The neuroplasticity marker PSA-NCAM: Insights into new therapeutic avenues for promoting neuroregeneration

Saini, Vedangana; Kaur, Taranjeet; Kalotra, Shikha; Kaur, Gurcharan

doi:10.1016/j.phrs.2020.105186

Cited by 12 publications

(8 citation statements)

References 173 publications

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“…In a recent report, this molecule is important in the maturation process of mouse cortical immature neurons since the removal of PSA accelerates the final development of these cells [126]. Most importantly, since PSA-NCAM is considered to be a potential target to facilitate repair/regeneration after CNS injury and disease [129], its expression/modulation should be investigated in studies asking whether the immature neurons can be activated in experimental conditions and disease models.…”

Section: Open Questions and Future Perspectivesmentioning

confidence: 99%

The PSA-NCAM-Positive “Immature” Neurons: An Old Discovery Providing New Vistas on Brain Structural Plasticity

Bonfanti

Seki

2021

Cells

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Studies on brain plasticity have undertaken different roads, tackling a wide range of biological processes: from small synaptic changes affecting the contacts among neurons at the very tip of their processes, to birth, differentiation, and integration of new neurons (adult neurogenesis). Stem cell-driven adult neurogenesis is an exception in the substantially static mammalian brain, yet, it has dominated the research in neurodevelopmental biology during the last thirty years. Studies of comparative neuroplasticity have revealed that neurogenic processes are reduced in large-brained mammals, including humans. On the other hand, large-brained mammals, with respect to rodents, host large populations of special “immature” neurons that are generated prenatally but express immature markers in adulthood. The history of these “immature” neurons started from studies on adhesion molecules carried out at the beginning of the nineties. The identity of these neurons as “stand by” cells “frozen” in a state of immaturity remained un-detected for long time, because of their ill-defined features and because clouded by research ef-forts focused on adult neurogenesis. In this review article, the history of these cells will be reconstructed, and a series of nuances and confounding factors that have hindered the distinction between newly generated and “immature” neurons will be addressed.

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Section: Open Questions and Future Perspectivesmentioning

confidence: 99%

The PSA-NCAM-Positive “Immature” Neurons: An Old Discovery Providing New Vistas on Brain Structural Plasticity

Bonfanti

Seki

2021

Cells

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“…Three main isoforms have been identified; two are transmembrane forms NCAM-140 and NCAM-180, while the third, NCAM-120 is anchored to the cell membrane through glycosylphosphatidylinositol (GPI) linkage ( Cox et al, 2009 ). Additionally, there is the polysialylated form of the neural cell adhesion molecule called PSA-NCAM; it is well documented that during CNS development, the PSA-NCAM is involved in precursor migration and in neuronal differentiation ( Hu et al, 1996 ; Petridis et al, 2004 ; Bonfanti, 2006 ; Rutishauser, 2008 ; Schuster et al, 2020 ), and also in the regulation of synaptic plasticity in adult brain ( Seki and Arai, 1993 ; Muller et al, 2000 ; Saini et al, 2020 ).…”

Section: Neural Cell Adhesion Molecule: Structure and Functionmentioning

confidence: 99%

Altering Cell-Cell Interaction in Prenatal Alcohol Exposure Models: Insight on Cell-Adhesion Molecules During Brain Development

Licheri

Brigman

2021

Front. Mol. Neurosci.

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Alcohol exposure during pregnancy disrupts the development of the brain and produces long lasting behavioral and cognitive impairments collectively known as Fetal Alcohol Spectrum Disorders (FASDs). FASDs are characterized by alterations in learning, working memory, social behavior and executive function. A large body of literature using preclinical prenatal alcohol exposure models reports alcohol-induced changes in architecture and activity in specific brain regions affecting cognition. While multiple putative mechanisms of alcohol’s long-lasting effects on morphology and behavior have been investigated, an area that has received less attention is the effect of alcohol on cell adhesion molecules (CAMs). The embryo/fetal development represents a crucial period for Central Nervous System (CNS) development during which the cell-cell interaction plays an important role. CAMs play a critical role in neuronal migration and differentiation, synaptic organization and function which may be disrupted by alcohol. In this review, we summarize the physiological structure and role of CAMs involved in brain development, review the current literature on prenatal alcohol exposure effects on CAM function in different experimental models and pinpoint areas needed for future study to better understand how CAMs may mediate the morphological, sensory and behavioral outcomes in FASDs.

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“…First, interference with the expression and/or function of these molecules in knock-out mice models or pharmacologically by the administration of antibodies, peptides, enzymes, or antisense oligonucleotides results in impaired long term potentiation (LTP) (Cremer et al, 2000;Eckhardt et al, 2000;Duncan et al, 2021) and learning and memory deficits (Cremer et al, 1994;Arami et al, 1996;Becker et al, 1996;Cambon et al, 2003;Seymour et al, 2008;Bisaz et al, 2009). Second, the converse evidence, i.e., improved LTP and enhanced learning abilities, has been achieved by mimicking NCAM function (Cambon et al, 2004) or by L1 or PSA-NCAM over-expression (Wolfer et al, 1998;Rendeiro et al, 2014;Saini et al, 2020). Third, mRNA and protein expression of NCAM, PSA-NCAM, and L1 in different Abbreviations: NCAM, neural cell adhesion molecule; LTP, long term potentiation; CS, conditioned stimulus; US, unconditioned stimulus; PSA, polysialic acid; EMG, electromyographic; OO, orbicularis oculi; CR, conditioned response; Ipsi, ipsilateral; Contra, contralateral. brain areas is regulated by learning and LTP (Ronn et al, 2000;Hartz and Rønn, 2010;Saini et al, 2020;Duncan et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

