scholarly journals Choroid Plexus Epithelium of the Fourth Ventricle

2020 ◽  
Author(s):  
Author(s):  
B. Van Deurs ◽  
J. K. Koehler

The choroid plexus epithelium constitutes a blood-cerebrospinal fluid (CSF) barrier, and is involved in regulation of the special composition of the CSF. The epithelium is provided with an ouabain-sensitive Na/K-pump located at the apical surface, actively pumping ions into the CSF. The choroid plexus epithelium has been described as “leaky” with a low transepithelial resistance, and a passive transepithelial flux following a paracellular route (intercellular spaces and cell junctions) also takes place. The present report describes the structural basis for these “barrier” properties of the choroid plexus epithelium as revealed by freeze fracture.Choroid plexus from the lateral, third and fourth ventricles of rats were used. The tissue was fixed in glutaraldehyde and stored in 30% glycerol. Freezing was performed either in liquid nitrogen-cooled Freon 22, or directly in a mixture of liquid and solid nitrogen prepared in a special vacuum chamber. The latter method was always used, and considered necessary, when preparations of complementary (double) replicas were made.


PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150945 ◽  
Author(s):  
Nathalie Strazielle ◽  
Rita Creidy ◽  
Christophe Malcus ◽  
José Boucraut ◽  
Jean-François Ghersi-Egea

2013 ◽  
Vol 305 (7) ◽  
pp. R679-R688 ◽  
Author(s):  
Allyson C. Marshall ◽  
Hossam A. Shaltout ◽  
Nancy T. Pirro ◽  
James C. Rose ◽  
Debra I. Diz ◽  
...  

Antenatal betamethasone (BM) therapy accelerates lung development in preterm infants but may induce early programming events with long-term cardiovascular consequences. To elucidate these events, we developed a model of programming whereby pregnant ewes are administered BM (2 doses of 0.17 mg/kg) or vehicle at the 80th day of gestation and offspring are delivered at term. BM-exposed (BMX) offspring develop elevated blood pressure; decreased baroreflex sensitivity; and alterations in the circulating, renal, and brain renin-angiotensin systems (RAS) by 6 mo of age. We compared components of the choroid plexus fourth ventricle (ChP4) and cerebral spinal fluid (CSF) RAS between control and BMX male offspring at 6 mo of age. In the choroid plexus, high-molecular-weight renin protein and ANG I-intact angiotensinogen were unchanged between BMX and control animals. Angiotensin-converting enzyme 2 (ACE2) activity was threefold higher than either neprilysin (NEP) or angiotensin 1-converting enzyme (ACE) in control and BMX animals. Moreover, all three enzymes were equally enriched by approximately 2.5-fold in ChP4 brush-border membrane preparations. CSF ANG-(1–7) levels were significantly lower in BMX animals (351.8 ± 76.8 vs. 77.5 ± 29.7 fmol/mg; P < 0.05) and ACE activity was significantly higher (6.6 ± 0.5 vs. 8.9 ± 0.5 fmol·min−1·ml−1; P < 0.05), whereas ACE2 and NEP activities were below measurable limits. A thiol-sensitive peptidase contributed to the majority of ANG-(1–7) metabolism in the CSF, with higher activity in BMX animals. We conclude that in utero BM exposure alters CSF but not ChP RAS components, resulting in lower ANG-(1–7) levels in exposed animals.


2020 ◽  
Vol 143 ◽  
pp. 152-157
Author(s):  
Riccardo Draghi ◽  
Lorenzo Mongardi ◽  
Riccardo Panzacchi ◽  
Umberto Godano ◽  
Ilaria Barni ◽  
...  

