Comparison of Plasticity In Vivo and In Vitro in the Developing Visual Cortex of Normal and Protein Kinase A RIβ-Deficient Mice

Hensch, Takao K.; Gordon, Joshua A.; Brandon, Eugene P.; McKnight, G. Stanley; Idzerda, Rejean L.; Stryker, Michael P.

doi:10.1523/jneurosci.18-06-02108.1998

Cited by 117Neuroscience and Neuropharmacology ResearchVisual perception and processing mechanismsNeurogenesis and neuroplasticity mechanisms

Comparison of Plasticity In Vivo and In Vitro in the Developing Visual Cortex of Normal and Protein Kinase A RIβ-Deficient Mice

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Hensch, Takao K., Gordon, Joshua A., Brandon, Eugene P., McKnight, G. Stanley, Idzerda, Rejean L., Stryker, Michael P.·1998·The Journal of Neuroscience

DOI 10.1523/jneurosci.18-06-02108.1998PMC PMC2553093

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Abstract

Developing sensory systems are sculpted by an activity-dependent strengthening and weakening of connections. Long-term potentiation (LTP) and depression (LTD)in vitro have been proposed to model this experience-dependent circuit refinement. We directly compared LTP and LTD induction in vitro with plasticity in vivo in the developing visual cortex of a mouse mutant of protein kinase A (PKA), a key enzyme implicated in the plasticity of a diverse array of systems. In mice lacking the RIβ regulatory subunit of PKA, we observed three abnormalities of synaptic plasticity in layer II/III of visual cortex in vitro. These included an absence of (1) extracellularly recorded LTP, (2) depotentiation or LTD, and (3) paired-pulse facilitation. Potentiation was induced, however, by pairing low-frequency stimulation with direct depolarization of individual mutant pyramidal cells. Together these findings suggest that the LTP defect in slices lacking PKA RIβ lies in the transmission of sufficient net excitation through the cortical circuit. Nonetheless, functional development and plasticity of visual cortical responses in vivo after monocular deprivation did not differ from normal. Moreover, the loss of all responsiveness to stimulation of the originally deprived eye in most cortical cells could be restored by reverse suture of eyelids during the critical period in both wild-type and mutant mice. Such an activity-dependent increase in response would seem to require a mechanism like potentiation in vivo. Thus, the RIβ isoform of PKA is not essential for ocular dominance plasticity, which can proceed despite defects in several common in vitro models of neural plasticity.

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Postnatal maturation of GABA-mediated inhibition and cortical interneurons controls the timing of critical period plasticity in rodent primary visual cortex.
“The postnatal maturation of GABA-mediated inhibition and cortical interneurons is crucial for controlling the timing of critical period plasticity in rodent primary visual cortex (17,18).”
From MeCP2 regulates the timing of critical period plasticity that shapes functional connectivity in primary visual cortex (2015) · cites this paper as [17]