“…Second, the converse evidence, i.e., improved LTP and enhanced learning abilities, has been achieved by mimicking NCAM function (Cambon et al, 2004) or by L1 or PSA-NCAM over-expression (Wolfer et al, 1998;Rendeiro et al, 2014;Saini et al, 2020). Third, mRNA and protein expression of NCAM, PSA-NCAM, and L1 in different Abbreviations: NCAM, neural cell adhesion molecule; LTP, long term potentiation; CS, conditioned stimulus; US, unconditioned stimulus; PSA, polysialic acid; EMG, electromyographic; OO, orbicularis oculi; CR, conditioned response; Ipsi, ipsilateral; Contra, contralateral. brain areas is regulated by learning and LTP (Ronn et al, 2000;Hartz and Rønn, 2010;Saini et al, 2020;Duncan et al, 2021). Specifically, the expression of these CAMs is modulated in the hippocampus 1-24 h after LTP induction, by training in a memory task (Fazeli et al, 1994;Schuster et al, 1998;Ronn et al, 2000), or after a variety of hippocampaldependent training experiences including passive avoidance training (Doyle et al, 1992a;Fox et al, 1995Fox et al, , 2000Brandewiede et al, 2014), contextual fear conditioning (Merino et al, 2000;Sandi et al, 2003;Maćkowiak et al, 2009), and olfactory (Knafo et al, 2005a,b), and spatial (Sandi, 2004;Venero et al, 2006;Yamagishi et al, 2018) learning tests.…”

Section: Introductionmentioning

confidence: 99%

“…Both molecules also play a key role in regulating the structural synaptic changes underlying learning acquisition and memory formation ( Sandi, 2004 ; Bisaz et al, 2009 ; Conboy et al, 2010 ; Hartz and Rønn, 2010 ; Duncan et al, 2021 ). In addition, post-translational attachment of polysialic acid to NCAM (PSA-NCAM), a reaction shown to downregulate NCAM adhesion properties ( Rutishauser and Landmesser, 1996 ; Colley, 2010 ; Hildebrandt et al, 2010 ), has also been implicated in synaptic remodeling after learning experiences ( O’Malley et al, 2000 ; Kiss et al, 2001 ; El Maarouf and Rutishauser, 2010 ; Gascon et al, 2010 ; Saini et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

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Acquisition-dependent modulation of hippocampal neural cell adhesion molecules by associative motor learning

et al. 2022

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It is widely accepted that some types of learning involve structural and functional changes of hippocampal synapses. Cell adhesion molecules neural cell adhesion molecule (NCAM), its polysialylated form polysialic acid to NCAM (PSA-NCAM), and L1 are prominent modulators of those changes. On the other hand, trace eyeblink conditioning, an associative motor learning task, requires the active participation of hippocampal circuits. However, the involvement of NCAM, PSA-NCAM, and L1 in this type of learning is not fully known. Here, we aimed to investigate the possible time sequence modifications of such neural cell adhesion molecules in the hippocampus during the acquisition of a trace eyeblink conditioning. To do so, the hippocampal expression of NCAM, PSA-NCAM, and L1 was assessed at three different time points during conditioning: after one (initial acquisition), three (partial acquisition), and six (complete acquisition) sessions of the conditioning paradigm. The conditioned stimulus (CS) was a weak electrical pulse separated by a 250-ms time interval from the unconditioned stimuli (US, a strong electrical pulse). An acquisition-dependent regulation of these adhesion molecules was found in the hippocampus. During the initial acquisition of the conditioning eyeblink paradigm (12 h after 1 and 3 days of training), synaptic expression of L1 and PSA-NCAM was transiently increased in the contralateral hippocampus to the paired CS-US presentations, whereas, when the associative learning was completed, such increase disappeared, but a marked and bilateral upregulation of NCAM was found. In conclusion, our findings show a specific temporal pattern of hippocampal CAMs expression during the acquisition process, highlighting the relevance of NCAM, PSA-NCAM, and L1 as learning-modulated molecules critically involved in remodeling processes underlying associative motor-memories formation.

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The neuroplasticity marker PSA-NCAM: Insights into new therapeutic avenues for promoting neuroregeneration

Cited by 12 publications

References 173 publications

The PSA-NCAM-Positive “Immature” Neurons: An Old Discovery Providing New Vistas on Brain Structural Plasticity

The PSA-NCAM-Positive “Immature” Neurons: An Old Discovery Providing New Vistas on Brain Structural Plasticity

Altering Cell-Cell Interaction in Prenatal Alcohol Exposure Models: Insight on Cell-Adhesion Molecules During Brain Development

Acquisition-dependent modulation of hippocampal neural cell adhesion molecules by associative motor learning

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