The distribution, activity, and function of the cilia in the frog brain

Nelson, Deborah J.; Wright, Ernest M.

doi:10.1113/jphysiol.1974.sp010742

Cited by 72 publications

(34 citation statements)

References 30 publications

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“…The choroidal epithelium is very folded, with several rims and folds branching off the central rim (see Nelson & Wright, 1974, plate 1). The percentage of successful penetrations was largest on the central rim, Furthermore, the epithelium at this central rim was flat over an area of 100 by 300 gm and perpendicular to the symmetry axis of the chamber.…”

Section: Resultsmentioning

confidence: 99%

Epithelial potassium transport: Tracer and electrophysiological studies in choroid plexus

Zeuthen

Wright

1981

J. Membrain Biol.

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Summary. Transport of potassium by bullfrog choroid plexus was studied using tracers and ion-selective microelectrodes. 1) Tracers."We measured unidirectional uptakes of 42K across each surface of the plexus, efflux of 42K from loaded tissues, intracellular potassium pools, and [3H]-ouabain binding. 42K uptake across the brush border membrane was composed of diffusional and saturable components. The saturable component exhibited kinetics of a two-site model with Km's of 0.3mM and a Vma~ of 81amol cm -2 hr -1. Ouabain inhibited uptake across the brush border membrane with a Ki of 1 • 10 7 M. Ethacrynic acid, phloretin, amiloride, and low sodium concentrations inhibited uptake, whereas bicarbonate ions increased transport up to 100%. The rate of ouabain-sensitive uptake across the serosal surface was only 6% of that across the ventricular surface. The efflux of potassium across the brush border membrane could account for most of the efflux from the epithelium. Potassium was accumulated within the plexus to a concentration in excess of 100 mM. 42K in the extracellular compartments exchanged with 40-55% of the intracellular potassium. Ouabain bound to the brush border membrane with a K,~ of 8 • 10 -7 M, a ks of 3.8 x 104 mol-1 min-~ and a k_ 1 of 3 • 10 -2 rain 2. Ouabain binding was blocked by cymarin and gitoxigin.2) Electrodes." Under control conditions the intracellular electrical potential, E ~c, was -45 mV and the apparent intracellular K+-concentration, K3, was 90 raM. K § ions appeared to be actively accumulated within the epithelium. E ~c and K~ + were followed under three experimental conditions: (i) treating the tissue with ouabain; (ii)varying the ventricular K § concentration; and (iii)passing transmural currents. It is concluded that the permeability of the ventricular membrane to potassium (1-5 x 10 -s cm sec -~) was much greater than the permeability of the serosal membrane and that the rate of K pumping into the epithelium was 0.35-0.55x10-9mol cm 2 sec 1 96% of the transmural current was paracellular, and the resistance of the serosal membrane was nine times greater than that of the ventricular membrane. Increasing K[ produced Nernstian changes in E ~c and E[ c, but the cells only depolarized by 0.13 mV for each mV increase in the chemical potential of the ventricular solutions.Both types of experiments are consistent with a model of the epithelium where the cells are predominantly K+-permeable (at the ventricular membrane) and there is a large paracellular shunt. K § is actively transported into the cells by a brush border Na/Kpump, only to leave the cell passively across the same membrane. The pump, which is electrogenic, transports two K ions into the cell for every three Na ions pumped out. There are about 10 • 106 pumps/ cell, and each pump turns over 10 times/sec. The choroid epithelium behaves as predicted by the model proposed first by Koefoed-Johnsen, V., Ussing, H.H. (1958) Acta Physiol. Scand. 42:298. The frog choroid plexus secretes cerebrospinal fluid (CSF) into the ventricles of t...

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Section: Resultsmentioning

confidence: 99%

Epithelial potassium transport: Tracer and electrophysiological studies in choroid plexus

Zeuthen

Wright

1981

J. Membrain Biol.

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“…Ciliary beating of the ependymal cells lining the ventricular system is responsible for the laminar flow of CSF occurring on the ventricular surface [16,17,63,64]. In the human brain, ciliary beating is essential for maintaining adequate CSF flow [65].…”

Section: At Late Gestational Stages Vz Disruption In the Telencephalmentioning

confidence: 99%

“…3f). In human embryos, there is also an early division of labor between the medial and the laterodorsal walls of the lateral ventricles, with the former probably engaged in the laminar flow of CSF [16,17] driven by multiciliated ependymal cells and the latter involved in neurogenesis (Fig. 2c, d).…”

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confidence: 99%

Neural Stem Cells and Fetal-Onset Hydrocephalus

Rodríguez¹,

Guerra²

2017

Pediatr Neurosurg

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Fetal-onset hydrocephalus is not only a disorder of cerebrospinal fluid (CSF) dynamics, but also a brain disorder. How can we explain the inborn and, so far, irreparable neurological impairment in children born with hydrocephalus? We hypothesize that a cell junction pathology of neural stem cells (NSC) leads to two inseparable phenomena: hydrocephalus and abnormal neurogenesis. All neurons, glial cells, and ependymal cells of the mammalian central nervous system originate from the NSC forming the ventricular zone (VZ) and the neural progenitor cells (NPC) forming the subventricular zone. Several genetic mutations and certain foreign signals all convey into a final common pathway leading to cell junction pathology of NSC and VZ disruption. VZ disruption follows a temporal and spatial pattern; it leads to aqueduct obliteration and hydrocephalus in the cerebral aqueduct, while it results in abnormal neurogenesis in the telencephalon. The disrupted NSC and NPC are released into the CSF and may transform into neurospheres displaying a junctional pathology similar to that of NSC of the disrupted VZ. These cells can then be utilized to investigate molecular alterations underlying the disease and open an avenue into possible NSC therapy.

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“…Winne 1976). Although the activity of cilia associated with a planar epithelium, like the frog choroid plexus, produces a mixing of the fluid within approximately 100 gm of the cell surface (Nelson and Wright 1974), molecules in the bulk phase must still diffuse through an unstirred layer above the fluid mixed by the cilia. This unstirred layer can be hundreds of microns thick (Nelson and Wright 1974).…”

Section: Discussionmentioning

confidence: 99%