Abstract
Gama amino butyric acid (GABA) inhibition plays an important role in the onset and offset of the critical period for ocular dominance (OD) plasticity in the primary visual cortex. Previous studies have focused on the involvement of GABAA receptors, while the potential contribution of GABAB receptors to OD plasticity has been neglected. In this study, the GABAB receptor antagonist SCH50911 or agonist baclofen was infused into the primary visual cortex of cats concurrently with a period of monocular deprivation (MD). Using single-unit recordings we found that the OD shift induced by four days of MD during the critical period was impaired by infusion of the antagonist SCH50911, but enhanced by infusion of the agonist baclofen. In contrast, seven days of MD in adult cats did not induce any significant OD shift, even when combined with the infusion of SCH50911 or baclofen. Together, these findings indicate that an endogenous GABAB receptor-mediated inhibition contributes to juvenile, but not adult, OD plasticity.
Highlights
Altering visual experience by monocular deprivation (MD) results in the rewiring of cortical circuitry with visual representation shifting predominantly to the open eye
Since long-term depression (LTD) and long-term potentiation (LTP) at inhibitory and excitatory synapses have been hypothesized to be crucial for the attenuation of deprived eye responses and the strengthening of open eye responses, we have investigated the contribution of GABAB receptors in ocular dominance (OD) plasticity using cortical infusion of the antagonist SCH50911 and agonist baclofen in juvenile and adult cats
Blockade of GABAB receptors impaired OD plasticity during the critical period At the peak of the critical period for ocular dominance plasticity (4–5 weeks of age), kittens received an infusion of the GABAB receptor antagonist SCH50911 (20 mM) into the left visual cortex
Summary
Altering visual experience by MD (a model of amblyopia) results in the rewiring of cortical circuitry with visual representation shifting predominantly to the open eye. Knockout of the GABA synthetic enzyme GAD65 prevents the onset of the critical period [3], while reducing intracortical GABAergic inhibition promotes OD plasticity in adults [4,5,6,7]. Many of these effects are blocked by diazepam [3, 6], indicating a requirement for GABAA receptor activation, but cortical inhibition may be mediated by GABAB receptors
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