Impaired GABAergic transmission disrupts normal homeostatic plasticity in rat cortical networks.

Nicolas Le Roux (1, 2) , Muriel Amar (1, 2) , Alexandre Moreau (1, 2) , Gérard Baux (1, 2) , Philippe Fossier (1, 2)

1 INAF - Institut de Neurobiologie Alfred Fessard
2 NBCM - Laboratoire de neurobiologie cellulaire et moléculaire

In the cortex, homeostatic plasticity appears to be a key process for maintaining neuronal network activity in a functional range. This phenomenon depends on close interactions between excitatory and inhibitory circuits. We previously showed that application of a high frequency of stimulation (HFS) protocol in layer 2/3 induces parallel potentiation of excitatory and inhibitory inputs on layer 5 pyramidal neurons, leading to an unchanged excitation/inhibition (E/I) balance. These coordinated long-term potentiations of excitation and inhibition correspond to homeostatic plasticity of the neuronal networks. We showed here, on the rat visual cortex, that blockade (with gabazine) or overactivation (with 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol) of GABA(A) receptors enhanced the E/I balance and prevented the potentiation of excitatory and inhibitory inputs after an HFS protocol. These impairements of the GABAergic transmission led to a long-term depression-like effect after an HFS protocol. We also observed that the blockade of inhibition reduced excitation (by 60%), and conversely, the blockade of excitation decreased inhibition (by 90%). These results support the idea that inhibitory interneurons are critical for recurrent interactions underlying homeostatic plasticity in cortical networks.

Mots clés: homeostatic plasticity; GABAA receptors; cortical networks

Domaines: Neurobiologie

Nicolas Le Roux, Muriel Amar, Alexandre Moreau, Gérard Baux, Philippe Fossier. Impaired GABAergic transmission disrupts normal homeostatic plasticity in rat cortical networks.. European Journal of Neuroscience, 2008, 27 (12), pp.3244-56. ⟨10.1111/j.1460-9568.2008.06288.x⟩. ⟨hal-00303327⟩