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Review
. 2016 Sep;110(1-2):29-36.
doi: 10.1016/j.jphysparis.2016.11.003. Epub 2016 Nov 10.

Nicotinic Regulation of Experience-Dependent Plasticity in Visual Cortex

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Free PMC article
Review

Nicotinic Regulation of Experience-Dependent Plasticity in Visual Cortex

Masato Sadahiro et al. J Physiol Paris. .
Free PMC article

Abstract

While the cholinergic neuromodulatory system and muscarinic acetylcholine receptors (AChRs) have been appreciated as permissive factors for developmental critical period plasticity in visual cortex, it was unknown why plasticity becomes limited after the critical period even in the presence of massive cholinergic projections to visual cortex. In this review we highlighted the recent progresses that started to shed light on the role of the nicotinic cholinergic neuromodulatory signaling on limiting juvenile form of plasticity in the adult brain. We introduce the Lynx family of proteins and Lynx1 as its representative, as endogenous proteins structurally similar to α-bungarotoxin with the ability to bind and modulate nAChRs to effectively regulate functional and structural plasticity. Remarkably, Lynx family members are expressed in distinct subpopulations of GABAergic interneurons, placing them in unique positions to potentially regulate the convergence of GABAergic and nicotinic neuromodulatory systems to regulate plasticity. Continuing studies of the potentially differential roles of Lynx family of proteins may further our understanding of the fundamentals of molecular and cell type-specific mechanisms of plasticity that we may be able to harness through nicotinic cholinergic signaling.

Keywords: Cholinergic; Lynx1; Lypd6; Nicotinic; Plasticity; Visual cortex.

Conflict of interest statement

The authors declare no competing financial interests

Figures

Figure 1
Figure 1. The expression timecourse of cholinergic innervation, nicotinic acetylcholinergic receptors, and Lynx1 in the primary visual cortex
Cholinergic innervations of the V1 (denoted as ChAT expression) and expression of nAChRs, sharply elevate from birth and continue to follow along the rise of critical period after eye opening. In adulthood, while cholinergic signaling remains robust, Lynx1 increases to actively dampen nicotinic cholinergic signaling to effectively suppress plasticity.
Figure 2
Figure 2. The Lynx family of proteins as novel class of nicotinic cholinergic signaling modulators for regulating plasticity
A. Lynx1 and Lypd6 are representatives of the Ly-6/neurotoxin gene superfamily (Lynx family) of proteins and are negative and positive modulators of nAChR signaling respectively. Lynx1 elevates in expression while Lypd6 expression declines into adulthood. These expression patterns collectively dampen nAChR signaling in adult V1, and well positioned to subsequently suppress cortical plasticity. B. Lynx1 and Lypd6 are both preferably enriched in GABAergic interneurons than glutamatergic neurons in the V1, and furthermore within the GABAergic interneuronal subpopulations, they distinctly prefer PV and SST interneurons respectively. While future work should aim to investigate the PV interneuron-specific role of Lynx1 in suppressing cortical plasticity in adulthood, it would be of equal interest to investigate the potential involvement of SST interneurons and the associated nAChR subtype in mediating cortical plasticity where the expression of Lypd6 during the critical period could modulate their impact. The cortical circuit positioning of the SST interneurons as well Lypd6 being a positive modulator of nicotinic cholinergic signaling highlights an ideal position to drive inhibition that can efficiently mediate experience-dependent plasticity mechanisms.

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