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Welcome to the Pacific Cascade Chapter of the Society for Neuroscience
We exist to promote understanding of the nervous system, both among practicing neuroscientists and the public at large. We count among our members about 300 students, staff, and faculty members at the University of Washington and other local institutions in the Puget Sound area.
Our main activities are to co-sponsor an annual meeting of neuroscientists in the Pacific Northwest and to help enhance teaching of neuroscience to local school children. We aim to sponsor travel fellowships to support participation of students in national or international meetings.
We are part of the Society for Neuroscience based in Washington DC. Please feel free to contact us if you have any questions. Carol L. Thompson, Ph.D. Amy Rebecca Furay, Ph.D. Congratulations to Will Marrs, recipient of a SfN 2009 Chapters Graduate Student Travel Award Upon joining the Stella lab two years ago, I was introduced to the finding that a microglial cell line commonly used in the lab hydrolyzes (inactivates) 2-AG despite the fact that these cells don't express MAGL (which was the only enzyme known to mediate 2-AG hydrolysis at the time). I decided to spearhead a project to identify this unknown enzymatic activity, and discovered that this 2-AG-hydrolyzing activity is due to a previously uncharacterized serine hydrolase known as ABHD6. We then found that ABHD6 is also expressed in mouse brain as well as in neurons in primary culture. Furthermore, we demonstrated that this novel enzyme mediates half of the total 2-AG hydrolysis in neuron homogenates, that it functions as a rate-limiting step in the accumulation of 2-AG in intact neurons, and that inhibiting ABHD6 in mouse cortical slices unmasks CB1-dependent LTD at glutamatergic synapses. Thus, like MAGL, ABHD6 regulates cannabinoid receptor activation in the brain by controlling the level of 2-AG accumulation. My future plans are to explore the therapeutic potential of targeting ABHD6.
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The endocannabinoid signaling system consists of the cannabinoid receptors (CB1 and CB2), the endogenous cannabinoids (AEA and 2-AG), and the metabolic enzymes that produce and inactivate these lipid neuromodulators. CB1 is the most abundant G-protein-coupled receptor in the brain, where it regulates neurotransmission and is involved in a variety of cognitive processes. 2-AG is a full agonist at cannabinoid receptors, and is the most abundant endocannabinoid in the brain. A novel approach to targeting this signaling system is to inhibit the enzymes that inactivate the endocannabinoids, which results in increased activation of cannabinoid receptors only where and when these ligands are being endogenously produced. This approach has great therapeutic potential, as it provides many advantages over targeting cannabinoid receptors directly with exogenous compounds.