic plasticity in cortical, hippocampal and cerebellar neurons. Activation and inactivation properties of ionic channels in the axon determine the short-term dynamics of axonal propagation and synaptic transmission. Activation of glutamate receptors initiates a long-term modification in neuronal excitability that may represent the substrate for the mnesic engram and for the stabilization of the epileptic state. Similarly to synaptic plasticity, long-lasting intrinsic plasticity appears to be reversible and to express a certain level of input or cellular specificity. These non-synaptic forms of plasticity affect the signal propagation in the axon, the dendrites and the soma. They not only share common learning rules and induction pathways with the better known synaptic plasticity such as NMDA receptor-dependent LTP and LTD but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram.