Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Keith, Richard A.; Mangano, Thomas J.; Salama, Andre I.

doi:10.1111/j.1476-5381.1989.tb14604.x

Cited by 16 publications

(11 citation statements)

References 26 publications

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“…However, in our preparation it is clear that N-type Ca 2 + channels are implicated in the alterations in the [Ca 2 + ] i . Furthermore, it was previously shown that these channels play a small but significant role in neurotransmiter release induced by kainate (Keith et al, 1989). P-type Ca 2 + channels, which are predominantly located in nerve terminals (Ambró sio et al, 1997) did not contribute to the increase in the [Ca 2 + ] i in the hippocampal cell cultures, probably because we are mainly looking at changes in neuronal cell bodies.…”

Section: Effect Of Cbz On Kainate-mediated [Ca 2 + ] I Responsesmentioning

confidence: 84%

Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists

et al. 1999

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In order to better understand the mechanism(s) of action of carbamazepine (CBZ), we studied its effects on the increase in [Ca 2 + ] i and [Na + ] i stimulated by glutamate ionotropic receptor agonists, in cultured rat hippocampal neurons, as followed by indo-1 or SBFI fluorescence, respectively. CBZ inhibited the increase in [Ca 2 + ] i stimulated either by glutamate, kainate, a-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA), or N-methyl-D-aspartate (NMDA), in a concentration-dependent manner. In order to discriminate the effects of CBZ on the activation of glutamate receptors from possible effects on Ca 2 + channels, we determined the inhibitory effects of Ca 2 + channel blockers on [Ca 2 + ] i changes in the absence or in the presence of CBZ. The presence of 1 mM nitrendipine, 0.5 mM v-conotoxin GVIA (v-CgTx GVIA), or of both blockers, inhibited the kainate-stimulated increase in [Ca 2 + ] i by 51.6, 32.9 or 68.7%, respectively. In the presence of both 100 mM CBZ and nitrendipine, the inhibition was similar (54.1%) to that obtained with nitrendipine alone, but in the presence of both CBZ and v-CgTx GVIA, the inhibition was greater (54%) than that caused by v-CgTx GVIA alone. However, CBZ did not inhibit the increase in [Na + ] i stimulated by the glutamate receptor agonists, but inhibited the increase in [Na + ] i due to veratridine. Tetrodotoxin, or MK-801, did not inhibit the influx of Na + stimulated by kainate, indicating that Na + influx occurs mainly through the glutamate ionotropic non-NMDA receptors. Moreover, LY 303070, a specific AMPA receptor antagonist, inhibited the [Na + ] i response to kainate or AMPA by about 70 or 80%, respectively, suggesting that AMPA receptors are mainly involved. Taken together, the results suggest that CBZ inhibits L-type Ca 2 + channels and Na + channels, but does not inhibit activation of glutamate ionotropic receptors.

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Section: Effect Of Cbz On Kainate-mediated [Ca 2 + ] I Responsesmentioning

confidence: 84%

Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists

et al. 1999

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“…However, when a Ca2+/Me-free buffer was used, the loss of LDH was very large. Second, the release of LDH caused by Ca2+ withdrawal was accompanied by the efflux of DA and, in the case of incubation in Ca2+/Mg2+free buffer, a large depletion of tissue DA (see also Jones et al, 1987;Keith et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Incubation of Tissue Slices in the Absence of Ca²⁺ and Mg²⁺ Can Cause Nonspecific Damage

Lónárt

Zigmond

1991

Journal of Neurochemistry

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Superfusion of striatal slices with a medium deficient in Ca2+ and Mg2+ caused a large and sustained increase in release of lactate dehydrogenase, a finding indicative of the disruption of plasma membranes. This was associated with an efflux of dopamine (DA) and the depletion of DA from the tissue. In addition, whereas DA efflux was stimulated by either D-amphetamine (10 microM) or L-glutamate (10 mM) in the absence of Ca2+, these effects were greatly reduced when Mg2+ also was withdrawn from the buffer. These results suggest that (a) incubation in a Ca2+/Mg2(+)-free buffer disrupts plasma membranes, (b) this disruption affects dopaminergic neurons as well as those of other striatal elements, and (c) the failure of a treatment to stimulate DA release in a Ca2+/Mg2(+)-free buffer cannot be used as a test of Ca2+ dependence.

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“…The blockade of these channels has been shown to inhibit the release of several neurotransmitters [24][25][26][27] and inhibits glutamatergic synaptic transmission in the hippocampus [23,28]. We have also previously shown that these channels have a major contribution to the [Ca 2+ ] i signal in isolated hippocampal nerve terminals [29].…”

Section: L-type Camentioning

confidence: 98%

Differential Contribution of L-, N-, and P/Q-type Calcium Channels to [Ca2+]i Changes Evoked by Kainate in Hippocampal Neurons

Santiago

Carvalho

et al. 2008

Neurochem Res

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We investigated the contribution of L-, N-and P/Q-type Ca 2+ channels to the [Ca 2+ ] i changes, evoked by kainate, in the cell bodies of hippocampal neurons, using a pharmacological approach and Ca 2+ imaging. Selective Ca 2+ channel blockers, namely nitrendipine, x-Conotoxin GVIA (x-GVIA) and x-Agatoxin IVA (x-AgaIVA) were used. The [Ca 2+ ] i changes evoked by kainate presented a high variability, and were abolished by NBQX, a AMPA/ kainate receptor antagonist, but the N-methyl-D-aspartate (NMDA) receptor antagonist, D-AP5, was without effect. Each Ca 2+ channel blocker caused differential inhibitory effects on [Ca 2+ ] i responses evoked by kainate. We grouped the neurons for each blocker in three subpopulations: (1) neurons with responses below 60% of the control; (2) neurons with responses between 60% and 90% of the control, and (3) neurons with responses above 90% of the control. The inhibition caused by nitrendipine was higher than the inhibition caused by x-GVIA or x-AgaIVA. Thus, in the presence of nitrendipine, the percentage of cells with responses below 60% of the control was 41%, whereas in the case of x-GVIA or x-AgaIVA the values were 9 or 17%, respectively. The results indicate that hippocampal neurons differ in what concerns their L-, N-and P/Q-type Ca 2+ channels activated by stimulation of the AMPA/ kainate receptors.

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Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Cited by 16 publications

References 26 publications

Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists

Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists

Incubation of Tissue Slices in the Absence of Ca²⁺ and Mg²⁺ Can Cause Nonspecific Damage

Differential Contribution of L-, N-, and P/Q-type Calcium Channels to [Ca2+]i Changes Evoked by Kainate in Hippocampal Neurons

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Inhibition of N‐methyl‐D‐aspartate‐ and kainic acid‐induced neurotransmitter release by ω‐conotoxin GVIA

Cited by 16 publications

References 26 publications

Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists

Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists

Incubation of Tissue Slices in the Absence of Ca2+ and Mg2+ Can Cause Nonspecific Damage

Differential Contribution of L-, N-, and P/Q-type Calcium Channels to [Ca2+]i Changes Evoked by Kainate in Hippocampal Neurons

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Incubation of Tissue Slices in the Absence of Ca²⁺ and Mg²⁺ Can Cause Nonspecific Damage