Published online Nov 26, 2019. doi: 10.4252/wjsc.v11.i11.982
Peer-review started: March 26, 2019
First decision: August 1, 2019
Revised: September 8, 2019
Accepted: October 1, 2019
Article in press: October 1, 2019
Published online: November 26, 2019
Processing time: 227 Days and 11.9 Hours
Neural stem cells (NSC) act as a versatile tool for neuronal cell replacement strategies to treat neurodegenerative disorders in which functional neurorestorative mechanisms are limited. While the beneficial effects of such cell-based therapy have already been documented in terms of neurodegeneration of various origins, a neurophysiological basis for improvement in the recovery of neurological function is still not completely understood. This overview briefly describes the cumulative evidence from electrophysiological studies of NSC-derived neurons, aimed at establishing the maturation of differentiated neurons within a host microenvironment, and their integration into the host circuits, with a particular focus on the neurogenesis of NSC grafts within the post-ischemic milieu. Overwhelming evidence demonstrates that the host microenvironment largely regulates the lineage of NSC grafts. This regulatory role, as yet underestimated, raises possibilities for the favoured maturation of a subset of neural phenotypes in order to gain timely remodelling of the impaired brain tissue and amplify the therapeutic effects of NSC-based therapy for recovery of neurological function.
Core tip: Electrophysiology combined with post-hoc immunohistochemistry was utilized for monitoring the maturation of neural stem cell (NSC)-derived hippocampal neurons within a host tissue, aimed at establishing the neurogenesis of NSC grafts between physiological and post-ischemic endogenous milieus. Understanding the timing maturation of the neurophysiological properties of differentiated neurons within the microenvironment of a host brain tissue will provide an assessment of the effects of cell-based therapy with regard to neurodegenerative disorders of varied aetiology.