Anat Cell Biol.  2011 Mar;44(1):50-59. 10.5115/acb.2011.44.1.50.

The effects of electrical shock on the expressions of aquaporin subunits in the rat spinal cords

• Yeo SI
• Ryu HJ
• Kim JE
• Chun W
• Seo CH
• Lee BC
• Choi IG
• Sheen SH
• Kang TC

• KMID: 2168868
• DOI: http://doi.org/10.5115/acb.2011.44.1.50

Abstract

We analyzed aquaporin (AQP) expression in the rat spinal cord following an electrical shock (ES) to elucidate the roles of AQP in spinal cord injury (SCI) induced by an electrical burn. In control animals, AQP1 immunoreactivity was observed in the small diameter dorsal horn fibers of laminae I and II and in astrocytes and neurons in the spinal cord. Both AQP4 and AQP9 immunoreactivity were detected in astrocytes. One week after the ES, AQP1 immunoreactivity in dorsal horn fibers was downregulated to 83, 61, and 33% of control levels following a 1-, 4-, or 6-second ES, respectively. However, AQP1 immunoreactivity in ventral horn neurons increased to 1.3-, 1.5-, and 2.4-fold of control levels following a 1-, 4-, or 6-second ES, respectively. AQP4 immunoreactivity was upregulated after an ES in laminae I and II astrocytes in a stimulus-intensity independent manner. Unlike AQP1 and AQP4, AQP9 immunoreactivity was unaffected by the ES. These findings indicate that altered AQP immunoreactivity may be involved in SCI following an ES.

Keyword

Aquaporins; Astrocytes; Neurons; Spinal cord; Electrical shock

MeSH Terms

Animals
Anterior Horn Cells
Aquaporins
Astrocytes
Burns
Horns
Neurons
Rats
Shock
Spinal Cord
Spinal Cord Injuries
Aquaporins

Figure

• 

  Fig. 1 Aquaporin (AQP)1 immunoreactivity in rat spinal cord following an electrical shock (ES). (A) Control. (B) 1 s ES. (C) 4 s ES. (D) 6 s ES. In control rats, AQP1 immunoreactivity was observed in the small diameter dorsal horn fibers in laminae I and II. After the ES, AQP1 immunoreactivity in dorsal horn fibers was downregulated in a stimulus-intensity dependent manner (arrows, column 2). However, AQP1 immunoreactivity in neurons within the ventral horn was clearly upregulated in a stimulus-intensity dependent manner (arrows, column 3). Rectangles in column 1 indicate a region in columns 2 and 3, respectively. Scale bar=400 µm (column 1), 50 µm (columns 2, 3). (E) Quantitative analyses of AQP1 in the spinal cord following an ES (mean±SEM). Significant differences from control animals, *P<0.05, **P<0.01.

• 

  Fig. 2 Double immunofluorescent staining for aquaporins (AQPs), NeuN, or glial fibrillary acidic protein (GFAP) in the spinal cord. AQP1 immunoreactivity (A1, arrow) was not detected in NeuN-positive dorsal horn neurons of the 6-s electrical shock (ES) animals (A2, arrow). In the ventral horn, AQP1 immunoreactivity (B1, C1) was observed in GFAP astrocytes (B2, arrows) and NeuN-positive neurons (C2, arrows). AQP4 (D1, arrows) and AQP9 (E1, arrows) immunoreactivity was detected in GFAP astrocytes (D2, E2, arrows). Blue (column 3) is DAPI counterstaining. Column 4 is a merged-image. Scale bar=12.5 µm.

• 

  Fig. 3 Aquaporin (AQP)4 immunoreactivity in the rat spinal cord following an electrical shock (ES). (A) Control. (B) 1 s ES. (C) 4 s ES. (D) 6 s ES. After the ES, AQP4 immunoreactivity was upregulated in astrocytes within laminae I and II in a stimulus-intensity independent manner (column 2). However, AQP4 immunoreactivity in the ventral horn was unaffected by the ES. Rectangles in column 1 indicate a region in columns 2 and 3, respectively. Scale bar=400 µm (column 1), 50 µm (columns 2, 3). (E) Quantitative analyses of AQP4 in the spinal cord following an ES (mean±SEM). Significant differences from control animals, *P<0.05, **P<0.01.

• 

  Fig. 4 Aquaporin (AQP)9 immunoreactivity in the rat spinal cord following an electrical shock (ES). (A) Control. (B) 1 s ES. (C) 4 s ES. (D) 6 s ES. Unlike AQP1 and AQP4, AQP9 immunoreactivity was unaffected by the ES. Rectangles in column 1 indicate a region in columns 2 and 3, respectively. Scale bar=400 µm (column 1), 50 µm (columns 2, 3). (E) Quantitative analyses of AQP9 in the spinal cord following an ES (mean±SE). Significant differences from control animals.

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