Kainic acid-induced convulsions cause prolonged changes in the chondroitin sulfate proteoglycans neurocan and phosphacan in the limbic structures

Okamoto, Masahiro; Sakiyama, Junko; Mori, Shuji; Kurazono, Sekiko; Usui, Shinichi; Hasegawa, Masatoshi; Oohira, Atsuhiko

doi:10.1016/s0014-4886(03)00251-6

Cited by 52 publications

(50 citation statements)

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“…Previous western blot and immunohistochemical analyses show that neurocan increases and phosphacan decreases within 24 h after KA treatment in the rat hippocampus (Okamoto et al, 2003). Consistent with these data, we found that Neurocan …”

Section: Accepted Manuscriptsupporting

confidence: 92%

“…Dysregulation of PNNs is implicated in various neurological and psychiatric disorders including epilepsy, Alzheimer's disease, bipolar disorder, schizophrenia, and traumatic brain injury (Baig et al, 2005;McRae and Porter, 2012;Morawski et al, 2010;Okamoto et al, 2003;Pantazopoulos et al, 2015;Yi et al, 2012). Additionally, alteration of C6ST-1 expression and CS sulfation patterns are reportedly evident in brains of human patients with bipolar disorder or schizophrenia and mice with cortical brain injury (Okuda et al, 2014;Pantazopoulos et al, 2015;Yi et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Reportedly, alteration of CS sulfation patterns and/or PNNs is evident in various neurological and psychiatric disorders including epilepsy, Alzheimer's disease, ischemic stroke, bipolar disorder, schizophrenia, and traumatic brain injury(Baig et al, 2005;Bonneh-Barkay and Wiley, 2009;Cabungcal et al, 2013; Hobohm et al, 2005;Okamoto et al, 2003;Pantazopoulos et al, 2015;Swarup et al, 2013;Yi et al, 2012). For example, postmortem analysis of amygdala indicates that 6-sulfated CS chains recognized by CS-56 are less numerous in brains from patients with schizophrenia or bipolar disorder than in control brains.…”

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confidence: 99%

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Involvement of chondroitin 6-sulfation in temporal lobe epilepsy

Yutsudo

Kitagawa

2015

Experimental Neurology

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Section: Accepted Manuscriptsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Involvement of chondroitin 6-sulfation in temporal lobe epilepsy

Yutsudo

Kitagawa

2015

Experimental Neurology

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“…The structural and molecular organization of PNNs is heterogeneous and depends on the neuronal cell types consisting of tenascin-R, aggrecan and neurocan that enwraps the perikaryon of several neurons [48,49]. PNNs dysfunction has been implicated in several neuropsychiatric disorders, including epilepsy [50,51]. Brain-specific CSPG includs aggrecan and neurocan in the developing and mature rat brain and has been demonstrated to control axonal extension or regeneration via inhibition of neuronal cell migration and neurite extension from surviving neurons [52–54].…”

Section: Discussionmentioning

confidence: 99%

AMPA Receptor Antagonist NBQX Decreased Seizures by Normalization of Perineuronal Nets

Chen

Gao

et al. 2016

PLoS ONE

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Epilepsy is a serious brain disorder with diverse seizure types and epileptic syndromes. AMPA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzoquinoxaline-2,3-dione (NBQX) attenuates spontaneous recurrent seizures in rats. However, the anti-epileptic effect of NBQX in chronic epilepsy model is poorly understood. Perineuronal nets (PNNs), specialized extracellular matrix structures, surround parvalbumin-positive inhibitory interneurons, and play a critical role in neuronal cell development and synaptic plasticity. Here, we focused on the potential involvement of PNNs in the treatment of epilepsy by NBQX. Rats were intraperitoneally (i.p.) injected with pentylenetetrazole (PTZ, 50 mg/kg) for 28 consecutive days to establish chronic epilepsy models. Subsequently, NBQX (20 mg/kg, i.p.) was injected for 3 days for the observation of behavioral measurements of epilepsy. The Wisteria floribundi agglutinin (WFA)-labeled PNNs were measured by immunohistochemical staining to evaluate the PNNs. The levels of three components of PNNs such as tenascin-R, aggrecan and neurocan were assayed by Western blot assay. The results showed that there are reduction of PNNs and decrease of tenascin-R, aggrecan and neurocan in the medial prefrontal cortex (mPFC) in the rats injected with PTZ. However, NBQX treatment normalized PNNs, tenascin-R, aggrecan and neurocan levels. NBQX was sufficient to decrease seizures through increasing the latency to seizures, decrease the duration of seizure onset, and reduce the scores for the severity of seizures. Furthermore, the degradation of mPFC PNNs by chondroitinase ABC (ChABC) exacerbated seizures in PTZ-treated rats. Finally, the anti-epileptic effect of NBQX was reversed by pretreatment with ChABC into mPFC. These findings revealed that PNNs degradation in mPFC is involved in the pathophysiology of epilepsy and enhancement of PNNs may be effective for the treatment of epilepsy.

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“…Phosphacan/RPTPbeta isoforms might also play active roles in the regulation of cellular changes associated with pathologies in the CNS. Indeed, the level of expression of the isoforms has been found to be regulated in a specific manner in penetrant lesions of the CNS (Deller et al 1997;McKeon et al 1999;Dobbertin et al 2003), and phosphacan has been recently shown to be specifically upregulated in the dentate gyrus of epileptic mice (Okamoto et al 2003;Heck et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Cortical neurons express PSI, a novel isoform of phosphacan/RPTPbeta

et al. 2005

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Phosphacan is a chondroitin sulfate proteoglycan representing the secreted extracellular part of a transmembrane receptor protein tyrosine phosphatase (RPTP-beta). These isoforms have been implicated in cell-extracellular matrix signaling events associated with myelination, axon growth, and cell migration in the developing central nervous system and may play critical roles in the context of brain pathologies. Recently, we have reported the identification of a new isoform of phosphacan, the phosphacan short isoform (PSI), the expression of which peaks in the second postnatal week. PSI interacts with the neuronal receptors L1 and F3/contactin and can promote neurite growth of cortical neurons. In this study, we have assessed, by in situ hybridization, the expression profile of PSI in the rat brain at postnatal day 7. PSI is largely expressed in the gray matter of the developing cerebral cortex in which it colocalizes with phosphacan, whereas the expression of RPTPbeta receptor forms is restricted to the ventricular area in which PSI has not been observed. Neurons from all layers of the cortex express PSI. In the cerebellum, on the other hand, no expression of PSI has been detected, although the other phosphacan/RPTP-beta isoforms show strong PSI expression here. Overall, our study suggests that PSI is expressed during the postnatal period in differentiated neurons of the cortex but is absent from structures in which proliferation and migration occur. The significance of these observations is discussed in the context of previous models of phosphacan/RPTP-beta functions.

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Kainic acid-induced convulsions cause prolonged changes in the chondroitin sulfate proteoglycans neurocan and phosphacan in the limbic structures

Cited by 52 publications

References 49 publications

Involvement of chondroitin 6-sulfation in temporal lobe epilepsy

Involvement of chondroitin 6-sulfation in temporal lobe epilepsy

AMPA Receptor Antagonist NBQX Decreased Seizures by Normalization of Perineuronal Nets

Cortical neurons express PSI, a novel isoform of phosphacan/RPTPbeta

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