Involvement of P-type calcium channels in high potassium-elicited release of neurotransmitters from rat brain slices

Kimura, M.; Yamanishi, Yoshihiro; Hanada, Takahisa; Kagaya, Toshitaka; Kuwada, Manabu; Watanabe, Tomohiro; Katayama, Kouichi; Nishizawa, Yuji

doi:10.1016/0306-4522(95)00023-c

Cited by 57 publications

(29 citation statements)

References 24 publications

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“…In granule neurons, clearly VAs inhibit the cur- (22,30) as observed in these experiments ( Figure 2c); and P/Q-type channel blockade was associated with the greatest decrease in neurotransmitter release (36). Electrophysiological studies (17,37) have shown the presence of five distinct Ca channels with differing toxin sensitivity in CG neurons in culture.…”

Section: Discussionsupporting

confidence: 58%

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Lynch¹,

Miao²,

Nagao³

et al. 2017

J Anesth Perioper Med

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Section: Discussionsupporting

confidence: 58%

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Lynch¹,

Miao²,

Nagao³

et al. 2017

J Anesth Perioper Med

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“…This approach has been used in studies of the hippocampus (Lonart and Johnson, 1995;Katona et al, 1999) [Ca 2+ ] o -independent processes, e.g., miniature synaptic potentials and re-uptake. To the contrary, high potassium-depolarization evoked hippocampal [ 3 H]-NE release was more than 99% dependent on the presence of extracellular Ca 2+ , as reported previously (Kimura et al, 1995;Lonart et al, 1998). Similarly, measurements of evoked [ 3 H]-NE release from the amygdala (97%, Fig.…”

Section: Extracellular Ca 2+ Concentration-([ca 2+supporting

confidence: 86%

“…] o ) dependence of neurotransmitter release-Under physiological conditions, invasion of action potentials into the noradrenergic nerve terminals of the hippocampus evokes neurotransmitter release by activation P/Q and Ntype calcium channels followed by the influx of extracellular Ca 2+ (Kimura et al, 1995;Lonart et al, 1998;Khvotchev et al, 2000) leading to vesicular exocytosis. In contrast, GABA release may contain both [Ca 2+ ] o -dependent and independent components (Bernath, 1992;During et al, 1995;Wang et al, 1996;Sciancalepore et al, 1998).…”

Section: Extracellular Ca 2+ Concentration-([ca 2+mentioning

confidence: 99%

Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices

2007

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Presentation of a tonal cue that previously had been associated with a fearful experience (footshock) produces alterations in arousal and sleep that occur after the fearful cue is no longer presented. To begin investigating neurochemical mechanisms that may underlie the effects of fearful cue presentation, we measured release of Depolarization-evoked release of [ 3 H]-NE from amygdalar slices of mice, which were trained to recognize a tone as a fearful cue, was suppressed at 2-3hrs after exposure of animals to the fearful cue, but recovered after 4-5 hrs. Interestingly, depolarization-evoked release of [ 14 C]-GABA was significantly increased in the amygdala, and also showed a tendency for enhancement in the hippocampus, NPO, and DRN at 2-3 hrs after cue presentation. The changes in [ 14 C]-GABA release were also transient; 4-5 hrs after cue presentation no significant differences were detected between samples derived from experimental groups which experienced fearful or neutral cues. The similar time course of fearful cue-induced changes in neurotransmitter release and changes in arousal and REM sleep suggests that alterations in amygdalar neurotransmission may be involved changes in arousal and sleep that occur after fear.

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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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Involvement of P-type calcium channels in high potassium-elicited release of neurotransmitters from rat brain slices

Cited by 57 publications

References 24 publications

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Volatile Anesthetic Depression of Ca2+ Entry Into and Glutamate Release from Cultured Cerebellar Granule Neurons

Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices

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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