Neuregulin-Dependent Regulation of Fast-Spiking Interneuron Excitability Controls the Timing of the Critical Period

Gu, Yu; Tran, Trinh; Murase, Sachiko; Borrell, Andrew; Kirkwood, Alfredo; Quinlan, Elizabeth

doi:10.1523/jneurosci.4242-15.2016

Cited by 63 publications

(73 citation statements)

References 53 publications

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“…Several proteins that regulate synaptic strength and/or number are highly enriched at excitatory synapses onto PV interneurons and impact the timing of the critical period and NRG1 (NARP: Chang et al, 2010; Gu et al, 2013, Pelkey et al, 2015; Gu et al, 2016; kaplan et al, 2016; Sun et al, 2016). Accordingly, NARP-deficient mice fail to initiate a critical period unless rescued by enhancing the strength of the inhibitory output or excitatory drive onto PV interneurons (Gu et al, 2013; Gu et al, 2016). …”

Section: Inhibition and Critical Period Inductionmentioning

confidence: 99%

“…Hence, the critical period can be reopened in adulthood by pharmacological reduction of inhibition (Harazouv et al, 2010) or by the knockdown of Otx2 (Beurdeley et al, 2012; Spatazza et al, 2013). Treatment with an NRG1 peptide induces a precocious termination of the critical period, while inhibition of the activity of the NRG receptor (ErbB) reactivates the critical period in adults (Gu et al, 2016). Indeed, a developmental reduction of plasticity at excitatory synapses onto FS interneurons may explain the requirement for longer durations of MD with age (Kameyama et al, 2010).…”

Section: Inhibition and Critical Period Inductionmentioning

confidence: 99%

“…In contrast, dark exposure decreases the excitability of PV interneurons, and the reactivated plasticity can be reversed by increasing the strength of their excitatory synaptic inputs (Gu et al, 2016). A loss of specific neurofilament protein associated with cytoskeletal stability is observed in the LGN following dark exposure, which may further contribute to the reactivation of structural OD plasticity (O’Leary et al, 2012; Duffy et al, 2016).…”

Section: Environmental Reactivation Of Critical Period In Adulthoodmentioning

confidence: 99%

“…The SSRI antidepressant fluoxetine reduces the basal levels of extracellular GABA (Maya Vetencourt et al, 2008) and the number of PV interneurons surrounded by dense perineuronal nets (Guirado et al, 2014). Similarly, dark exposure may rejuvenate intracortical inhibition by reducing the excitatory drive onto PV neurons (Gu et al, 2016) (Fig. 2).…”

Section: Reactivating Plasticity To Enhance Recoverymentioning

confidence: 99%

“…It has been demonstrated that shortly after eye opening, V1 neurons exhibit orientation tuning and respond to visual stimulation of either eye; however, the orientation preference through each eye, which is initially mismatched, becomes tuned to similar orientations during the critical period (Wang et al, 2010). Indeed, manipulations that prolong V1 plasticity, such as environmental enrichment, accelerate binocular matching of the stimulus selectivity in the developing mouse primary visual cortex (Gu et al, 2016). In contrast, manipulations that accelerate plasticity in the cortex, such as heterozygous loss of Mecp2 , prevent the acquisition of matched stimulus selectivity (Krishnan et al, 2015).…”

Section: Expanding the Focus Beyond Ocular Dominancementioning

confidence: 99%

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Critical periods in amblyopia

2018

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The shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.

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Section: Inhibition and Critical Period Inductionmentioning

confidence: 99%

Section: Inhibition and Critical Period Inductionmentioning

confidence: 99%

Section: Environmental Reactivation Of Critical Period In Adulthoodmentioning

confidence: 99%

Section: Reactivating Plasticity To Enhance Recoverymentioning

confidence: 99%

Section: Expanding the Focus Beyond Ocular Dominancementioning

confidence: 99%

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Critical periods in amblyopia

2018

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Neuregulin directed molecular mechanisms of visual cortical plasticity

Grieco

Holmes

2018

J of Comparative Neurology

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Experience-dependent critical period (CP) plasticity has been extensively studied in the visual cortex. Monocular deprivation during the CP affects ocular dominance, limits visual performance, and contributes to the pathological etiology of amblyopia. Neuregulin-1 (NRG1) signaling through its tyrosine kinase receptor ErbB4 is essential for the normal development of the nervous system and has been linked to neuropsychiatric disorders such as schizophrenia. We discovered recently that NRG1/ErbB4 signaling in PV neurons is critical for the initiation of CP visual cortical plasticity by controlling excitatory synaptic inputs onto PV neurons and thus PV-cell mediated cortical inhibition that occurs following visual deprivation. Building on this discovery, we review the existing literature of neuregulin signaling in developing and adult cortex and address the implication of NRG/ErbB4 signaling in visual cortical plasticity at the cellular and circuit levels. NRG-directed research may lead to therapeutic approaches to reactivate plasticity in the adult cortex.

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Neuregulin and ErbB expression is regulated by development and sensory experience in mouse visual cortex

Grieco

Wang

Mahapatra

et al. 2019

J of Comparative Neurology

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Neuregulins (NRGs) are protein ligands that impact neural development and circuit function. NRGs signal through the ErbB receptor tyrosine kinase family. NRG1/ErbB4 signaling in parvalbumin-expressing (PV) inhibitory interneurons is critical for visual cortical plasticity. There are multiple types of NRGs and ErbBs that can potentially contribute to visual cortical plasticity at different developmental stages. Thus, it is important to understand the normal developmental expression profiles of NRGs and ErbBs in specific neuron types in the visual cortex, and to study whether and how their expression changes in PV inhibitory neurons and excitatory neurons track with sensory perturbation. Cell type-specific translating ribosome affinity purification and qPCR was used to compare mRNA expression of nrg1,2,3,4 and erbB1,2,3,4 in PV and excitatory neurons in mouse visual cortex. We show that the expression of nrg1 and nrg3 decreases in PV neurons at the critical period peak, postnatal day 28 (P28) after monocular deprivation and dark rearing, and in the adult cortex (at P104) after 2-week long dark exposure. In contrast, nrg1 expression by excitatory neurons is unchanged at P28 and P104 following sensory deprivation, whereas nrg3 expression by excitatory neurons shows changes depending on the age and the mode of sensory deprivation. ErbB4 expression in PV neurons remains consistently high and does not appear to change in response to sensory deprivation. These data provide new important details of cell type-specific NRG/ErbB expression in the visual cortex and support that NRG1/ErbB4 signaling is implicated in both critical period and adult visual cortical plasticity.

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Neuregulin-Dependent Regulation of Fast-Spiking Interneuron Excitability Controls the Timing of the Critical Period

Cited by 63 publications

References 53 publications

Critical periods in amblyopia

Critical periods in amblyopia

Neuregulin directed molecular mechanisms of visual cortical plasticity

Neuregulin and ErbB expression is regulated by development and sensory experience in mouse visual cortex

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