Blood-brain barrier permeability towards small and large tracers in a mouse model of osmotic demyelination syndrome

A primary cilium in oligodendrocytes: a fine structure signal of repairs in thalamic Osmotic Demyelination Syndrome (ODS)

“…This fine structure investigation complements others made with neurophysiology, histology, immunohistochemistry and molecular biochemistry [15][16][17][18][19] included four groups. Group 1 were normonatremic or Sham mice (NN; n = 13) sacrificed at day 0; Group 2 were hyponatremic mice (HN; n = 11) sacrificed 4 days after the induction of hyponatremia (day 0 + 4-day treatment period named 'chronic hyponatremia' as described in the ODS protocol (in a) and in.…”

“…Those changes were revealed along with astrogliosis as well as with clasmatodendrosis (cell body swelling with fragmentation of distal processes 16,17,42 ). They were linked to other myelin repression or damages of molecular markers and losses [15][16][17]43 accompanied by a local, restricted microglial cell's reactivity, [15][16][17][18][19] verified by ultrastructure. [15][16][17] In ODS, the delimited CNS EPM cytotoxic events of the thalamic injuries do not involve irreversible damages in the CNS neurons, demonstrating resilience in the same demyelinated regions.…”

“…[1][2][3][4][5][6][7][8] The ODS neuropathologic syndrome is caused by a hastily adjustment of a temporary or chronic deficiency of the homeostatic sodium gradient as it can be pertinent to diverse homeostatic hormonal sodic perturbations such as those afflicted by exaggerated body fluid losses and emergently treated for alcoholism, diabetes as well as to defective dialysis. [1][2][3][9][10][11][12][13][14] A large reference list of ODS literature was recently cited [15][16][17][18][19] and it appeared that EPM lesions can appear before any CPM ones [19][20][21][22][23][24][25] and ODS in human EPM cases would be more frequent than CPM ones. 23 There, ODS can frequently appear clinically in the elderly, hospitalized population.…”

“…4,[31][32][33][34][35][36][37][38][39][40][41] Future development of genetically modified mouse models may further clarify the pathophysiology of ODS, its associated disorders, as well as its resolution. Several murine investigations have already provided clarifications on the ODS trigger events and, there, a breach in the blood-brain barrier (BBB) suggested a leak of some circulating compound(s) 19 that eventually would trigger astrocytic signaling(s) toward oligodendrocytes causing a rapid myelin loss of APC (Adenomatous Polyposis Coli) and proteolipid protein (PLP) immunoreactivity that culminated 48 h post-correction of hyponatremia. Those changes were revealed along with astrogliosis as well as with clasmatodendrosis (cell body swelling with fragmentation of distal processes 16,17,42 ).…”

“…[15][16][17][18] This report again analyzes the same groups of mice that have revealed ODS extrapontine tissue's changes in [15][16][17][18] and further comforts all those data of this murine model of osmotic demyelinating syndrome (ODS) where the relay ventral posterolateral (VPL) and ventral posteromedial (VPM) thalamic nuclei have been shown susceptible toward osmotic-induced demyelination. 19 It adds information about ongoing ODS oligodendrocyte changes and repairs. At 12-hour post rebalancing osmolarity, ultrastructural examination revealed a primary or single cilium in oligodendrocytes in vivo while morphologic hyperchromaticity have been featured as in.…”