Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland.
نویسندگان
چکیده
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.
منابع مشابه
Synaptic-like microvesicles, synaptic vesicle counterparts in endocrine cells, are involved in a novel regulatory mechanism for the synthesis and secretion of hormones.
Microvesicles in endocrine cells are the morphological and functional equivalent of neuronal synaptic vesicles. Microvesicles accumulate various neurotransmitters through a transmitter-specific vesicular transporter energized by vacuolar H(+)-ATPase. We found that mammalian pinealocytes, endocrine cells that synthesize and secrete melatonin, accumulate l-glutamate in their microvesicles and sec...
متن کاملAcetylcholine triggers L-glutamate exocytosis via nicotinic receptors and inhibits melatonin synthesis in rat pinealocytes.
Rat pinealocytes, melatonin-secreting endocrine cells, contain peripheral glutaminergic systems. L-Glutamate is a negative regulator of melatonin synthesis through a metabotropic receptor-mediated inhibitory cAMP cascade. Previously, we reported that depolarization of pinealocytes by externally added KCl and activation of L-type Ca2+ channels resulted in secretion of L-glutamate by microvesicle...
متن کاملEvaluation of Glutamate Dehydrogenase Activity and Insulin Secretion in Mice Exposed to Dexamethasone
Background and Aims: Diabetes is one of the most important endocrine disrupters and is associated with various hormones, including those that can lead to diabetes. Glucocorticoid use may lead to insulin resistance. Dexamethasone is one of these glucocorticoid compounds. Glutamate dehydrogenase plays a key role in the production of glutamate in the secretion of insulin. Based on these hormonal i...
متن کاملO 3:Therapeutic Potential of a Novel NMDA Receptor Subunit 2B Antagonist in a Mouse Model of Autoimmune Neuroinflammation
Glutamate-mediated excitotoxicity and neurodegeneration have been shown as pathophysiological hallmarks of multiple sclerosis (MS) and other autoimmune inflammatory CNS disorders. N‑Methyl‑D‑Aspartate (NMDA) receptors play a pivotal role in the mediation of neuronal glutamate excitotoxicity leading to cellular damage and apoptotic cell death. Current treatment approaches targeting glutamate exc...
متن کاملIdentification of a vesicular aspartate transporter.
Aspartate is an excitatory amino acid that is costored with glutamate in synaptic vesicles of hippocampal neurons and synaptic-like microvesicles (SLMVs) of pinealocytes and is exocytosed and stimulates neighboring cells by binding to specific cell receptors. Although evidence increasingly supports the occurrence of aspartergic neurotransmission, this process is still debated because the mechan...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- The Journal of neuroscience : the official journal of the Society for Neuroscience
دوره 28 43 شماره
صفحات -
تاریخ انتشار 2008