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Fig. 1 | Fluids and Barriers of the CNS

Fig. 1

From: Preclinical update on regulation of intracranial pressure in relation to idiopathic intracranial hypertension

Fig. 1

CSF secretion modulation at the choroid plexus. Simplified schematics of choroid plexus epithelial (CPe) cells. (Left cell) CSF secretion at CPe cells, whereby the activity of carbonic anhydrase (CA) generates carbonic acid which dissociates to a proton and a bicarbonate ion, these drive the sodium/hydrogen exchanger (NHE) and anion exchanger (AE2) respectively, transporting sodium and chloride ions into CPe cells. Additionally the basolateral sodium bicarbonate transporter (NBCn1) transports bicarbonate and sodium ions into the cell. These provide the ionic gradients to drive both the Na+/K+ ATPase and the NKCC1 channel to transport sodium into the ventricular spaces, this facilitates the osmosis of water via aquaporin 1 (AQP1). Furthermore the action of NKCC1 independently draws water from the cytosol to the ventricular space. The mechanisms of basolateral water transport remain unelucidated. Blue arrows represent the movement of water. CPe cell to the right represents current and proposed drug targets for modulating CSF secretion at the choroid plexus where the majority directly modifies the transport or generation of ions. The exceptions lie with somatostatin receptor (SST) agonist octreotide whose function and effect on ICP are unclear, and glucagon like peptide 1 receptor (GLP-1R) agonist exenatide which inhibits Na+/K+ATPase actity

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