We examined calcium influx under physiological conditions in mouse DRG neurons lacking GD3s and found no major alterations in the responses of calcium channels when the cultures were incubated in KCl or ATP. This result suggests that 9-O-acetyl GD3 regulates integrin assembly by promoting b1 subunit expression/trafficking along the growing neurites. Therefore, DRGs induced to depolarize might lose the ability to regulate Ca2+ entry, resulting in impairments in neurite outgrowth and attachment to the ECM. Another finding regarding nerve morphology was that the myelin thickness was reduced in adult mice lacking GD3s. It is well understood that during development and regeneration, peripheral nerve axons and glia control Schwann cell survival and fate, modulating the myelinated or non-myelinated state of the axons. The levels of neuregulin-1 produced by neurons Remdesivir GS-5734 increase with axonal thickness. This factor binds to Erb-B2 receptors on Schwann cells and induces myelination. We found no differences in Erb-B2 expression in Schwann cells or in neuregulin-1 expression in DRG neurons from genetically modified versus WT mice. The axonal thickness was not altered despite the reduced number of axons in the nerves lacking GD3s. One possible explanation for the reduction in the myelin thickness may be the reduced number of axons during late steps of nerve development, which would reduce the average neuregulin-1 levels. To better understand the mechanisms underlying this change, further studies are required. It is well established that the ganglioside 9-O-acetyl GD3 is expressed prenatally by neurons and glia along the course of neural development in rodents. Its expression is strongly reduced on E20, which correlates with the end of axonal growth and the establishment of functional connections between neurons, including the DRG, the lumbar spinal cord and peripheral nerves. Curiously, when axons are lesioned in adult rats, the expression of this molecule is upregulated for a period that correlates to WD and the initiation of axonal regeneration. We found that the peak of ganglioside expression is on day 7 after nerve crush lesioning, and its expression then gradually reduces to basal levels by day 10 after lesioning. We examined selected parameters of WD, including axonal breakdown, macrophage invasion and cell proliferation, specifically including Schwann cell proliferation, at the distal stump. All of these processes acted in synchrony for Schwann cells to form the bands of Bu¨ngner, allowing axons to regenerate. Potential changes in the behavior of these cells could represent a possible explanation for the upregulation of 9-Oacetyl GD3 during early steps of nerve regeneration.