| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2005: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2004: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
GABA is known to produce a depolarization or secretion in adrenal medullary (AM) cells of various species. However, whether the GABAergic system is intrinsic or extrinsic in the adrenal medulla is ambiguous. Thus, we addressed this issue using immunological techniques and RT-PCR. The immunoblotting and immunohistochemistry revealed that GAD, a GABA synthesizing enzyme, was present in rat AM cells, but not adrenal cortical cells. VGAT, a vesicular GABA transporter, was also found in the rat AM. Similarly, PCR products for GAD67, one isoform of GAD, and for VGAT were amplified in cDNAs samples of rat adrenal medulla, but not adrenal cortex. Interestingly, GAT, which is responsible for the termination of an GABAergic inhibitory transmission in the brain, was not found at the mRNA level in the adrenal medulla. Perfusion of 30 μM GABA-containing solution in the rat adrenal medulla loaded with fluo-4 resulted in an increase in Ca^<2+> signal in some, but not all, of AM cells that responded to the electrical stimulation. The maximum response of Ca^<2+> signal evoked by both the electrical stimulation and GABA did not exceed that elicited by the electrical stimulation alone. The immunoblot and RT-PCR showed that GABA receptors in rat AM cells consisted of at least α1,α3,β3, and γ2 subunits. The results suggest that GABA functions as a paracrine or autocrine in rat AM cells.
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