1995
DOI: 10.1111/j.1460-9568.1995.tb00698.x
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Stimulation of Ca2+‐Activated Non‐specific Cationic Channels by Phospholipase C‐linked Glutamate Receptors in Synaptoneurosomes?

Abstract: The regulation of intracellular Ca2+ concentration ([Ca2+]i) by glutamate metabotropic receptors (mGluR) was studied in 8-day-old rat forebrain synaptoneurosomes using spectrofluorimetric methods. Here we demonstrate that metabotropic glutamate agonists induce in rat brain synaptoneurosomes a Ca2+ influx largely dependent upon the presence of Ca2+ in the external medium. The pharmacological profile of this influx is strongly correlated with the pharmacological profile of the activation of phosphoinositide hydr… Show more

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Cited by 10 publications
(3 citation statements)
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References 43 publications
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“…This interpretation does not preclude the possibility that fetal ethanol exposure may have altered other mGluR-mediated responses that regulate neurotransmitter release. Other mGluR-stimulated PLC-/PKCdependent mechanisms that affect neurotransmitter release include IP 3 -triggered release of internal calcium stores (Vignes et al, 1995), decreased permeability of potassium channels that antagonize voltage-dependent calcium entry into nerve terminals (Abdul-Ghani et al, 1996;Gerber and Gahwiler, 1994;Luthi et al, 1996), and inhibition of group II or group III mGluRs that mediate decreased N-and P-type voltage-sensitive calcium channel permeability at nerve terminals (Herrero et al, 1996;Macek et al, 1998). Prenatal ethanol exposure might also affect mGluR-stimulated phospholipase D (PLD)-dependent generation of arachidonic acid (Boss and Conn, 1992;Pellegrini-Giampietro et al, 1996).…”
Section: Discussionmentioning
confidence: 99%
“…This interpretation does not preclude the possibility that fetal ethanol exposure may have altered other mGluR-mediated responses that regulate neurotransmitter release. Other mGluR-stimulated PLC-/PKCdependent mechanisms that affect neurotransmitter release include IP 3 -triggered release of internal calcium stores (Vignes et al, 1995), decreased permeability of potassium channels that antagonize voltage-dependent calcium entry into nerve terminals (Abdul-Ghani et al, 1996;Gerber and Gahwiler, 1994;Luthi et al, 1996), and inhibition of group II or group III mGluRs that mediate decreased N-and P-type voltage-sensitive calcium channel permeability at nerve terminals (Herrero et al, 1996;Macek et al, 1998). Prenatal ethanol exposure might also affect mGluR-stimulated phospholipase D (PLD)-dependent generation of arachidonic acid (Boss and Conn, 1992;Pellegrini-Giampietro et al, 1996).…”
Section: Discussionmentioning
confidence: 99%
“…The reciprocal facilitatory interaction also occurs postsynaptically since activation of group I mGlu receptors potentiates depolarization induced by NMDA in the hippocampus (Fitzjohn et al, 1996). A Ca2+-dependence in mGlu-stimulated phosphoinositide breakdown in synaptosomes has been demonstrated (Vignes et al, 1995a) so it is also possible that NMDA and mGlu receptor interactions can occur presynaptically.…”
Section: Discussionmentioning
confidence: 99%
“…Complex interactions between group I metabotropic glutamate receptors (mGluR‐I), intracellular Ca 2+ stores and Ca 2+ ‐permeable cation channels in the plasma membrane of neurons have been identified in the cortex, hippocampus and cerebellum (Linden et al ., 1994; Vignes et al ., 1995; Abdul‐Ghani et al ., 1996; Fagni et al ., 2000; Nakamura et al ., 2000; Gee et al ., 2003).…”
Section: Introductionmentioning
confidence: 99%