Effects of Salt Loading on the Morphology of Astrocytes in the Ventral Glia Limitans of the Rat Supraoptic Nucleus Journal Articles uri icon

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abstract

  • In the ventral glial limitans (VGL) of the supraoptic nucleus (SON) of the rat, a unique astrocyte type is found with an ability to undergo striking morphological plasticity in response to a wide range of physiological stimulations such as chronic hypernatraemia. This includes a thinning of the VGL, which contains the somata and proximal processes of these astrocytes, as well as an almost complete withdrawal of their vertically‐oriented distal processes. Currently, there is little information available on the types of astrocytes that reside in the SONVGL and which of these exhibit state‐dependent structural plasticity. To address this, we enabled the visualisation of single SONVGL glia using two novel cell labelling techniques with fluorescence microscopy. First, we used an inducible genetic reporter mouse line that allowed the specific labelling of a low density of astrocytes expressing glutamate and aspartate transporter (GLAST)/excitatory amino acid transporter 1. This approach revealed a high degree of variability in the morphology of mouse SONVGL astrocytes, in contrast to what has been reported for cortical astrocytes. Next, we used the DiOlistlic labelling approach to label single glial cells with DiI in the SONVGL of rats. Astrocytes observed using this approach shared the morphological features of GLAST‐expressing astrocytes in the mouse SONVGL. Specific structural aspects of these cells were modified by chronic hypernatraemia achieved by 7‐day salt loading. Notably, the average area of cells exhibiting protoplasmic features was significantly reduced in the horizontal plane, and the size of varicosities present on fibrous projections was significantly enlarged. These observations indicate that novel cell labelling methods can significantly advance our understanding of SONVGL cells and reveal specific forms of morphological plasticity that can be driven by chronic hypernatraemia.

authors

  • Choe, Katrina
  • Prager‐Khoutorsky, M
  • Farmer, WT
  • Murai, KK
  • Bourque, CW

publication date

  • April 2016