Microglia are the resident immune cells of the central nervous system that mediate an array of critical functions like neuronal development and connectivity as well as protecting their environment from unwelcome invaders^1,7. On the other hand, microglia are also implicated in a variety of inflammatory and neurological disorders such as Alzheimer's disease, epilepsy, and schizophrenia⁵.

Microglia originate from a dedicated pool of yolk sac-derived cells that infiltrate into the brain during the early embryonic stage⁷. Later on, it was discovered that a pan of molecular cues pertaining the tyrosine kinase activity of CSF-1 receptor and the transcription factor IRF-8 are critical factors for their commitment to this particular cell lineage and to maintain their long-term survival⁷.

More recently, interest in microglia has resurfaced after numerous evidence implicated them in regulating neuronal connectivity³. These studies also demonstrated that microglia cells could form synaptic connections between neurons during embryonic stage or during synaptic plasticity processes to enhance neuronal function³.

Despite their fundamental role in maintaining normal neuronal function, abnormal microglial activity has been reported in several cases of mental disorders and neuroinflammatory conditions^2,5. In Alzheimer's disease, for example, postmortem studies implied the possibility of dysfunctional microglia as evident from their close proximity to amyloid beta particulates^5,6. Further genetic studies uncovered a common mutation in TREM2, a cell surface receptor important for phagocytosis of amyloid beta fibrils⁵. Moreover, in light of the inflammatory nature of Alzheimer's disease, several studies underscored the prominent involvement of ion channels like the voltage-gated potassium ions and the purinergic receptors to activate inflammatory signaling cascades in microglia and consequently, instigate local inflammatory reactions⁴.

In summary, microglia are essential components of the brain parenchyma, contributing to its normal physiological function. Nevertheless, in some cases, abnormal microglial activity can inflict severe damage and propagate neuroinflammatory diseases. As such, a better understanding of ion channels activity in such devastating medical conditions could spell relieve in such circumstances.