Neurosurgery ◽  
2003 ◽  
Vol 52 (6) ◽  
pp. 1400-1410 ◽  
Author(s):  
M. Faik Özveren ◽  
Uğur Türe ◽  
M. Memet Özek ◽  
M. Necmettin Pamir

Abstract OBJECTIVE Compared with other lower cranial nerves, the glossopharyngeal nerve (GPhN) is well hidden within the jugular foramen, at the infratemporal fossa, and in the deep layers of the neck. This study aims to disclose the course of the GPhN and point out landmarks to aid in its exposure. METHODS The GPhN was studied in 10 cadaveric heads (20 sides) injected with colored latex for microsurgical dissection. The specimens were dissected under the surgical microscope. RESULTS The GPhN can be divided into three portions: cisternal, jugular foramen, and extracranial. The rootlets of the GPhN emerge from the postolivary sulcus and course ventral to the flocculus and choroid plexus of the lateral recess of the fourth ventricle. The nerve then enters the jugular foramen through the uppermost porus (pars nervosa) and is separated from the vagus and accessory nerves by a fibrous crest. The cochlear aqueduct opens to the roof of this porus. On four sides in the cadaver specimens (20%), the GPhN traversed a separate bony canal within the jugular foramen; no separate canal was found in the other cadavers. In all specimens, the Jacobson's (tympanic) nerve emerged from the inferior ganglion of the GPhN, and the Arnold's (auricular branch of the vagus) nerve also consisted of branches from the GPhN. The GPhN exits from the jugular foramen posteromedial to the styloid process and the styloid muscles. The last four cranial nerves and the internal jugular vein pass through a narrow space between the transverse process of the atlas (C1) and the styloid process. The styloid muscles are a pyramid shape, the tip of which is formed by the attachment of the styloid muscles to the styloid process. The GPhN crosses to the anterior side of the stylopharyngeus muscle at the junction of the stylopharyngeus, middle constrictor, and hyoglossal muscles, which are at the base of the pyramid. The middle constrictor muscle forms a wall between the GPhN and the hypoglossal nerve in this region. Then, the GPhN gives off a lingual branch and deepens to innervate the pharyngeal mucosa. CONCLUSION Two landmarks help to identify the GPhN in the subarachnoid space: the choroid plexus of the lateral recess of the fourth ventricle and the dural entrance porus of the jugular foramen. The opening of the cochlear aqueduct, the mastoid canaliculus, and the inferior tympanic canaliculus are three landmarks of the GPhN within the jugular foramen. Finally, the base of the styloid process, the base of the styloid pyramid, and the transverse process of the atlas serve as three landmarks of the GPhN at the extracranial region in the infratemporal fossa.


2019 ◽  
Vol 40 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Ken Yanase ◽  
Naoya Uemura ◽  
Yoichi Chiba ◽  
Ryuta Murakami ◽  
Ryuji Fujihara ◽  
...  

2007 ◽  
Vol 292 (4) ◽  
pp. C1409-C1416 ◽  
Author(s):  
Boglarka Banizs ◽  
Peter Komlosi ◽  
Mark O. Bevensee ◽  
Erik M. Schwiebert ◽  
Phillip D. Bell ◽  
...  

Tg737 orpk mice have defects in cilia assembly and develop hydrocephalus in the perinatal period of life. Hydrocephalus is progressive and is thought to be initiated by abnormal ion and water transport across the choroid plexus epithelium. The pathology is further aggravated by the slow and disorganized beating of motile cilia on ependymal cells that contribute to decreased cerebrospinal fluid movement through the ventricles. Previously, we demonstrated that the hydrocephalus phenotype is associated with a marked increase in intracellular cAMP levels in choroid plexus epithelium, which is known to have regulatory effects on ion and fluid movement in many secretory epithelia. To evaluate whether the hydrocephalus in Tg737 orpk mutants is associated with defects in ion transport, we compared the steady-state pHi and Na+-dependent transport activities of isolated choroid plexus epithelium tissue from Tg737 orpk mutant and wild-type mice. The data indicate that Tg737 orpk mutant choroid plexus epithelium have lower pHi and higher Na+-dependent HCO3− transport activity compared with wild-type choroid plexus epithelium. In addition, wild-type choroid plexus epithelium could be converted to a mutant phenotype with regard to the activity of Na+-dependent HCO3− transport by addition of dibutyryl-cAMP and mutant choroid plexus epithelium toward the wild-type phenotype by inhibiting PKA activity with H-89. Together, these data suggest that cilia have an important role in regulating normal physiology of choroid plexus epithelium and that ciliary dysfunction in Tg737 orpk mutants disrupts a signaling pathway leading to elevated intracellular cAMP levels and aberrant regulation of pHi and ion transport activity.


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