Relationship between arterial and cisternal CSF oxygen tension in rabbits

1979 ◽  
Vol 236 (3) ◽  
pp. F220-F225
Author(s):  
L. Jankowska ◽  
P. Grieb
Keyword(s):  
Cerebrospinal Fluid ◽  
Linear Regression ◽  
Choroid Plexus ◽  
Oxygen Tension ◽  
Linear Regression Equation ◽  
Mechanically Ventilated ◽  
Fluid Formation ◽  
And Function ◽  
Ionic Exchanges ◽  
Arterial Po2

Oxygen tension was measured in samples of blood and cisternal cerebrospinal fluid taken from anesthetized, paralyzed, and mechanically ventilated rabbits at various levels of arterial PO2. Cerebrospinal fluid oxygen tension (CSF PO2) was correlated with arterial PO2 (linear regression equation PCSFO2 = 0.2472 Pao2 + 42.34). During hypoxia CSF PO2 was higher than arterial PO2 in most experiments. These data can be attributed to the Bohr effect, which would increase the PO2 of the blood in choroid plexus capillaries as a result of its acidification. The acidification was suggested by Maren (Am. J. Physiol. 222: 885-889, 1972) to be a part of the ionic exchanges involved in cerebrospinal fluid formation. Such a mechanism may be of importance for supporting choroid plexus metabolism and function during hypoxia. This mechanism is most clearly seen in the rabbit.

Choroid plexus Na+/K+-activated adenosine triphosphatase and cerebrospinal fluid formation

Neurosurgery ◽  
1985 ◽  
Vol 17 (5) ◽  
pp. 768???72 ◽  
Author(s):  
M Pollay ◽  
B Hisey ◽  
E Reynolds ◽  
P Tomkins ◽  
F A Stevens ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Adenosine Triphosphatase ◽  
Fluid Formation

Benzodiazepine receptors and cerebrospinal fluid formation

1990 ◽  
Vol 72 (5) ◽  
pp. 759-762 ◽  
Author(s):  
Gregg L. Williams ◽  
Michael Pollay ◽  
Thomas Seale ◽  
Brent Hisey ◽  
P. Alex Roberts
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Binding Sites ◽  
Benzodiazepine Receptors ◽  
Secretory Activity ◽  
Assay Method ◽  
Content Type ◽  
High Affinity ◽  
Fluid Formation

✓ There is autoradiographic evidence that peripheral-type benzodiazepine ligands bind with high affinity to the membranes of choroid plexus tissue. In this study, the binding of a 4′-chloro analog of diazepam (Ro 5-4864) to rabbit choroid plexus and cerebral cortex was accomplished utilizing an in vitro radioactive assay method. A kinetic analysis of this binding revealed a relatively high affinity of this ligand (KD) for peripheral binding sites in plexus tissue (KD = 16.1 nM/mg protein). There was a 4.6-fold greater density of binding sites (total receptor density (Bmax) = 2.3 pmol/mg) in choroidal membrane as compared to cortical tissue (Bmax = 0.5 pmol/mg). In 40 rabbits in which a ventricular perfusion system was used, the rate of cerebrospinal fluid (CSF) formation was observed to decrease some 48% in the presence of 10−4 M Ro 5-4864, although some inhibition of secretory activity was still noted at a CSF concentration of 10−8 M. The choroid plexus tissue levels of adenosine 3′,5′cyclic monophosphate (cAMP) and adenosine triphosphatase (ATPase) were not affected by 10−4 M Ro 5-4864. The results of this study support the notion that the specific benzodiazepine peripheral binding sites in choroid plexus serve to modulate CSF formation. The mechanism of action is poorly understood but does not involve the transport ATPase system or the second messenger cAMP.

Maturational differences in acetazolamide-altered pH and HCO3 of choroid plexus, cerebrospinal fluid, and brain

1992 ◽  
Vol 262 (5) ◽  
pp. R909-R914 ◽  
Author(s):  
C. E. Johanson ◽  
Z. Parandoosh ◽  
M. L. Dyas
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Cortex ◽  
Carbonic Anhydrase ◽  
Choroid Plexus ◽  
Intracellular Ph ◽  
Ph Regulation ◽  
Secretory Process ◽  
Sprague Dawley ◽  
Infant Rats ◽  
Fluid Formation

