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onsdag 20 mars 2013

Aivoselkäydinneste (1)

Aineistoa suomennettavaksi:
1)  2007
Pflugers Arch. 2007 Apr;454(1):1-18. Epub 2006 Nov 21.

Water and solute secretion by the choroid plexus.

Source

The Water and Salt Research Center & Institute of Anatomy, University of Aarhus, Wilhelm Meyers Allé, 8000 Aarhus, Denmark. jp@ana.au.dk

Abstract

The cerebrospinal fluid (CSF) provides mechanical and chemical protection of the brain and spinal cord. This review focusses on the contribution of the choroid plexus epithelium to the water and salt homeostasis of the CSF, i.e. the secretory processes involved in CSF formation. The choroid plexus epithelium is situated in the ventricular system and is believed to be the major site of CSF production. Numerous studies have identified transport processes involved in this secretion, and recently, the underlying molecular background for some of the mechanisms have emerged. The nascent CSF consists mainly of NaCl and NaHCO(3), and the production rate is strictly coupled to the rate of Na(+) secretion. In contrast to other secreting epithelia, Na(+) is actively pumped across the luminal surface by the Na(+),K(+)-ATPase with possible contributions by other Na(+) transporters, e.g. the luminal Na(+),K(+),2Cl(-) cotransporter. The Cl(-) and HCO(3) (-) ions are likely transported by a luminal cAMP activated inward rectified anion conductance, although the responsible proteins have not been identified. Whereas Cl(-) most likely enters the cells through anion exchange, the functional as well as the molecular basis for the basolateral Na(+) entry are not yet well-defined. Water molecules follow across the epithelium mainly through the water channel, AQP1, driven by the created ionic gradient. In this article, the implications of the recent findings for the current model of CSF secretion are discussed. Finally, the clinical implications and the prospects of future advances in understanding CSF production are briefly outlined.

(2) 2001

Microsc Res Tech. 2001 Jan 1;52(1):49-59.

Mechanisms of CSF secretion by the choroid plexus.

Source

School of Biological Sciences, University of Manchester, Manchester M13 9PT, United Kingdom.

Abstract

The epithelial cells of the choroid plexus secrete cerebrospinal fluid (CSF), by a process that involves the movement of Na(+), Cl(-) and HCO(3)(-) from the blood to the ventricles of the brain. This creates the osmotic gradient, which drives the secretion of H(2)O. The unidirectional movement of the ions is achieved due to the polarity of the epithelium, i.e., the ion transport proteins in the blood-facing (basolateral) are different to those in the ventricular (apical) membranes. Saito and Wright (1983) proposed a model for secretion by the amphibian choroid plexus, in which secretion was dependent on activity of HCO(3)(-) channels in the apical membrane. The patch clamp method has now been used to study the ion channels expressed in rat choroid plexus. Two potassium channels have been observed that have a role in maintaining the membrane potential of the epithelial cell, and in regulating the transport of K(+) across the epithelium. An inward-rectifying anion channel has also been identified, which is closely related to ClC-2 channels, and has a significant HCO(3)(-) permeability. This channel is expressed in the apical membrane of the epithelium where it may play an important role in CSF secretion. A model of CSF secretion by the mammalian choroid plexus is proposed that accommodates these channels and other data on the expression of transport proteins in the choroid plexus.
Copyright 2001 Wiley-Liss, Inc.

(2) 2009 Kloridin jakautumahäiriö  aivoautonomian alueella.

J Neurol Sci. 2009 Oct 15;285(1-2):146-8. doi: 10.1016/j.jns.2009.06.026. Epub 2009 Jul 12.

Decreased chloride levels of cerebrospinal fluid in patients with amyotrophic lateral sclerosis.

Source

Department of Internal Medicine, Division of Neurology, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan. watasho@hyo-med.ac.jp

Abstract

Recent studies have suggested that the elevation of intracellular chloride contributes to excitotoxic cell death in motor neuron and can be related to the pathogenesis of amyotrophic lateral sclerosis (ALS). We investigated whether chloride levels in cerebrospinal fluid (CSF) and serum were lower in ALS patients than in control patients with other neurological diseases (OND). We also examined the relationship between chloride levels and clinical ALS phenotypes. We measured chloride levels (CSF and serum) in 27 ALS patients and 33 age- and gender-matched OND controls admitted to our hospital for diagnosis. The CSF chloride levels were lower in ALS patients (117 [range 102-130] mmol/L) than in OND controls (126 [range 114-134] mmol/L) . There was no significant difference in CSF chloride levels among the sub-groups of ALS patients classified according to their age, gender, duration of illness, clinical state and type of onset (P>0.05). CSF chloride levels already significantly decreased in ALS patients at the time of diagnosis. We conclude that the elevation of intracellular chloride would cause the reduction of chloride in CSF and be related to the pathogenesis of ALS.

  •  (4) 1969 Aivoselkäydinnesteen kloridipitoisuus on korkeampi kuin muissa kehon nesteissä
 Vanha Harper antaa kloridin distribuutiotiedot tähän tapaan, mitä voi pitää viiteellisenä 1960 luvulta. :
Koko veri 250 mg  100 millissä
Plasma tai seerum  365 mg  100 millissä.
Solut 190  mg  100 millissä
Aivoselkäydinneste 440 mg  100 millissä
Lihaskudos 40  mg 100 millissä
Hermokudos 171  mg 100 millissä.

Kloridin tarvpeen määritelyssä varman tuo likvorin  pitoisuus  on merkitsevä seikka.  Tosin siinä on  indiffusible - momentti,   aivo retentoi kloridia tuohon aivotyynyosaan, likvoriin.
likvori taas vaihtuu aika nopeasti useita  kertoja päivässä. Miten siinä  resoptiovaiheessa koridi toimii? Ei ainakaan pyri  suuremmalti erittymään poispäin.

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