Hyponatriämie im Alter (II) – eine klare Therapie

Hofmann, Werner; Flägel, Kristina; Gosch, Markus

doi:10.1007/s00391-020-01758-7

Cited by 1 publication

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References 27 publications

(23 reference statements)

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“…Considering the latest information about demyelinating defects and some remyelinating potentials illustrated here one still remain to know whether with delayed time after ODS damages, a sort of modus vivendi between astrocytes, oligodendrocytes, and neurons signals in making remyelination to return ODS thalamus or other CNS-damaged regions completely able to retrieve standard structures and functions. Possibly, similar repairs occurred in human ODS where most patients appeared to have a favorable clinical prognosis in the short-term post-hospitalization even though, retrospectively, there were and are still concerns for a range of 10 to 25% fatal outcomes [22,28,45,[107][108][109][110][111][112][113][114][115][116][117][118][119][120]123,259,260], or other neurologic defects [112,261], especially due other underlying disease states [45,[259][260][261][262].…”

Section: The Ais and Arl13b Label Marker Significancementioning

confidence: 99%

Thalamic Neuron Resilience during Osmotic Demyelination Syndrome (ODS) Is Revealed by Primary Cilium Outgrowth and ADP-ribosylation factor-like protein 13B Labeling in Axon Initial Segment

Gilloteaux,

De Swert,

Suain

et al. 2023

IJMS

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A murine osmotic demyelinating syndrome (ODS) model was developed through chronic hyponatremia, induced by desmopressin subcutaneous implants, followed by precipitous sodium restoration. The thalamic ventral posterolateral (VPL) and ventral posteromedial (VPM) relay nuclei were the most demyelinated regions where neuroglial damage could be evidenced without immune response. This report showed that following chronic hyponatremia, 12 h and 48 h time lapses after rebalancing osmolarity, amid the ODS-degraded outskirts, some resilient neuronal cell bodies built up primary cilium and axon hillock regions that extended into axon initial segments (AIS) where ADP-ribosylation factor-like protein 13B (ARL13B)-immunolabeled rod-like shape content was revealed. These AIS-labeled shaft lengths appeared proportional with the distance of neuronal cell bodies away from the ODS damaged epicenter and time lapses after correction of hyponatremia. Fine structure examination verified these neuron abundant transcriptions and translation regions marked by the ARL13B labeling associated with cell neurotubules and their complex cytoskeletal macromolecular architecture. This necessitated energetic transport to organize and restore those AIS away from the damaged ODS core demyelinated zone in the murine model. These labeled structures could substantiate how thalamic neuron resilience occurred as possible steps of a healing course out of ODS.

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