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Long-Term Potentiation and Memory
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Activity-regulated genes as mediators of neural circuit plasticity
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Two Forms of Synaptic Plasticity with Distinct Dependence on Age, Experience, and NMDA Receptor Subtype in Rat Visual Cortex
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Environmental enrichment from birth enhances visual acuity but not place learning in mice
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Mouse visual cortex
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Cyclic AMP-dependent protein kinase mediates ocular dominance shifts in cat visual cortex
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Impairment of Neocortical Long-Term Potentiation in Mice Deficient of Endothelial Nitric Oxide Synthase
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Developmentally Restricted Synaptic Plasticity in a Songbird Nucleus Required for Song Learning
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Gabaa receptor maturation in relation to eye opening in the rat visual cortex
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Developmental synaptic plasticity at the thalamocortical input to barrel cortex: Mechanisms and roles
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PRKAR1B mutation associated with a new neurodegenerative disorder with unique pathology
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Experience-dependent plasticity without long-term depression by type 2 metabotropic glutamate receptors in developing visual cortex
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Requirement for the RIIβ Isoform of PKA, But Not Calcium-Stimulated Adenylyl Cyclase, in Visual Cortical Plasticity
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Reduced presynaptic efficiency of excitatory synaptic transmission impairs LTP in the visual cortex of BDNF‐heterozygous mice
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NMDA Antagonists in the Superior Colliculus Prevent Developmental Plasticity But Not Visual Transmission or Map Compression
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Ocular Dominance Columns: Enigmas and Challenges
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Sensory Deprivation Unmasks a PKA-Dependent Synaptic Plasticity Mechanism that Operates in Parallel with CaMKII
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Reversible blockade of experience-dependent plasticity by calcineurin in mouse visual cortex
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LTP and LTD vary with layer in rodent visual cortex
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What's Critical for the Critical Period in Visual Cortex?
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Bidirectional Trafficking of Prostaglandin E2Receptors Involved in Long-Term Potentiation in Visual Cortex
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The Adult Visual Cortex Expresses Dynamic Synaptic Plasticity That Is Driven by the Light/Dark Cycle
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Transient PKA Activity Is Required for Initiation But Not Maintenance of BDNF-Mediated Protection from Nitric Oxide-Induced Growth-Cone Collapse
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The Two Regulatory Subunits ofAplysiacAMP-Dependent Protein Kinase Mediate Distinct Functions in Producing Synaptic Plasticity
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Core Differences in Synaptic Signaling Between Primary Visual and Dorsolateral Prefrontal Cortex
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Monocular Cells Without Ocular Dominance Columns
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AKAP‐independent localization of type‐II protein kinase A to dynamic actin microspikes
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Cyclic Nucleotides Modulate Genioglossus and Hypoglossal Responses to Excitatory Inputs in Rats
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α/β-tubulin are A kinase anchor proteins for type I PKA in neurons
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Experience‐dependent regulation of functional maps and synaptic protein expression in the cat visual cortex
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Candidate genes in ocular dominance plasticity
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Kv3.1 channels regulate the rate of critical period plasticity
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Comparison of plasticity in vivo and in vitro in the developing visual cortex of normal and protein kinase A RIbeta-deficient mice
Hensch, T. K., Gordon, J. A., Br, E. P., McKnight, G. S., Idzerda, R. L., & Stryker, M. P. (1998)
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Authors: Hensch, T. K., Gordon, J. A., Brandon, E. P., McKnight, G. S., Idzerda, R. L., & Stryker, M. P.
Affiliations: University of California, San Francisco (US)
University of Washington (US)
ORCID: Hensch, Takao K.
Gordon, Joshua A.
Brandon, Eugene P.
McKnight, G. Stanley
Stryker, Michael P.
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 1998-03-15
Volume: 18
Issue: 6
Pages: 2108-2117
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.18-06-02108.1998
PMC: PMC2553093
OpenAlex: W2171569315
Cited by: 117
References: 98
Citations by year: 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2018: 1 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 2 · 2013: 2 · 2012: 3
FWCI: 3.83
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 184 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (EY02874)
National Eye Institute (R01EY002874, EY-02874, R37EY002874)
National Institute of General Medical Sciences (GM32875, R01GM032875)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cognitive Neuroscience › Visual perception and processing mechanisms
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: visual cortex development, synaptic plasticity, long-term potentiation, long-term depression, depotentiation, paired-pulse facilitation, monocular deprivation, ocular dominance, critical period, pyramidal neurons, layer 2/3
MeSH terms: Action Potentials, Aging, Animals, Extracellular Space, Functional Laterality, Neuronal Plasticity, Ocular Physiological Phenomena, Reference Values, Sensory Deprivation, Synapses, Visual Cortex, Vision, Monocular, Long-Term Potentiation, Cyclic AMP-Dependent Protein Kinases, Patch-Clamp Techniques, Mice, Cyclic AMP-Dependent Protein Kinase RIbeta Subunit

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Comparison of Plasticity In Vivo and In Vitro in the Developing Visual Cortex of Normal and Protein Kinase A RIβ-Deficient Mice

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