Different inflammatory reactions to vitamin D3 among the lateral, third and fourth ventricular choroid plexuses of the rat

Levine, Seymour; Saltzman, Arthur; Ginsberg, Stephen D.

doi:10.1016/j.yexmp.2008.06.003

Cited by 3 publications

(1 citation statement)

References 27 publications

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“…Ventricular CP variations include epithelial cell pH, K + /Na + , organic anion transport capability, water content, and blood flow (Harbut and Johanson 1986; Murphy and Johanson 1990; Pappenheimer, Heisey, and Jordan 1961; Szmydynger-Chodobska, Chodobski, and Johanson 1994). Inflammatory responses also vary in third ventricle CP versus the structure of the CP in other regions (Levine, Saltzman, and Ginsberg 2008). Given the regional differences in CP baseline physiology and structure, one expects variations in how a particular CP responds to pathogens and toxic agents.…”

Section: Introductionmentioning

confidence: 99%

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

et al. 2010

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Bordering the ventricular cerebrospinal fluid (CSF) are epithelial cells of choroid plexus (CP), ependyma and circumventricular organs (CVOs) that contain homeostatic transporters for mediating secretion/reabsorption. The distributional pathway (''nexus'') of CP-CSF-ependyma-brain furnishes peptides, hormones, and micronutrients to periventricular regions. In disease/toxicity, this nexus becomes a conduit for infectious and xenobiotic agents. The sleeping sickness trypanosome (a protozoan) disrupts CP and downstream CSF-brain. Piperamide is anti-trypanosomic but distorts CP epithelial ultrastructure by engendering hydropic vacuoles; this reflects phospholipidosis and altered lysosomal metabolism. CP swelling by vacuolation may occlude CSF flow. Toxic drug tools delineate injuries to choroidal compartments: cyclophosphamide (vasculature), methylcellulose (interstitium), and piperazine (epithelium). Structurally perturbed CP allows solutes to penetrate the ventricles. There, CSF-borne pathogens and xenobiotics may permeate the ependyma to harm neurogenic stem cell niches. Amoscanate, an anti-helmintic, potently injures rodent ependyma. Ependymal/brain regions near CP are vulnerable to CSF-borne toxicants; this proximity factor links regional barrier breakdown to nearby periventricular pathology. Diverse diseases (e.g., African sleeping sickness, multiple sclerosis) take early root in choroidal, circumventricular, or perivascular loci. Toxicokinetics informs on pathogen, anti-parasitic agent, and auto-antibody distribution along the CSF nexus. CVOs are susceptible to plasma-borne toxicants/pathogens. Countering the physico-chemical and pathogenic insults to the homeostasis-mediating ventricle-bordering cells sustains brain health and fluid balance.

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Section: Introductionmentioning

confidence: 99%

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

et al. 2010

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The Blood–Cerebrospinal Fluid Barrier: Structure and Functional Significance

Johanson

Stopa

McMillan

2010

Methods in Molecular Biology

193

163

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The choroid plexus (CP) of the blood-CSF barrier (BCSFB) displays fundamentally different properties than blood-brain barrier (BBB). With brisk blood flow (10 × brain) and highly permeable capillaries, the human CP provides the CNS with a high turnover rate of fluid (∼400,000 μL/day) containing micronutrients, peptides, and hormones for neuronal networks. Renal-like basement membranes in microvessel walls and underneath the epithelium filter large proteins such as ferritin and immunoglobulins. Type IV collagen (α3, α4, and α5) in the subepithelial basement membrane confers kidney-like permselectivity. As in the glomerulus, so also in CP, the basolateral membrane utrophin A and colocalized dystrophin impart structural stability, transmembrane signaling, and ion/water homeostasis. Extensive infoldings of the plasma-facing basal labyrinth together with lush microvilli at the CSF-facing membrane afford surface area, as great as that at BBB, for epithelial solute and water exchange. CSF formation occurs by basolateral carrier-mediated uptake of Na+, Cl-, and HCO3-, followed by apical release via ion channel conductance and osmotic flow of water through AQP1 channels. Transcellular epithelial active transport and secretion are energized and channeled via a highly dense organelle network of mitochondria, endoplasmic reticulum, and Golgi; bleb formation occurs at the CSF surface. Claudin-2 in tight junctions helps to modulate the lower electrical resistance and greater permeability in CP than at BBB. Still, ratio analyses of influx coefficients (Kin) for radiolabeled solutes indicate that paracellular diffusion of small nonelectrolytes (e.g., urea and mannitol) through tight junctions is restricted; molecular sieving is proportional to solute size. Protein/peptide movement across BCSFB is greatly limited, occurring by paracellular leaks through incomplete tight junctions and low-capacity transcellular pinocytosis/exocytosis. Steady-state concentration ratios, CSF/plasma, ranging from 0.003 for IgG to 0.80 for urea, provide insight on plasma solute penetrability, barrier permeability, and CSF sink action to clear substances from CNS.

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Vacuolar Pathology in the Median Eminence of the Hypothalamus After Hyponatremia

Levine¹,

Saltzman²,

Ginsberg³

2011

J Neuropathol Exp Neurol

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The median eminence of the hypothalamus is an important conduit by which neurosecretory hormones from hypothalamic nuclei are delivered to the pars nervosa (neural lobe) of the pituitary en route to the bloodstream. Dilutional hyponatremia was produced in adult rats to determine the effect on the morphology of the median eminence of the hypothalamus. Hyponatremia was caused by reducing electrolyte and organic osmolyte reserves in order to block the excretion of water through delivery of the nephrotoxin mercuric chloride (HgCl2). Histological examination of the brain 1 day following a hyponatremic insult revealed vacuolation within the median eminence of the hypothalamus. No other lesions were found in other parts of the brain following hyponatremia. The hyponatremic lesion consisted of a band of closely packed vacuoles that crossed the floor of the third ventricle. Vacuoles associated with hyponatremia were predominantly in the subependymal, fiber, reticular, and palisade layers of the median eminence. Vacuolation was not observed in the tanycyte layer of the median eminence. This study indicates that the median eminence is a potentially vulnerable site in human hyponatremic conditions that should be evaluated further in relevant animal models.

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Different inflammatory reactions to vitamin D3 among the lateral, third and fourth ventricular choroid plexuses of the rat

Cited by 3 publications

References 27 publications

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

The Blood–Cerebrospinal Fluid Barrier: Structure and Functional Significance

Vacuolar Pathology in the Median Eminence of the Hypothalamus After Hyponatremia

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