Hydrocephalus disorders: their biophysical and neuroendocrine impact on the choroid plexus epithelium

Abstract

Publisher Summary This chapter discusses that choroid plexus (CP) epithelial cells carry out a wide variety of secretory and reabsorptive functions that, by way of cerebrospinal fluid (CSF) volume transmission, contribute to the stability of the neuronal extracellular environment. During fetal development, the brain critically depends upon the CP–CSF nexus for a steady supply of micronutrients and trophic factors to support normal growth. In adulthood, the CP reacts to biochemical and physical perturbations, associated with disease and trauma by secreting into CSF a wide array of growth factors, transport (carriage) proteins, and neuropeptides. Arginine vasopressin (AVP) and basic fibroblast growth factor (FGF–2) colocalize in the choroid epithelium. Release of these peptides at the blood–CSF barrier in response to ischemia and augmented intracranial pressure helps to repair injured tissue, and adjust CSF formation and pressure. The chapter discusses that as a part of homeostatic mechanisms to modulate extracellular fluid parameters, in the face of CSF distortions, such as ventriculomegaly, there is plasticity in regard to CP receptor targets for AVP and atrial natriuretic peptide (ANP). Functional and ultrastructural evidence is offered to support the model of a CSF neuroendocrine system, the histological substrate, of which is the “dark” epithelium in CP. The response of the AVP, ANP, and nitrergic (nNOS) systems to hydrocephalus provides insight on the fluid dynamics in the basolateral space between choroid epithelial cells.