Perisynaptic schwann cells
Perisynaptic Schwann Cells (PSCs) contribute to the tripartite synapse organization in combination with the pre-synaptic nerve and the post-synaptic muscle fiber.
[1] PSCs are considered to be the glial component of the Neuromuscular Junction (NMJ) and have a similar functionality to that of Astrocytes in the Central Nervous System.
This balance between external and internal influences creates a range of PSCs that are present in the many Neuromuscular Junctions of the Peripheral Nervous System.
Perisynaptic (Terminal) Schwann Cells were first discovered by Louis-Antoine Ranvier in 1878 when he observed branching networks surrounding the motor end plate (neural portion of NMJ).
These cells were distinguished from muscle fibre nuclei and the motor end plate, making the third component of the tripartite synaptic model.
[1] It was found that these newly discovered cells were present in nerve degeneration models, showing their non-neural nature.
The proximity of PSCs to the motor end plate raised questions about their functionality, but little was known up until the vast research conducted in the past two decades.
[1] As mentioned in the development section, Schwann cell precursors accompany growing axons as they reach their associated muscles.
[5] This TGF-ß1 appears to stop nerve growth in order to promote the nerve-muscle synapse formation, however its role in vivo is unknown.
In frog ablation models, there is observable difference in NMJ properties that arise approximately seven days after PSCs were selectively removed.
Motor-end plate potentials were unaltered in the pre-ablated and the 5 hour ablated models, showing that PSCs are not essential for short-term maintenance of the NMJ.
The mammalian PSC, when treated with antibodies against gangliosides in Miller-Fisher Syndrome, show not change in NMJ properties in the short-term, but long-term data has not collected.
It can be gathered that PSCs play an important role in long-term maintenance of frog NMJ, but it is unknown if the same effects are true in mammalian NMJs.
[1] This increase in intracellular calcium levels is not observed in the myelinating Schwann cells that line the axon, but only in the PSCs present at the NMJ.
The recovering axon grows along a scaffolding of basal lamina left from the damaged Schwann cells and reaches the proximal PSC site (nearest NMJ).
These PSC bridges are seen in vivo following complement-mediated injury in a murine model, showing that this role of PSCs are present in mammalian NMJs.
