Abstract
Activity-dependent neuronal plasticity is a fundamental mechanism through which the nervous system adapts to sensory experience. Several lines of evidence suggest that parvalbumin (PV+) interneurons are essential in this process, but the molecular mechanisms underlying the influence of experience on interneuron plasticity remain poorly understood. Perineuronal nets (PNNs) enwrapping PV+ cells are long-standing candidates for playing such a role, yet their precise contribution has remained elusive. We show that the PNN protein Brevican is a critical regulator of interneuron plasticity. We find that Brevican simultaneously controls cellular and synaptic forms of plasticity in PV+ cells by regulating the localization of potassium channels and AMPA receptors, respectively. By modulating Brevican levels, experience introduces precise molecular and cellular modifications in PV+ cells that are required for learning and memory. These findings uncover a molecular program through which a PNN protein facilitates appropriate behavioral responses to experience by dynamically gating PV+ interneuron function.
Original language | English |
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Article number | E10 |
Pages (from-to) | 639-655 |
Journal | Neuron |
Volume | 95 |
Issue number | 3 |
Early online date | 14 Jul 2017 |
DOIs | |
Publication status | Published - 2 Aug 2017 |
Keywords
- Parvalbumin interneurons
- inhibitory circuitries
- perineuronal nets
- synapse maturation
- AMPA receptors
- Kv channels
- learning and memory
- plasticity
- activity-dependent