Plates-Formes de Recherche en Neurosciences

logo amu logo cnrs

Plates-formes PFRN

Accueil > Bibliographie > Role of drebrin A in dendritic spine plasticity and synaptic function : (...)

Role of drebrin A in dendritic spine plasticity and (...)

Commun Integr Biol. 2009 May ;2(3):268-70
Role of drebrin A in dendritic spine plasticity and synaptic function : Implications in neurological disorders.
Ivanov A, Esclapez M, Ferhat L.

Drebrin A is one of the most abundant neuron-specific binding proteins of F-actin and its expression is increased in parallel with synapse formation. Drebrin A is particularly concentrated in dendritic spines, postsynaptic sides of excitatory glutamatergic synapses. More recently, Ferhat and colleagues reported the functional role of drebrin A in regulating synaptic transmission. Indeed, our study showed that overexpression of drebrin A induced an increase of glutamatergic but not GABAergic synapses and resulted in the alteration of the normal excitatory-inhibitory ratio in favor of excitation in mature hippocampal neurons. Downregulation of drebrin A expression by antisense oligonucleotides resulted in the decrease of both miniature- glutamatergic and GABAergic synaptic activities without affecting the excitatory-inhibitory ratio. Studies performed in heterologous cells revealed that drebrin A reorganized the actin filaments and stabilized them and that these effects are depend upon its actin-binding domain. These results suggest that drebrin A regulates dendritic spine morphology, size and density, presumably via regulation of actin cytoskeleton remodeling and dynamics. These data demonstrate for the first time that an actin-binding protein such as drebrin A regulates both glutamatergic and GABAergic synaptic transmissions, probably through an increase of active synaptic site density for glutamatergic transmission and through homeostatic mechanisms for the GABAergic one.It is appealing to suggest that abnormalities in the expression of drebrin A may result in aberrant synapse development and/or loss of synapses leading to synaptic dysfunction, which underlies cognitive impairment accompanying neurological disorders such as Alzheimer’s disease, Down syndrome as well as normal aging.

PubMed

    Ils nous font confiance

  • logo amu
  • logo cnrs
  • logo inserm
  • logo AP-HM
  • logo F�d�ration pour la Recherche sur le Cerveau
  • logo Fondation pour la Recherche Medical en France
  • logo IBiSA
  • logo Europe programme FEDER
  • logo Agence Nationale de la Recherche
  • logo Plateforme Technologique Aix-Marseille
  • logo Vect-Horus
  • logo Neuron Experts