Abstract
In peripheral myelinated axons of mammalian spinal motor neurons, Ca
2+
influx was thought to occur only in pathological conditions such as ischaemia.
Using Ca
2+
imaging in mouse large motor axons, we find that physiological stimulation with trains of action potentials transiently elevates axoplasmic [Ca
2+
] around nodes of Ranvier.
These stimulation‐induced [Ca
2+
] elevations require Ca
2+
influx, and are partially reduced by blocking T‐type Ca
2+
channels (e.g. mibefradil) and by blocking the Na
+
/Ca
2+
exchanger (NCX), suggesting an important contribution of Ca
2+
influx via reverse‐mode NCX activity.
Acute disruption of paranodal myelin dramatically increases stimulation‐induced [Ca
2+
] elevations around nodes by allowing activation of sub‐myelin L‐type (nimodipine‐sensitive) Ca
2+
channels.
The Ca
2+
that enters myelinated motor axons during normal activity is likely to contribute to several signalling pathways; the larger Ca
2+
influx that occurs following demyelination may contribute to the axonal degeneration that occurs in peripheral demyelinating diseases.
