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

Abstract

A murine osmotic demyelination syndrome (ODS) model of the central nervous system included the relay thalamic ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei. Morphologic comparisons between treatments have revealed oligodendrocyte changes and, already 12 hours following the osmolality restoration, some heavily contrasted oligodendrocytes formed a unique intracellular primary cilium. This unique structure, found in vivo, in mature CNS oligodendrocytes, could account for a local awakening of some of the developmental proteome as it can be expressed in oligodendrocyte precursor cells. This resilience accompanied the emergence of arl13b protein expression along with restoration of nerve cell body axon hillocks shown in a previous issue of this journal. Additionally, the return of several thalamic oligodendrocyte fine features (nucleus, organelles) was shown 36 h later, including some mitosis. Those cell restorations and recognized translational activities comforted that local repairs could again take place, due to oligodendrocyte resilience after ODS instead or added to a postulated immigration of oligodendrocyte precursor cells distant from the sites of myelinolysis.

Loss of Ephaptic Contacts in the Murine Thalamus during Osmotic Demyelination Syndrome

“…This report comforts and completes other ODS investigations made in our murine model with neurophysiology, histology, molecular markers, immunohistochemistry, and electron microscopy techniques [1][2][3][4][5][6] where we detected the thalamus VRM and VPL relay nuclei to contain many adjoined neurons that appeared in histology sections as duos or, rarely, as triplets of nerve cell bodies. [1][2][3][4]6 Our data also encompass other description of neuron's injuries within the core of demyelinated zones, and the concomitant changes that altered joined neurons according to their location in or outside the demyelinating ODS zone of the thalamus, associated with chronic hyponatremia, at 12 h and at 48 h time lapses after reinstatement of natremia.…”

“…A murine model used for the study of osmotic demyelination syndrome (ODS), induced by arginine-vasopressin (AVP) analog, revealed with light microscopy large number of contiguous neurons, in the relay posterolateral (VPL) and ventral posteromedial (VPM) thalamic nuclei, whether intact or associated with various damages in this extrapontine myelinolysis (EPM), [1][2][3][4][5][6] as suggested with another previous report of rat brain damages. 7 In the past, such neuron's close contacts were defined in 1942 with the Greek root 'ἔφαψις 'or "ephapsis" as of "touching" (plural: ephapses) by Angélique Arvanitaki 8,9 when she investigated adjoined neurons of the nudibranch Mollusc Aplysia nervous system.…”

“…ODS induction was based on the correction of a chronic hyponatremia, adapted protocol from, 1 again described in. [2][3][4][5][6][7] Briefly, an osmotic minipump (Model 1004, Alzet, Cupertino, CA), filled with desmopressin acetate (2 µg/ml; Minirin, Ferring, Saint-Prex, Switzerland) was inserted subcutaneously under anesthesia into the mice's back at day 0. Standard pellets and water fed control mice, while treated mice received a low-sodium liquid diet (AIN76A, MP Biomedicals, Santa Ana, CA, USA), for a period of 4 days, ad libitum (Figure 1).…”

“…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. [1][2][3][4][5][6] Groups 3 and 4 were mice that underwent the 4-day "chronic hyponatremia" abruptly provided with normonatremia bore both the acronym "ODS." Group 3 included mice sacrificed 12 h after a fast restoration of normal natremia, thus named ODS 12 h group (ODS12h; n = 6) while Group 4 mice encompassed mice sacrificed 48 h post fast osmotic correction, hence named ODS48 h (n = 9).…”

“…[1][2][3][4]6 Our data also encompass other description of neuron's injuries within the core of demyelinated zones, and the concomitant changes that altered joined neurons according to their location in or outside the demyelinating ODS zone of the thalamus, associated with chronic hyponatremia, at 12 h and at 48 h time lapses after reinstatement of natremia. The mere existence of nerve cell body ephaptic contacts that remained throughout the VPL and VPM relay nuclei of the least thalamus damages can suggest these associations can bring support for some of the neuron's resilience in ODS defect, 5 maintaining some of the dispatching thalamus functions and, probably later, through plasticity, would favor functional recovery amongst these thalamus regions and others of the CNS that have undergone ODS damages.…”