Contribution of the GABAergic system to cortical plasticity

• Autorzy: Kossut M.
• Języki publikacji: EN

Abstrakty

EN

Experience-induced plastic changes in the cerebral cortex are accompanied by alterationsin excitatory and inhibitory transmission. Increased excitatory drive, necessary for plasticity, precedes the occurrence of plastic change, while decreased inhibitory signaling often facilitates plasticity. However, an increase of inhibitory interactions was noted in some instances of experience-dependent changes. We found upregulation of the number of inhibitory markers in the barrel cortex of mice after classical conditioning engaging vibrissae, observed concurrently with enlargement of the cortical representational area of the row of vibrissae receiving conditioned stimulus (CS). We also observed that an increase of GABA level accompanied the conditioning. Moreover, Npas4, a transcription factor important for structural and functional neuronal plasticity and identified as an element of the program controlling inhibitory synapse development, was affected by conditioning. With real-time PCR on laser-dissected individual rows of barrels we found that Npas4 mRNA level was upregulated following conditioning. In order to find whether unaltered GABAergic signaling is necessary for learning-dependent rewiring in the murine barrel cortex, we locally decreased GABA production in the barrel cortex or reduced transmission through GABAA receptors at the time of the conditioning. Both treatments prevented learninginduced enlargement of the conditioned vibrissae representation. At the behavioral level, consolidation of the conditioned response (cessation of head movements in response to CS) was impaired. These results show that appropriate functioning of the GABAergic system is required for both manifestation of functional cortical representation plasticity and for the development of a conditioned response.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2015
• Tom: 75
• Numer: Supl.
• Opis fizyczny: p.S31

Twórcy

autor

Kossut M.

• Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland