Kv1.1 channels regulate early postnatal neurogenesis in mouse hippocampus via the TrkB signaling pathway

In the postnatal brain, neurogenesis occurs only within a few regions, such as the hippocampal sub-granular zone (SGZ). Postnatal neurogenesis is tightly regulated by factors that balance stem cell renewal with differentiation, and it gives rise to neurons that participate in learning and memory formation (Anacker and Hen, 2017; Bond et al., 2015; Toda et al., 2019). The Kv1.1 channel, a voltage-gated potassium channel, was previously shown to suppress postnatal neurogenesis in the SGZ in a cell-autonomous manner. In this study, we clarified the physiological and molecular mechanisms underlying Kv1.1-dependent postnatal neurogenesis. First, we discovered that the membrane potential of neural progenitor cells is highly dynamic during development. We further established a multinomial logistic regression model for cell type classification based on the biophysical characteristics and corresponding cell markers. We found that loss of Kv1.1 channel activity causes significant depolarization of type 2b neural progenitor cells. This depolarization is associated with increased tropomyosin receptor kinase B (TrkB) signaling and proliferation of neural progenitor cells; suppressing TrkB signaling reduces the extent of postnatal neurogenesis. Thus, our study defines the role of the Kv1.1 potassium channel in regulating the proliferation of postnatal neural progenitor cells in the mouse hippocampus.

Systematic Review of Nicotine Exposure’s Effects on Neural Stem and Progenitor Cells

While various modalities of chronic nicotine use have been associated with numerous negative consequences to human health, one possible benefit of nicotine exposure has been uncovered. The discovery of an inverse correlation between smoking and Parkinson’s disease, and later Alzheimer’s disease as well, motivated investigation of nicotine as a neuroprotective agent. Some studies have demonstrated that nicotine elicits improvements in cognitive function. The hippocampus, along with the subventricular zone (SVZ), is a distinct brain region that allow for ongoing postnatal neurogenesis throughout adulthood and plays a major role in certain cognitive behaviors like learning and memory. Therefore, one hypothesis underlying nicotine-induced neuroprotection is possible effects on neural stem cells and neural precursor cells. On the other hand, nicotine withdrawal frequently leads to cognitive impairments, particularly in hippocampal-dependent behaviors, possibly suggesting an impairment of hippocampal neurogenesis with nicotine exposure. This review discusses the current body of evidence on nicotine’s effects on neural stem cells and neural progenitors. Changes in neural stem cell proliferation, survival, intracellular dynamics, and differentiation following acute and chronic nicotine exposure are examined.

Broadening the functional and evolutionary understanding of postnatal neurogenesis using reptilian models

ABSTRACTThe production of new neurons in the brains of adult animals was first identified by Altman and Das in 1965, but it was not until the late 20th century when methods for visualizing new neuron production improved that there was a dramatic increase in research on neurogenesis in the adult brain. We now know that adult neurogenesis is a ubiquitous process that occurs across a wide range of taxonomic groups. This process has largely been studied in mammals; however, there are notable differences between mammals and other taxonomic groups in how, why and where new neuron production occurs. This Review will begin by describing the processes of adult neurogenesis in reptiles and identifying the similarities and differences in these processes between reptiles and model rodent species. Further, this Review underscores the importance of appreciating how wild-caught animals vary in neurogenic properties compared with laboratory-reared animals and how this can be used to broaden the functional and evolutionary understanding of why and how new neurons are produced in the adult brain. Studying variation in neural processes across taxonomic groups provides an evolutionary context to adult neurogenesis while also advancing our overall understanding of neurogenesis and brain plasticity.