The carbonic anhydrase inhibitor acetazolamide is useful for analyzing ion transport, pH regulation, and fluid formation in developing central nervous system. We used the 14C-labeled dimethadione technique to measure alterations in steady-state pH, and to estimate the HCO3 concentration [HCO3], in choroid plexus (CP), cerebrospinal fluid (CSF), and cerebral cortex of 1- and 3-wk-old Sprague-Dawley rats treated with acetazolamide or probenecid. These drugs can suppress transport of HCO3 and other anions in some cells, consequently altering intracellular pH. In 1-wk-old infant rats whose CSF secretory process is incompletely developed, 1 h of acetazolamide treatment did not significantly change CP intracellular pH or [HCO3]. However, in 3-wk-old rats, in which the ability of CP to secrete ions and fluids is almost fully developed, acetazolamide caused marked increases in CP cell intracellular pH and [HCO3]. In contrast, acetazolamide-induced alkalinization was not observed in CSF or cerebral cortex of the 1- and 3-wk-old animals. The other test agent, probenecid (an inhibitor of anion transport but not of carbonic anhydrase), did not alter the pH of any region at any age investigated. Overall, the results are interpreted in light of developmental changes in carbonic anhydrase and previous findings from kinetic analyses of ion-translocating systems in CP. Acetazolamide may interfere with a CP apical membrane HCO3 extrusion mechanism not fully operational in infant rats.

Cotransport of sodium and chloride by the adult mammalian choroid plexus

1990 ◽  
Vol 258 (2) ◽  
pp. C211-C216 ◽  
Author(s):  
C. E. Johanson ◽  
S. M. Sweeney ◽  
J. T. Parmelee ◽  
M. H. Epstein
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Drug Effects ◽  
Disulfonic Acid ◽  
Base Line ◽  
Sprague Dawley ◽  
Disulfonic Stilbene ◽  
Fluid Formation ◽  
Vitro Analysis

Cerebrospinal fluid formation stems primarily from the transport of Na and Cl in choroid plexus (CP). To characterize properties and modulation of choroidal transporters, we tested diuretics and other agents for ability to alter ion transport in vitro. Adult Sprague-Dawley rats were the source of CPs preincubated with drug for 20 min and then transferred to cerebrospinal fluid (CSF) medium containing 22Na or 36Cl with [3H]mannitol (extracellular correction). Complete base-line curves were established for cellular uptake of Na and Cl at 37 degrees C. The half-maximal uptake occurred at 12 s, so it was used to assess drug effects on rate of transport (nmol Na or Cl/mg CP). Bumetanide (10(-5) and 10(-4) M) decreased uptake of Na and Cl with maximal inhibition (up to 45%) at 10(-5) M. Another cotransport inhibitor, furosemide (10(-4) M), reduced transport of Na by 25% and Cl by 33%. However, acetazolamide (10(-4) M) and atriopeptin III (10(-7) M) significantly lowered uptake of Na (but not Cl), suggesting effect(s) other than on cotransport. The disulfonic stilbene 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 10(-4) M), known to inhibit Cl-HCO3 exchange, substantially reduced the transport of 36Cl. Bumetanide plus DIDS (both 10(-4) M) caused additive inhibition of 90% of Cl uptake, which provides strong evidence for the existence of both cotransport and antiport Cl carriers. Overall, this in vitro analysis, uncomplicated by variables of blood flow and neural tone, indicates the presence in rat CP of the cotransport of Na and Cl in addition to the established Na-H and Cl-HCO3 exchangers.

scholarly journals The Wilms Tumor Gene wt1a Contributes to Blood-Cerebrospinal Fluid Barrier Function in Zebrafish

2022 ◽  
Vol 9 ◽  
Author(s):  
Vera L. Hopfenmüller ◽  
Birgit Perner ◽  
Hanna Reuter ◽  
Thomas J. D. Bates ◽  
Andreas Große ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Wilms Tumor ◽  
Barrier Properties ◽  
Suppressor Gene ◽  
Ependymal Cells ◽  
Urogenital Development ◽  
And Function ◽  
Dorsal Hindbrain

The Wilms tumor suppressor gene Wt1 encodes a zinc finger transcription factor, which is highly conserved among vertebrates. It is a key regulator of urogenital development and homeostasis but also plays a role in other organs including the spleen and the heart. More recently additional functions for Wt1 in the mammalian central nervous system have been described. In contrast to mammals, bony fish possess two paralogous Wt1 genes, namely wt1a and wt1b. By performing detailed in situ hybridization analyses during zebrafish development, we discovered new expression domains for wt1a in the dorsal hindbrain, the caudal medulla and the spinal cord. Marker analysis identified wt1a expressing cells of the dorsal hindbrain as ependymal cells of the choroid plexus in the myelencephalic ventricle. The choroid plexus acts as a blood-cerebrospinal fluid barrier and thus is crucial for brain homeostasis. By employing wt1a mutant larvae and a dye accumulation assay with fluorescent tracers we demonstrate that Wt1a is required for proper choroid plexus formation and function. Thus, Wt1a contributes to the barrier properties of the choroid plexus in zebrafish, revealing an unexpected role for Wt1 in the zebrafish brain.

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