Role of transthyretin in thyroxine transfer from cerebrospinal fluid to brain and choroid plexus

2006 ◽  
Vol 291 (5) ◽  
pp. R1310-R1315 ◽  
Author(s):  
Nouhad A. Kassem ◽  
Rashid Deane ◽  
Malcolm B. Segal ◽  
Jane E. Preston

The transport of 125I-labeled thyroxine (T4) from the cerebrospinal fluid (CSF) into brain and choroid plexus (CP) was measured in anesthetized rabbit [0.5 mg/kg medetomidine (Domitor) and 10 mg/kg pentobarbitonal sodium (Sagatal) iv] using the ventriculocisternal (V-C) perfusion technique. 125I-labeled T4 contained in artificial CSF was continually perfused into the lateral ventricles for up to 4 h and recovered from the cisterna magna. The %recovery of 125I-labeled T4 from the aCSF was 47.2 ± 5.6% ( n = 10), indicating removal of 125I-labeled T4 from the CSF. The recovery increased to 53.2 ± 6.3% ( n = 4) and 57.8 ± 14.8% ( n = 3), in the presence of 100 and 200 μM unlabeled-T4, respectively ( P < 0.05), indicating a saturable component to T4 removal from CSF. There was a large accumulation of 125I-labeled T4 in the CP, and this was reduced by 80% in the presence of 200 μM unlabeled T4, showing saturation. In the presence of the thyroid-binding protein transthyretin (TTR), more 125I-labeled T4 was recovered from CSF, indicating that the binding protein acted to retain T4 in CSF. However, 125I-labeled T4 uptake into the ependymal region (ER) of the frontal cortex also increased by 13 times compared with control conditions. Elevation was also seen in the hippocampus (HC) and brain stem. Uptake was significantly inhibited by the presence of endocytosis inhibitors nocodazole and monensin by > 50%. These data suggest that the distribution of T4 from CSF into brain and CP is carrier mediated, TTR dependent, and via RME. These results support a role for TTR in the distribution of T4 from CSF into brain sites around the ventricular system, indicating those areas involved in neurogenesis (ER and HC).

1979 ◽  
Vol 50 (5) ◽  
pp. 677-681 ◽  
Author(s):  
Steven K. Gudeman ◽  
Humbert G. Sullivan ◽  
Michael J. Rosner ◽  
Donald P. Becker

✓ The authors report a patient with bilateral papillomas of the choroid plexus of the lateral ventricles with documentation of cerebrospinal fluid (CSF) hypersecretion causing hydrocephalus. Special attention is given to the large volume of CSF produced by these tumors (removal of one tumor reduced CSF outflow by one-half) and to the fact that CSF diversion was not required after both tumors were removed. Since tumor removal alone was sufficient to stop the progression of hydrocephalus, we feel that this case supports the concept that elevated CSF production by itself is sufficient to cause hydrocephalus in patients with papillomas of the choroid plexus.


1989 ◽  
Vol 3 (10) ◽  
pp. 1559-1568 ◽  
Author(s):  
Lucy Y.-H. Tseng ◽  
Alexandra L. Brown ◽  
Yvonne W.-H. Yang ◽  
Joyce A. Romanus ◽  
Craig C. Orlowski ◽  
...  

1976 ◽  
Vol 51 (s3) ◽  
pp. 399s-402s ◽  
Author(s):  
P. Schelling ◽  
J. S. Hutchinson ◽  
U. Ganten ◽  
G. Sponer ◽  
D. Ganten

1. Anaesthetized, nephrectomized rats were infused intravenously with unlabelled angiotensin II (AII) or with [3H]angiotensin II (3H-labelled AII). The brain ventricular system was perfused with artificial cerebrospinal fluid. The perfusate was collected from the cisterna magna and analysed for AII by radioimmunological and biochemical methods. 2. No increase of immunoreactive AII in cerebrospinal fluid could be shown during intravenous infusion of AII. 3. During intravenous infusions of 3H-labelled AII at pressor doses small amounts of radioactivity were found in cerebrospinal fluid perfusate. 4. The radioactivity of cerebrospinal fluid outflow could not be related to AII.


