Changes in number of water-filled vesicles of choroid plexus in early and late phase of experimental rabbit subarachnoid hemorrhage model; the role of petrous ganglion of glossopharyngeal nerve

Aydın, Mehmet Dumlu; Kanat, Ayhan; Türkmenoğlu, Osman; Yolaş, Coşkun; Gündoğdu, Cemal

doi:10.1007/s00701-014-2088-7

Cited by 41 publications

(28 citation statements)

References 28 publications

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“…Hypersecretion of CSF may also be induced by stimulation of glossopharyngeal and vagus nerve endings that innervate the CP epithelium and arteries. An increase of cytoplasmic water vesicles in the acute phase of SAH is probably due to irritation of both nerves [191][192][193]. Moreover, a recent study suggests that AQP1 may also contribute to hypersecretion of CSF and post-hemorrhagic hydrocephalus.…”

Section: Hemorrhagic Strokementioning

confidence: 99%

“…↓ CSF secretion [198] ↑ mRNA for NF-κB, MCP-1, IL1R1, IL-8, IL-6, FAS, TNF-α expression [183] ↑ Iba-1+ and CD68+ epiplexus cells [186] ↑ Number of cytoplasmic water vesicles [191][192][193] ↑ HO-1 expression [183] ↑ AQP1 expression [194] Activation of TLR4 [182] Ischemic Apoptosis or necrosis according to the severity of ischemic injury [201] ↑ ED1+ number, CR3 receptors, expression of MHC I and MHC II antigens [217] ↑ Calcium transfer to CSF [210] Alteration in B-CSF barrier after middle cerebral artery occlusion [207] ↑ Apoptotic cells characterized by nuclear DNA fragmentation after middle cerebral artery occlusion [201] ↑ iNOS expression in epiplexus cells, Number of OX-42+ , ED1+ , OX-18+ , OX-6+ cells in epiplexus position [217] ↑ Permeability of B-CSF barrier for inulin after bilateral carotid occlusion [205] ↑ Expression of TGFβ1, brain-derived neurotrophic factor and other growth factors [216] ↑ MMP-9 expression in infiltrating macrophages [214] ↑ VEGF and eNOS expression [217,218] Plasma membrane and organelle damage; clumping of nuclear chromatin after forebrain ischemia [205,206] ↑ Number of macrophages [220] ↑ CP epithelial cell proliferation Expression of NeuN and GFAP after middle cerebral artery occlusion [215] CP as invasion route for T cells into the ischemic brain [219] Edema, apoptosis of CP epithelial cells after middle cerebral artery occlusion Indistinct epithelial membranes and varying degrees of pyknosis after middle cerebral artery occlusion [214] Desquamation of CP epithelial cells [199] ↓ AQP1 expression up to 24 h ↑ AQP1expression between 24-48 h after global cerebral ischemia [209] ↑ VCAM-1, MAdCAM-1, C3CL1, Nt5e expression [220] Traumatic TBI ↑ Intercellular spaces between CP epithelial cells [225] ↑ Macrophage number in epiplexus position after non-penetrative injury…”

Section: Transporters Othersmentioning

confidence: 99%

See 1 more Smart Citation

Choroid plexus and the blood–cerebrospinal fluid barrier in disease

Solar

Zamani

Kubíčková

et al. 2020

Fluids Barriers CNS

156

113

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The choroid plexus (CP) forming the blood-cerebrospinal fluid (B-CSF) barrier is among the least studied structures of the central nervous system (CNS) despite its clinical importance. The CP is an epithelio-endothelial convolute comprising a highly vascularized stroma with fenestrated capillaries and a continuous lining of epithelial cells joined by apical tight junctions (TJs) that are crucial in forming the B-CSF barrier. Integrity of the CP is critical for maintaining brain homeostasis and B-CSF barrier permeability. Recent experimental and clinical research has uncovered the significance of the CP in the pathophysiology of various diseases affecting the CNS. The CP is involved in penetration of various pathogens into the CNS, as well as the development of neurodegenerative (e.g., Alzheimer´s disease) and autoimmune diseases (e.g., multiple sclerosis). Moreover, the CP was shown to be important for restoring brain homeostasis following stroke and trauma. In addition, new diagnostic methods and treatment of CP papilloma and carcinoma have recently been developed. This review describes and summarizes the current state of knowledge with regard to the roles of the CP and B-CSF barrier in the pathophysiology of various types of CNS diseases and sets up the foundation for further avenues of research. Publisher's NoteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Section: Hemorrhagic Strokementioning

confidence: 99%

Section: Transporters Othersmentioning

confidence: 99%

Choroid plexus and the blood–cerebrospinal fluid barrier in disease

Solar

Zamani

Kubíčková

et al. 2020

Fluids Barriers CNS

156

113

View full text Add to dashboard Cite

show abstract

“…Aydin et al . showed an important link between petrous ganglion cells and water vesicles of CP were decreased in the late phase of SAH due to ischemic insult of the petrous ganglion network . Acute hydrocephalus is due to vasospasm of choroidal arteries, ependymal cell desquamation and also CSF acidosis …”

Section: Discussionmentioning

confidence: 99%

“…We previously showed that SAH causes cerebral fat embolism because of neurogenic lung edema and lung edema induces decreased blood pH values . CPs produce the most CSF to produce brain temperature …”

Section: Discussionmentioning

confidence: 99%

First definition of burned choroid plexus in acidic cerebrospinal fluid‐filled brain ventricles during subarachnoid hemorrhage: Experimental study

et al. 2020

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Blood and cerebrospinal fluid (CSF) acidosis is the most troubling complication in subarachnoid hemorrhage (SAH) if carotid body (CB) networks are disrupted. However, histopathological examination of the choroid plexus (CP) in acidic CSF has not been evaluated so far. In this study, we aimed to investigate the CP in acidic CSF following SAH. Twenty‐eight rabbits were used. Five rabbits were used to analyze CB network (control group; n = 5); seven rabbits were injected 1 mL of saline (Sham group; n = 7); and the rest 16 rabbits were given 1 mL of autologous arterial blood inject into the cisterna magna to create SAH (SAH group; n = 16). Blood and CSF pH values were recorded before/during/after the experimental procedures. Nuclear darkening, cellular shrinkage and pyknosis suggested the presence of apoptosis of epithelial cells of CP. The densities of normal and degenerated epithelial cells of CPs were estimated using stereological methods. The relationship between the pH values and degenerated epithelial cell densities of CPs were statistically compared by Mann–Whitney U‐test. The pH values of blood were estimated as 7.359 ± 0.039 in the control group, 7.318 ± 0.062 in the Sham group, 7.23 ± 0.013 in the SAH group. CSF pH values were 7.313 ± 0.028 in the control group, 7.296 ± 0.045 in the Sham group, and 7.224 ± 0.012 in the SAH group. Degenerated epithelial cell density of CP was 25 ± 7 in the control group, 226 ± 64 in the Sham group, and 2115 ± 635 in the SAH group. There was a considerable link between CSF pH values and degenerated epithelial cells of CP (P < 0.0001). This study shows that CB insult causes acidosis of CSF as well as cellular degeneration of CP during SAH. This is the first description of this in the literature.

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“…13 At present, neurosurgical practice is confronted by an explosion of technology. [16][17][18] However, our understanding of the mechanisms causing hydrocephalus in NMS is still not clear. A better understanding of the pathophysiology of hydrocephalus in this syndrome will lead to better patient outcome.…”

Section: Discussionmentioning

confidence: 99%