Water transport becomes uncoupled from K+ siphoning in brain contusion, bacterial meningitis, and brain tumours: immunohistochemical case review
- Department of Cellular and Molecular Sciences, St George’s Hospital Medical School, London SW20 0RE, UK
- Correspondence to: Dr M Papadopoulos Cellular and Molecular Sciences (Infectious Diseases), St George’s Hospital Medical School, Cranmer Terrace, Tooting, London SW20 0RE, UK; mpapadopsghms.ac.uk
- Accepted 6 June 2003
Abstract
Specimens of normal human brain, contused brain, brain with bacterial meningitis, and brain tumours were immunolabelled for aquaporin 4 (AQP4) and Kir4.1. In normal brain tissue, AQP4 and Kir4.1 were detected around the microvessels. In pathological brain tissue, AQP4 was upregulated in astrocytes in oedematous regions and Kir4.1 was upregulated in astrocytes in damaged brain. Changes in α syntrophin expression paralleled those of AQP4 and Kir4.1. The following hypothesis is proposed: in astrocytes, under normal conditions, AQP4 couples water transport with Kir4.1 mediated K+ siphoning, but in pathological states, AQP4 facilitates the flow of brain oedema fluid, and Kir4.1 buffers increased extracellular K+.