Cephalalgia ◽  
2016 ◽  
Vol 36 (14) ◽  
pp. 1379-1384 ◽  
Author(s):  
Kathrin Doppler ◽  
Morten Schütt ◽  
Claudia Sommer

Background Idiopathic intracranial hypertension is characterized by increased intracranial pressure. Its pathogenesis is largely unknown. Aquaporins may play a role in the homeostasis of cerebrospinal fluid. Methods We aimed to elucidate the role of aquaporins in idiopathic intracranial hypertension by measuring the level of aquaporin-1 and aquaporin-4 in the cerebrospinal fluid and plasma of 28 patients and 29 controls by enzyme-linked immunosorbent assay. The adipokines leptin and retinol-binding protein 4 were also measured. Results We found a reduction in aquaporin-4 in the cerebrospinal fluid of patients. Leptin levels were increased in the cerebrospinal fluid and plasma of patients and were correlated with weight, body mass index and body fat. There was no difference between patients and controls in the levels of aquaporin-4 and retinol-binding protein 4. Conclusion Our data suggest that an imbalance of aquaporin-4 in the cerebrospinal fluid of patients with idiopathic intracranial hypertension may contribute to the pathogenesis of this disorder.


1994 ◽  
Vol 80 (2) ◽  
pp. 321-323 ◽  
Author(s):  
Hirofumi Hirano ◽  
Kazuho Hirahara ◽  
Tetsuhiko Asakura ◽  
Tetsuro Shimozuru ◽  
Koki Kadota ◽  
...  

✓ A case is reported of hydrocephalus due to overproduction of cerebrospinal fluid (CSF) caused by villous hypertrophy of the choroid plexus in the lateral ventricles. A 7-year-old girl with mental retardation developed gait disturbance; hydrocephalus and a Dandy-Walker cyst were detected on computerized tomography. She was initially treated with a ventriculoperitoneal shunt; however, shunting failed to control the hydrocephalus. The excessive outflow of CSF suggested choroid plexus abnormality, and magnetic resonance (MR) imaging revealed enlargement of the choroid plexus in both lateral ventricles. The patient was therefore diagnosed as having hydrocephalus induced by overproduction of CSF, which was controlled by resection of the choroid plexus. Histological examination showed the structure typical of normal choroid plexus. This is a rare case of villous hypertrophy of the choroid plexus in which MR imaging assisted in the diagnosis.


Author(s):  
J. E. Michaels ◽  
P. A. Tornheim

In mammals, the caudal roof of the fourth ventricle consists of an inner layer of ependymal cells and an outer layer of leptomeningeal cells. It contains specializations in the form of tufts of choroid plexus for the elaboration of cerebrospinal fluid (CSF) as well as gross apertures that permit open communication between the ventricular system and the subarachnoid space, an essential feature for mammalian CSF circulation. In the bullfrog, as in most submammals, the roof of the fourth ventricle contains a rostral rhombencephalic choroid plexus with no gross evidence of fourth ventricular apertures. Communication between the ventricular system and the subarachnoid space in this animal, however, has been demonstrated to occur by way of microscopic openings or pores in the caudal roof of the hindbrain or the posterior rhombencephalic tela choroidea.


2019 ◽  
Vol 14 (9) ◽  
pp. 923-930 ◽  
Author(s):  
Natalia Egorova ◽  
Elie Gottlieb ◽  
Mohamed Salah Khlif ◽  
Neil J Spratt ◽  
Amy Brodtmann

Background Cerebrospinal fluid circulation is crucial for the functioning of the brain. Aging and brain pathologies such as Alzheimer’s disease have been associated with a change in the morphology of the ventricles and the choroid plexus. Despite the evidence from animal models that the cerebrospinal fluid system plays an important role in neuroinflammation and the restoration of the brain after ischemic brain injury, little is known about changes to the choroid plexus after stroke in humans. Aims Our goal was to characterize structural choroid plexus changes poststroke. Methods We used an automatic segmentation tool to estimate the volumes of choroid plexus and lateral ventricles in stroke and control participants at three time points (at baseline, 3 and 12 months) over the first year after stroke. We assessed group differences cross-sectionally at each time point and longitudinally. For stroke participants, we specifically differentiated between ipsi- and contra-lesional volumes. Statistical analyses were conducted for each region separately and included covariates such as age, sex, total intracranial volume, and years of education. Results We observed significantly larger choroid plexus volumes in stroke participants compared to controls in both cross-sectional and longitudinal analyses. Choroid plexus volumes did not exhibit any change over the first year after stroke, with no difference between ipsi- and contra-lesional volumes. This was in contrast to the volume of lateral ventricles that we found to enlarge over time in all participants, with more accelerated expansion in stroke survivors ipsi-lesionally. Conclusions Our results suggest that chronic stages of stroke are characterized by larger choroid plexus volumes, but the enlargement likely takes place prior to or very early after the stroke incident.


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