| Budget Amount *help |
¥4,200,000 (Direct Cost: ¥4,200,000)
Fiscal Year 1995: ¥4,200,000 (Direct Cost: ¥4,200,000)
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| Research Abstract |
In order to understand the molecular basis of behavior, we planned to raise transgenic mice systemically that overxpress or lack the particullar neuropeptide or its receptor. These studies were performed in collaboration with Dr. Linda C.Samuelson and Dr. Sally A.Camper of Michigan University. We focused on several neuropeptides such as neuropeptide Y (NPY), cholecystokinin (CCK), pancreatic polypetide (PP), and corticotropin-releasing factor (CRF), all of which were reported to have important roles on feeding, emotion, and learning behaviors.
NPY, one of the most abundant peptide transmitters in the mammalianbrain is assumed to play an important role in behavior and its disorders. To understand the long-term modulation of neuronal functions by NPY, we raised transgenic mice created with a novel neuron-specific expression vector of human Thy-1 gene fragment linked to mouse NPY cDNA.The transgenic mice displayd behavioral signs of anxiety, a moderate defect in spatial working memory, and hypertrophy of adrenal zona fasciculata cells, but no other behavioral defects were observed. These results suggest that brain NPY has a role in the anxiogenic behavior and that this genetic model provides an unique opportunity to study human anxiety and emotional disorders.
We are non trying to develop other novel transgenic models for understanding and treatment of human behavior and its disorders. Unfortunately, by the Kobe earthquake occurred on 17 January 1995 with a magnitude of 7.2 on the Richter scale, our hospitals equipped with modern medical facilities and technologies situated in the Kobe area sufferd severe structural as well as non-structural damage.
This resulted in considerable delay in our project.
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