The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) has received much attention in recent years and it is often used as a marker of neuronal cells undergoing structural and functional changes. The association of NCAM with chains of polysialic acid is finely tuned throughout nervous system development to confer the molecule a role as negative modulator of cell adhesive properties thereby allowing neurons to undergo plastic changes, such as neurite outgrowth and synaptic reorganization, in both embryonic and adult life. In adult mammals, PSA-NCAM expression persists in cerebral regions such as the hippocampus, the olfactory cortex, the medial prefrontal cortex, the amygdala, the hypothalamus, and terminal regions of primary sensory afferents where continuous remodelling has been described. In man, selected populations of central and peripheral neurons have been reported to express PSA-NCAM in normal conditions, supporting the concept of an involvement of this molecule in structural and functional plasticity throughout life. Accordingly, expression of PSA-NCAM is regulated in response to events involving synaptic structural plasticity such as learning, memory consolidation, chronic stress or chronic antidepressant treatment and different types of neuronal lesion models. Interestingly, its localization in subpopulations of primary sensory neurons suggests that PSA-NCAM may also have a part in the processing of somatosensory information. Here, by presenting both original observations from our laboratory and literature data, we review knowledge on the occurrence of the molecule in sensory ganglia, brainstem nuclei and hippocampal formation of the human nervous system at different developmental ages spanning from prenatal and postnatal to adult life. As morphological support of the possible interactions of PSA-NCAM with neurotrophic factors, data on PSA-NCAM codistribution with the neurotrophin BDNF in the brainstem are reviewed and novel findings on PSA-NCAM/BDNF codistribution and colocalization in the hippocampus are presented.
Polysialylated-neural cell adhesion molecole (PSA-NCAM) in the human nervous system at prenatal, postnatal, and adult ages
QUARTU, MARINA;SERRA, MARIA PINA;BOI, MARIANNA;DEMONTIS, ROBERTO;MELIS, TIZIANA;PODDIGHE, LAURA;
2013-01-01
Abstract
The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) has received much attention in recent years and it is often used as a marker of neuronal cells undergoing structural and functional changes. The association of NCAM with chains of polysialic acid is finely tuned throughout nervous system development to confer the molecule a role as negative modulator of cell adhesive properties thereby allowing neurons to undergo plastic changes, such as neurite outgrowth and synaptic reorganization, in both embryonic and adult life. In adult mammals, PSA-NCAM expression persists in cerebral regions such as the hippocampus, the olfactory cortex, the medial prefrontal cortex, the amygdala, the hypothalamus, and terminal regions of primary sensory afferents where continuous remodelling has been described. In man, selected populations of central and peripheral neurons have been reported to express PSA-NCAM in normal conditions, supporting the concept of an involvement of this molecule in structural and functional plasticity throughout life. Accordingly, expression of PSA-NCAM is regulated in response to events involving synaptic structural plasticity such as learning, memory consolidation, chronic stress or chronic antidepressant treatment and different types of neuronal lesion models. Interestingly, its localization in subpopulations of primary sensory neurons suggests that PSA-NCAM may also have a part in the processing of somatosensory information. Here, by presenting both original observations from our laboratory and literature data, we review knowledge on the occurrence of the molecule in sensory ganglia, brainstem nuclei and hippocampal formation of the human nervous system at different developmental ages spanning from prenatal and postnatal to adult life. As morphological support of the possible interactions of PSA-NCAM with neurotrophic factors, data on PSA-NCAM codistribution with the neurotrophin BDNF in the brainstem are reviewed and novel findings on PSA-NCAM/BDNF codistribution and colocalization in the hippocampus are presented.
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