Chondroitinase and Antidepressants Promote Plasticity by Releasing TRKB from Dephosphorylating Control of PTPσ in Parvalbumin Neurons
| Autor: | Hanna Antila, Plinio C. Casarotto, Eero Castrén, Frederike Winkel, Anna Steinzeig, Mikko Voipio, Caroline Biojone, Angelina Lesnikova, Senem Merve Fred, Juzoh Umemori |
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| Přispěvatelé: | Neuroscience Center, Helsinki Institute of Life Science HiLIFE, University of Helsinki |
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
PROTEOGLYCAN chABC Protein tyrosine phosphatase Tropomyosin receptor kinase B BRAIN PLASTICITY Mice RPTP sigma 0302 clinical medicine Neurotrophic factors PTPRS Phosphorylation Receptor Research Articles Cells Cultured Cerebral Cortex Neurons 0303 health sciences Mice Inbred BALB C Membrane Glycoproteins Neuronal Plasticity biology Chemistry General Neuroscience Perineuronal net musculoskeletal neural and ocular physiology Receptor-Like Protein Tyrosine Phosphatases Class 2 RECOVERY Protein-Tyrosine Kinases Antidepressive Agents Cell biology Parvalbumins embryonic structures Neurotrophin CSPG animal structures Development/Plasticity/Repair Mice Transgenic Dephosphorylation 03 medical and health sciences EXTRACELLULAR-MATRIX Animals Aggrecan 030304 developmental biology REACTIVATION perineuronal nets RECEPTOR Chondroitinase treatment 3112 Neurosciences Chondroitinases and Chondroitin Lyases OCULAR DOMINANCE PLASTICITY Mice Inbred C57BL enzymes and coenzymes (carbohydrates) 030104 developmental biology BDNF nervous system biology.protein RPTPσ CORTICAL PLASTICITY 030217 neurology & neurosurgery Parvalbumin NEUROTROPHIC FACTOR |
| Zdroj: | The Journal of Neuroscience BioRxiv bioRxiv |
| ISSN: | 1529-2401 0270-6474 |
| Popis: | Perineuronal nets (PNNs) are an extracellular matrix structure rich in chondroitin sulfate proteoglycans (CSPGs), which preferentially encase parvalbumin-containing (PV+) interneurons. PNNs restrict cortical network plasticity but the molecular mechanisms involved are unclear. We found that reactivation of ocular dominance plasticity in the adult visual cortex induced by chondroitinase ABC (chABC)-mediated PNN removal requires intact signaling by the neurotrophin receptor TRKB in PV+neurons. Additionally, we demonstrate that chABC increases TRKB phosphorylation (pTRKB), while PNN component aggrecan attenuates brain-derived neurotrophic factor (BDNF)-induced pTRKB in cortical neurons in culture. We further found that protein tyrosine phosphatase σ (PTPσ, PTPRS), receptor for CSPGs, interacts with TRKB and restricts TRKB phosphorylation. PTPσ deletion increases phosphorylation of TRKBin vitroandin vivoin male and female mice, and juvenile-like plasticity is retained in the visual cortex of adult PTPσ-deficient mice (PTPσ+/−). The antidepressant drug fluoxetine, which is known to promote TRKB phosphorylation and reopen critical period-like plasticity in the adult brain, disrupts the interaction between TRKB and PTPσ by binding to the transmembrane domain of TRKB. We propose that both chABC and fluoxetine reopen critical period-like plasticity in the adult visual cortex by promoting TRKB signaling in PV+neurons through inhibition of TRKB dephosphorylation by the PTPσ-CSPG complex.SIGNIFICANCE STATEMENTCritical period-like plasticity can be reactivated in the adult visual cortex through disruption of perineuronal nets (PNNs) by chondroitinase treatment, or by chronic antidepressant treatment. We now show that the effects of both chondroitinase and fluoxetine are mediated by the neurotrophin receptor TRKB in parvalbumin-containing (PV+) interneurons. We found that chondroitinase-induced visual cortical plasticity is dependent on TRKB in PV+neurons. Protein tyrosine phosphatase σ (PTPσ, PTPRS), a receptor for PNNs, interacts with TRKB and inhibits its phosphorylation, and chondroitinase treatment or deletion of PTPσ increases TRKB phosphorylation. Antidepressant fluoxetine disrupts the interaction between TRKB and PTPσ, thereby increasing TRKB phosphorylation. Thus, juvenile-like plasticity induced by both chondroitinase and antidepressant treatment is mediated by TRKB activation in PV+interneurons. |
| Databáze: | OpenAIRE |
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