Bassoon is required for adult ocular dominance plasticity and experience-induced changes in synapsin phosphorylation in visual cortex
Sensory stimulation enables experience-dependent fine tuning of brain circuits for optimal perception. In juvenile mice, brief closure of the contralateral eye reduces primary visual cortex (V1) activation through the deprived eye. In contrast, in adult animals, eye closure induces potentiated V1-responses to non-deprived eye visual stimulation. While considerable knowledge exists about postsynaptic mechanisms underlying this ocular dominance (OD) plasticity, little is known about contributing presynaptic molecules. Here we report that constitutive deletion of the presynaptic scaffolding protein bassoon (Bsn{Delta}Ex4/5) disrupted OD-plasticity in V1 of adult mice leaving juvenile OD-plasticity unaffected. Notably, in mice with a conditional deletion of Bsn only from cortical glutamatergic neurons (BsnEmx1), adult OD-plasticity was also impaired indicating that normal presynaptic plasticity of glutamatergic cortical synapses is selectively required in this process. While spatial vision was severely compromised in Bsn{Delta}Ex4/5 mice, it was preserved in BsnEmx1 mice, consistent with normal Bsn expression in subcortical circuit in these mice. Parallel experiments in cultured neurons revealed that deletion of Bsn left the inactivity-induced postsynaptic scaling of AMPA-responses mediated by increased AMPA receptor trafficking unchanged. However, presynaptic scaling was completely abolished as assessed by both electrophysiology and live-cell imaging of evoked synaptic vesicle fusion in cultured primary cortical neurons. Finally, monocular deprivation induced enhanced phosphorylation of synaptic vesicle-associated synapsin in contralateral V1 that was absent in BsnEmx1 mice. Overall, our data indicate that adult OD-plasticity requires Bsn-dependent presynaptic plasticity, involving experience-induced changes in synapsin phosphorylation. In contrast, juvenile OD-plasticity does not appear to be dependent on Bsn.