Involvement of Gap Junctional Communications Between Kndy Neurons and Glial Cells in Synchronized Discharges of Kndy Neurons in Mice
Presentation Number: SUN 483
Date of Presentation: April 2nd, 2017
Kana Ikegami*1, Nahoko Ieda1, Shiori Minabe1, Teppei Goto1, Alisa Sugimoto1, Sho Nakamura2, Naoko Inoue1, Kei-ichiro Maeda2, Hiroko Tsukamura1 and Yoshihisa Uenoyama1
1Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan, 2Department of Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan
Pulsatile release of the GnRH/LH is indispensable for puberty onset and reproductive activities at adulthood in mammals. KNDy neurons expressing kisspeptin (encoded by Kiss1 gene), neurokinin B and dynorphin A, localized in the hypothalamic arcuate nucleus, are thought to be a part of the GnRH pulse generator. The most of plausible explanation is that synchronous activity among KNDy neurons drive pulsatile GnRH release. It has been reported that gap junctional communications play a crucial role in the synchronizing activity in the brain. Thus, we hypothesized that gap junctional communications are involved in the synchronized activity of KNDy neurons. To address this hypothesis, we investigated morphological connections between KNDy neurons as well as between KNDy neurons and glial cells, gene expression of connexins in KNDy neurons, and effect of inhibitors for gap junctions on Ca2+ oscillations in KNDy neurons. GFP-labeled KNDy (KNDy-GFP) cells were collected from the fetal mediobasal hypothalamus of the transgenic mice expressing GFP under the control of the Kiss1 promoter and cultured on a glass-base dish for several weeks. Confocal microscopic analysis of cultured KNDy-GFP cells and neighboring glial cells, which have shown synchronized Ca2+ oscillations under the NK3R agonist (senktide) stimulation, revealed close contacts between KNDy-GFP cells as well as between KNDy-GFP cells and neighboring glial cells. Connexin-26 and -37 mRNA were found in isolated KNDy-GFP cells collected from adult female KNDy-GFP transgenic mice. Furthermore, gap junction inhibitors for neuron-neuron and neuron-glia communications attenuated senktide-induced Ca2+ oscillations in KNDy-GFP cells. Taken together, the present study suggests that both neuron-neuron and neuron-glia communications via gap junctions contribute to synchronized activity among KNDy neurons.
Nothing to Disclose: KI, NI, SM, TG, AS, SN, NI, KIM, HT, YU