Persistent cortical plasticity by upregulation of chondroitin 6-sulfation

In the citing paper

“As a result, transgenic mice overexpressing C6ST--1 retain a juvenile level of ocular dominance plasticity even in adulthood (Miyata et al., 2012).”

In the citing paper

“Overall then, there is a substantial increase in the 4--sulfation/6-sulfation (C4S/C6S) ratio during brain development (Kitagawa et al., 1997;Miyata et al., 2012).”

In the citing paper

“Specifically, 6--O--sulfation is dominant in the juvenile brain to produce C6S, which is more permissive (Lin et al., 2011;Miyata et al., 2012)”

In the citing paper

“While chondroitin 4-sulphates (C4S) are inhibitory [5], chondroitin 6-sulphates (C6S) are more permissive to plasticity and regeneration [173, 174], and the balance between C6S and C4S regulates neuroplasticity.”

In the citing paper

“The relative abundance of CS isomers incorporated into the CS-GAG chains has been linked to key biological functions within the brain including charged molecule diffusion (0S-CS (Nicholson & Hrabětová 2017)), neurocircuit plasticity (4S-CS and 6S-CS (Miyata et al. 2012; Yang et al. 2021)), glial scarring (4S6S-CS (Brown et al. 2012)), and neurite outgrowth (2S6S-CS (Shida et al. 2019; Clement et a”

In the citing paper

“Recent work suggests that microgliosis represents a potential mechanism driving PNN loss in models of neurodegeneration (Miyata et al. 2012; Miyata & Kitagawa 2016; Crapser et al. 2021)”

In the citing paper

“Second, PNN disruption prevents the persistent uptake of Otx2 homeoprotein into the enwrapped PV-cells required for their maintenance (27, 40, 41) (Fig. S3).”

In the citing paper

“Compromised PNNs prevent the persistent uptake of Otx2 homeoprotein into the enwrapped PV-cells needed for their maturation (including PNN maintenance itself) (27, 40, 41).”

In the citing paper

“This is further supported by the demonstration that the knock-out of specific sulfotranferases that modify the PNN structure interferes with Otx2 internalization and CP closure (Miyata et al., 2012)”

In the citing paper

“The model also stipulates that early sensory experience (sensory input) initiates expression of Otx2 binding sites on nascent PNNs (Beurdeley et al., 2012; Miyata et al., 2012), facilitating Otx2 import and opening a period of plasticity.”

In the citing paper

“where they form a reticular dendrosomatic structure around largely parvalbumin-expressing interneurons”

In the citing paper

“Chondroitin-4-sulfation (CS-4) and chondroitin-6 sulfation (CS-6) are the two most common sulfation patterns in the brain, with several variations depending on the position of the sulfation on the CS chains43, 44”

In the citing paper

“Numbers of CS chains and their patterns of sulfation fundamentally affect their functions, such as their ability to interact with other molecules including growth factors and cytokines.43”

In the citing paper

“Fourth, disruption of PNNs can alter the resting membrane potential of PV neurons (Miyata et al, 2012) and decrease the amplitudes of both inhibitory (Liu et al, 2013) and excitatory (Pyka et al, 2011) postsynaptic currents.”

In the citing paper

“Several studies suggest that ECM components, including PNNs, are critical regulators of synaptic plasticity (Do et al, 2015;Miyata et al, 2012;Morishita et al, 2015).”

In the citing paper

“For example, altered sulfation of N-acetylgalactosamine (GalNAc, a major disaccharide found in CSPGs) results in greatly reduced WFA labeling (Miyata et al, 2012).”

In the citing paper

“Interestingly, it has been recently shown that a developmental increase in the 4-sulfation/6-sulfation (4S/6S) ratio of CSPGs has a role in the closure of the critical period for ocular dominance plasticity in the mouse visual cortex, and condensation of CSPGs into PNNs is prevented by cell-autonomous overexpression of chondroitin 6-sulfation, which maintains a low 4S/6S ratio (Miyata et al., 2012”

In the citing paper

“Indeed, the maturation and phenotypic maintenance of PVI require incorporation of a non-cell autonomous homeobox protein, Otx2, through its affinity with PNN (Beurdeley et al., 2012; Miyata et al., 2012).”

In the citing paper

“Given the pivotal role of PVI, PNN, and myelin in regulating brain plasticity dynamics and active epochs (McGee et al., 2005; Miyata et al., 2012; Morishita and Hensch, 2008), the dysregulation of this “hub” could yield the slow emergence of clinical symptoms by altering the timing of key windows of critical period of brain plasticity (Morishita et al., 2010, abstract Neuroscience Meeting, 62.30).”