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Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland.
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- Author(s): Kim MH;Kim MH; Uehara S; Muroyama A; Hille B; Moriyama Y; Koh DS
- Source:
The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 2008 Oct 22; Vol. 28 (43), pp. 10852-63.
- Publication Type:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
- Language:
English
- Additional Information
- Source:
Publisher: Society for Neuroscience Country of Publication: United States NLM ID: 8102140 Publication Model: Print Cited Medium: Internet ISSN: 1529-2401 (Electronic) Linking ISSN: 02706474 NLM ISO Abbreviation: J Neurosci Subsets: MEDLINE
- Publication Information:
Publication: Washington, DC : Society for Neuroscience
Original Publication: [Baltimore, Md.] : The Society, c1981-
- Subject Terms:
- Abstract:
Glutamate transporters are expressed throughout the CNS where their major role is to clear released glutamate from presynaptic terminals. Here, we report a novel function of the transporter in rat pinealocytes. This electrogenic transporter conducted inward current in response to L-glutamate and L- or D-aspartate and depolarized the membrane in patch-clamp experiments. Ca2+ imaging demonstrated that the transporter-mediated depolarization induced a significant Ca2+ influx through voltage-gated Ca2+ channels. The Ca2+ rise finally evoked glutamate exocytosis as detected by carbon-fiber amperometry and by HPLC. In pineal slices with densely packed pinealocytes, glutamate released from the cells effectively activated glutamate transporters in neighboring cells. The Ca2+ signal generated by KCl depolarization or acetylcholine propagated through several cell layers by virtue of the regenerative "glutamate-induced glutamate release." Therefore, we suggest that glutamate transporters mediate synchronized elevation of L-glutamate and thereby efficiently downregulate melatonin secretion via previously identified inhibitory metabotropic glutamate receptors in the pineal gland.
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- Grant Information:
R01 GM083913 United States GM NIGMS NIH HHS; R01 GM083913-33 United States GM NIGMS NIH HHS; 27307C0011 United States ES NIEHS NIH HHS; 27398C0011 United States ES NIEHS NIH HHS; 27305C0011 United States ES NIEHS NIH HHS; GM083913 United States GM NIGMS NIH HHS
- Accession Number:
0 (Amino Acid Transport System X-AG)
0 (Chlorides)
0 (Enzyme Inhibitors)
0 (Excitatory Amino Acid Antagonists)
0 (Macrolides)
0 (benzyloxyaspartate)
1KSV9V4Y4I (Cesium)
30KYC7MIAI (Aspartic Acid)
3KX376GY7L (Glutamic Acid)
52497-36-6 (dihydrokainic acid)
660YQ98I10 (Potassium Chloride)
88899-55-2 (bafilomycin A1)
GNR9HML8BA (cesium chloride)
I38ZP9992A (Magnesium)
JL5DK93RCL (Melatonin)
SIV03811UC (Kainic Acid)
SY7Q814VUP (Calcium)
- Publication Date:
Date Created: 20081024 Date Completed: 20081201 Latest Revision: 20240615
- Publication Date:
20240615
- Accession Number:
PMC2596195
- Accession Number:
10.1523/JNEUROSCI.0894-08.2008
- Accession Number:
18945893
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