Neuroanatomical distribution of galectin-3 in the adult rat brain

Abstract

Galectin-3 is a member of the lectin subfamily that enables the specific binding of β-galactosides. It is expressed in a broad spectrum of species and organs, and is known to have various functions related to cell adhesion, signal transduction, and proinflammatory responses. Although, expression of galectin-3 in some activated neuroglia under neuroinflammation has been well documented in the central nervous system, little is known about the neuronal expression and distribution of galectin-3 in normal brain. To describe the cellular and neuroanatomical expression map of galectin-3, we performed galectin-3 immunohistochemistry on the entire normal rat brain and subsequently analyzed the neuronal distribution. Galectin-3 expression was observed not only in some neuroglia but also in neurons. Neuronal expression of galectin-3 was observed in many functional parts of the cerebral cortex and various other subcortical nuclei in the hypothalamus and brainstem. Neuroanatomical analysis revealed that robust galectin-3 immuno-signals were present in many hypothalamic nuclei related to a variety of physiological functions responsible for mediating anxiety responses, energy balance, and neuroendocrine regulation. In addition, the regions highly connected with these hypothalamic nuclei also showed intense galectin-3 expression. Moreover, multiple key regions involved in regulating autonomic functions exhibited high levels of galectin-3 expression. In contrast, the subcortical nuclei responsible for the control of voluntary motor functions and limbic system exhibited no galectin-3 immunoreactivity. These observations suggest that galectin-3 expression in the rat brain seems to be regulated by developmental cascades, and that functionally and neuroanatomically related brain nuclei constitutively express galectin-3 in adulthood.

Association between heart rate variability indices and features of spontaneous ventricular tachyarrhythmias in mice

“…Interestingly, we noticed significant differences, between TG and TG/KO mice, in a few nonlinear‐domain indices, including FuEn, SampEn and LZC, albeit HR or linear‐domain indices were not altered in TG/KO relative to that of TG mice. While there has been no report of altered autonomic nervous activities by deletion of Gal‐3 gene, this possibility cannot be excluded considering that Gal‐3 is expressed in rodent brain including regions that regulate autonomic nervous activity 13 . This, if confirmed by further investigation, would shed light on potential physiological action of Gal‐3 in the nervous system.…”

“…Indeed, Takemoto et al found that treatment with Gal‐3 inhibitor restored electrophysiological parameters implying that Gal‐3 exerts electrophysiological effect 12 . While there has been no report on regulation by Gal‐3 of autonomic nervous activities, expression of Gal‐3 has been shown in brain neurons including regions involved in regulating autonomic nervous functions 13 . It remains unknown whether Gal‐3 gene deletion in the TG mice might affect the severity of VTAs as well as HRVs.…”

Expression and role of Galectin-3 in the postnatal development of the cerebellum

“…Our results are in concordance, showing high expression of LGALS3 in the choroid plexus beneath the cerebellum and in the subependymal zone of the fourth ventricle. In the brain parenchyma, some studies have reported neuronal expression of LGALS3 in the hippocampus and cerebellum [24,33,34], while others did not detect any neuronal expression [19,35]. In the cerebellum in particular, low levels of mRNA expression were reported in Purkinje cells and granule cells in an analysis of Allen Brain Atlas data by John and Mishra [33].…”

Galectin-3-Mediated Glial Crosstalk Drives Oligodendrocyte Differentiation and (Re)myelination

“…However, Gal-3 has been immunocytochemically detected in immature (PDGFRα, A2B5, and O4) and mature (O1, MBP, CNPase, PLP) OLG isolated from primary rat cultures, with higher levels in mature ones ( Pasquini et al, 2011 ). Recent work also outlines Gal-3 occasional expression by Rip+ OLG in white matter from normal rat brains ( Yoo et al, 2017 ). Gal-3 appears to be cleaved in OPC by MMP2 and then stabilized in mature OLG, which suggests variations in its biological activity during OLG differentiation ( Pasquini et al, 2011 ).…”

“…In terms of cell populations, Gal-3 expression has been detected in fibroblasts, chondrocytes, osteoblasts, osteoclasts, keratinocytes, Schwann cells, gastric mucosa and endothelial cells from various tissues and organs (reviewed by Dumic et al, 2006 ). In addition to reports on neuronal and glial expression ( Yoo et al, 2017 ), Gal-3 has been shown expressed in vivo by astrocytes in the subventricular zone (SVZ), being indispensable for cytoarchitecture maintenance but dispensable for apoptosis and proliferation ( Comte et al, 2011 ). Gal-3 also maintains cell motility toward the olfactory bulb, possibly through EGFR phosphorylation modulation ( Comte et al, 2011 ).…”