1. Research themes 1.Describe the main scientific question and the big scientific picture you address. 2.Why is it important? 3.The knowledge gap (i.e. unanswered questions) so far. 1.Introduce the research methods you use in your study. 2.What your lab can provide for other PIs to enhance research? Our platforms Scientific Contributions Collaboration requests Explain the collaborations you are searching for as specific as possible. For example, you can declare the need of some technique or equipment for your research, a defined patient group, or an animal model/genotype. CNS Neuropharmacology (Research Title) Orexin, Nociceptin, Cannabinoid, Pain, Addiction, Schizophrenia, Electrophysiology (Key words for your research) Lih-Chu Chiou, PhD. Professor (PI’s name or All team members) Department of Pharmacology, College of Medicine, National Taiwan University (Main appointed department) Lab connections 1.Illustrate the core findings of your research. You can also demonstrate the research tools you provide. Figures below are just examples. 2.Please just briefly cite your important findings but NOT elaborately list your publications here. Briefly describe your research connections with other labs, especially the international groups that may provide help for our team members. Tips for poster preparation 1. To promote cross-talk and initiate integrated research in our community, we encourage researchers to present what they can offer in their lab platform and express what the platform they hope to collaborate with. 2. Words in blue color are just instructions, and those in black as well as figures are examples. Please delete them and replace with your content in your formal poster. 3. The black frame adjacent to the IBMP logo is for poster number. Please leave it blank. “N08” is just an example. (This is only a reminder. Please delete this box after reading.) Figure 1. A proposed model for how orexin A-induced inhibition of GABAergic transmission in the vlPAG ultimately leads to antinociception by activating the descending pain inhibitory pathway. The schema shows two GABAergic innervated neurons, with (right) and without (left) postsynaptic OX 1 receptors in the vlPAG before (A) and after (B) treatment with orexin A. Orexin A activates postsynaptic OX 1 receptors in the vlPAG neuron (right) and then, coupled by Gq protein, stimulates PLC to yield DAG which can be deacylated by DAGL to 2-AG, an endocannabinoid. 2-AG subsequently activates the presynaptic CB 1 receptors located on the GABAergic terminal of the same neuron as a retrograde messenger (right) or the CB 1 receptors on the adjacent GABAergic terminal as a heterosynaptic spillover messenger (left) to inhibit GABA release. Inhibition of the GABAergic transmission (disinhibition) in the vlPAG will activate the descending pain inhibitory pathway and reduce nociceptive responses. 2-AG can be degraded by the MGL located in GABAergic terminals. Thus, the MGL inhibitor enhances orexin A-induced IPSC depression. (Ho et al. 2011, J. Neurosci.) N08