Sanbing Shen

TL;DR: Mice carrying a null mutation of the VPAC(2) receptor for VIP and PACAP (Vipr2(-/-)) are incapable of sustaining normal circadian rhythms of rest/activity behavior and the role of intercellular neuropeptidergic signaling in maintenance of circadian function within the SCN is highlighted.

TL;DR: Transgenic embryos were generated carrying a Hoxb-8 transgene under control of the mouse RAR beta 2 promoter, which extends the normal expression domain to more anterior regions of the embryo, and showed mirror-image duplications in the forelimb, analogous to duplications observed in chick in response to transplantation of a ZPA to the anterior margin of the limb bud.

TL;DR: Disrupted-in-Schizophrenia-1 transgenic mice exhibit increased immobility and reduced vocalization in depression-related tests, and impairment in conditioning of latent inhibition, consistent with findings in severe schizophrenia.

TL;DR: Pulmonary hemodynamics and the development of hypoxia-induced pulmonary hypertension and pulmonary vascular remodeling in mice overexpressing the gene for the 5-HT transporter are investigated, providing a unique model that demonstrates differential mechanisms for familial pulmonary arterial hypertension and lungs with hypoxemia.

TL;DR: It is demonstrated that the VPAC2 receptor is necessary for the major part of the electrophysiological actions of VIP on SCN cells in vitro, and is of fundamental importance for the rhythmic and coherent expression of circadian rhythms governed by the SCN clock.