| First Author | Summers BS | Year | 2025 |
| Journal | eNeuro | Volume | 12 |
| Issue | 6 | PubMed ID | 40345851 |
| Mgi Jnum | J:368114 | Mgi Id | MGI:8213815 |
| Doi | 10.1523/ENEURO.0113-25.2025 | Citation | Summers BS, et al. (2025) Demyelination Produces a Shift in the Population of Cortical Neurons That Synapse with Callosal Oligodendrocyte Progenitor Cells. eNeuro 12(6):ENEURO.0113-25.2025 |
| abstractText | Oligodendrocyte progenitor cells (OPCs) receive synaptic input from a diverse range of neurons in the developing and adult brain. Understanding whether the neuronal populations that synapse with OPCs in the healthy brain is altered by demyelination and/or remyelination may support the advancement of neuroprotective or myelin repair strategies being developed for demyelinating diseases such as multiple sclerosis. To explore this possibility, we employed cre-lox transgenic technology to facilitate the infection of OPCs by a modified rabies virus, enabling the retrograde monosynaptic tracing of neuron-->OPC connectivity. In the healthy adult mouse, OPCs in the corpus callosum primarily received synaptic input from ipsilateral cortical neurons. Of the cortical neurons, approximately 50% were layer V pyramidal cells. Cuprizone demyelination reduced the total number of labeled neurons. However, the frequency/kinetics of mini-excitatory postsynaptic currents recorded from OPCs appeared preserved. Of particular interest, demyelination increased the number of labeled layer II/III pyramidal neurons and also increased at the expense of layer V pyramidal neurons, a change that was largely ameliorated by remyelination. These data suggest that in the healthy adult mouse brain, callosal OPCs primarily receive synaptic input from cortical layer V pyramidal neurons. However, callosal demyelination is associated with a population switch and OPCs equally synapse with layer II/III and V pyramidal neurons to synapse with OPCs, until myelin is restored. |
