Lynx1, a Cholinergic Brake, Limits Plasticity in Adult Visual Cortex
Open accessAbstract
Lynx Vision: Early in development, correct visual experiences during the so-called “critical period” build the foundations for visual function in adulthood. Hence, when one eye is not working together with the other, an adult may be left with imperfect vision. The plasticity characteristic of the critical period does not persist into adulthood, and later readjustments to visual function may not be fully successful. Morishita et al. (p. 1238 , published online 11 November; see the Perspective by Higley and Strittmatter ) have identified a gene in mice called Lynx1 , which shows increased expression after the critical period. The Lynx1 protein binds to and reduces the sensitivity of acetylcholine receptors, but if mice were treated to enhanced cholinergic signaling, their adult visual plasticity was improved and if mice lacked the Lynx1 gene altogether, they were able to recover visual function even in adulthood.
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Modulation of nicotinic function through the lynx1 protein is important for regulating the critical period for activity-dependent visual system development.
“modulation of nicotinic function through the lynx1 protein is also important for regulating the critical period for activity-dependent visual system development (Morishita et al. 2010).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Morishita et al. 2010
Various drugs, environmental manipulations, and genetic approaches have induced iPlasticity across several model systems and in people.
“Subsequently, several pharmacological treatments (Table 1) and environmental manipulations7,191–193, as well as genetic means, have been used to induce iPlasticity in several model systems and also in humans186.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [192]
Purely environmental manipulations, including enrichment or food restriction, can produce iPlasticity in visual cortex.
“iPlasticity can also be achieved in the visual cortex with purely environmental manipulations, such as environmental enrichment or food restriction in the visual cortex7,191–193.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [192]
Disruption of excitatory-inhibitory balance shifts the timing and quality of critical period development in primary visual cortex.
“Accordingly, disruption of E-I balance powerfully shifts the timing and quality of critical period development, as seen in the primary visual cortex (V1) (27–29).”
From Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons (2015) · cites this paper as [29]
An excessively plastic status may precede the progressive degenerative process as in other brain disorders.
“An excessively plastic status may precede the progressive degenerative process as in other brain disorders (29, 54).”
From Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons (2015) · cites this paper as [29]
Several molecular brakes relevant to schizophrenia, other than PNNs, limit critical period plasticity, including myelin signaling through NgR-PirB and dampened nicotinic receptor signaling by Lynx1.
“Several molecular brakes of relevance to schizophrenia (other than PNNs) have been identified to limit critical period plasticity, including myelin signaling through a NgR-PirB complex (2, 74, 75) or dampened nicotinic receptor signaling by Lynx1 (29, 76).”
From Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons (2015) · cites this paper as [29]
Signaling through nicotinic acetylcholine receptors is important for establishing critical periods for activity-dependent shaping of visual cortical function and maturation of thalamocortical and corticothalamic glutamatergic synapses.
“In addition, signaling through nAChRs is also important for establishing critical periods for activity-dependent shaping of visual cortical function (Morishita et al., 2010) and maturation of thalamocortical (Aramakis and Metherate, 1998; Aramakis et al., 2000; Hsieh et al., 2002) and corticothalamic (Heath et al., 2010; Horst et al., 2012; King et al., 2003; Picciotto et al., 1995) glutamatergic”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Morishita et al., 2010
ACh modulates cortical circuits over longer time scales by influencing the plasticity of cortical circuits.
“ACh also modulates cortical circuits over longer time scales by influencing the plasticity of cortical circuits.”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Morishita et al., 2010
In rodents, the protein Lynx1 suppresses nicotinic signaling in primary visual cortex, and its removal promotes ocular dominance plasticity in older animals.
“in rodents, the protein Lynx1 suppresses nicotinic signaling in primary visual cortex, and its removal promotes ocular dominance plasticity in older animals (Morishita et al., 2010).”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Morishita et al., 2010
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- Authors
- Morishita, H., Miwa, J. M., Heintz, N., & Hensch, T. K.
- Affiliations
- Boston Children's Hospital (US)
- California Institute of Technology (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Hensch, Takao K.
- Venue
- Science
- Published
- 2010-11-26
- Volume
- 330
- Issue
- 6008
- Pages
- 1238-1240
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3387538
- OpenAlex
- W2027220714
- Cited by
- 365
- References
- 36
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 8 · 2023: 12 · 2022: 15 · 2021: 22 · 2020: 31 · 2019: 23 · 2018: 29 · 2017: 26 · 2016: 24 · 2015: 31 · 2014: 31 · 2013: 33 · 2012: 36
- FWCI
- 12.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (DP1OD003699)
- National Institute on Drug Abuse (DA17279, R01DA017279)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- Lynx1, cholinergic neurotransmission, nicotinic acetylcholine receptors, adult visual cortex, experience-dependent plasticity, critical period, excitation-inhibition balance, cholinergic innervation
- MeSH terms
- Aging, Amblyopia, Animals, Cholinesterase Inhibitors, Evoked Potentials, Visual, Mecamylamine, Membrane Glycoproteins, Mice, Inbred C57BL, Neural Inhibition, Neuronal Plasticity, Neuropeptides, Physostigmine, Receptors, Nicotinic, Sensory Deprivation, Vision, Ocular, Visual Cortex, Visual Pathways, Signal Transduction, Mice, Knockout, Nicotinic Antagonists, Dominance, Ocular, Adaptor Proteins, Signal Transducing, Mice
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