Effects Of Deleting ErbB4in PV-positive Inter-Neurons On Adult Hippocampal Neurogenesis

Adult neurogenesis is a process continuously producing newborn neurons, which can integrate into the pre-existing neural circuits and play some specific functions. Adult hippocampal neurogenesis occurs in a complex neural niche. Interneurons in the niche attract wide attentions as they can project into the neural progenitor/stem cells (NPSCs) and their progeny cells. There are evidence that in adult hippocampal SGZ, local interneurons, mainly parvalbumin (parvalbumin, PV) positive neurons can sustainably release GABA, which can regulate the maturation of new neurons, development of dendrites and integration of synapses. ErbB4, a receptor tyrosine kinase, is mainly expressed in the interneurons, the parvalbumin positive neurons in particular. NRG1, through its receptor ErbB4, not only increases the excitability of PV interneurons but also promoted the release of GABA. However, whether ErbB4in PV interneurons affect the development of new neurons is unclear.In this study, we deleted the ErbB4specifically in the PV interneurons by taking advantage of the cre-loxp system.BrdU labeling together with NeuN staining experimental data showed that mice with the deletion of ErbB4in PV neurons have less newborn neurons in their hippocampus compared with that in control mice, suggesting that the survival of newborn neurons was impaired after deleting the ErbB4in PV interneurons. In addition, we examined the induction of LTP in CA1region between control and KO groups. In brain slice, field potential recordings showed no different LTP amplitude induced by TBS in the two groups. We also checked the induction of LTP in CA1in two additional mouse models in which the number of newborn neurons in the DG region has undergone significant decline. Compared with wild-type mice, however, the induction of LTP in CA1region did not show significant difference between groups. These results suggested that impaired neurogenesis may not affect the synaptic plasticity in CA1to change the overall behavior such as learning and memory, but whether it affects the synaptic plasticity in other brain regions need to be further investigated.