Norepinephrine efflux evoked by potassium chloride in cat sympathetic nerves: dual mechanism of action

Yamazaki, Toji; Akiyama, Tsuyoshi; Kawada, Toru; Kitagawa, Hirotoshi; Takauchi, Yuji; Yahagi, Naoki; Sunagawa, Kenji

doi:10.1016/s0006-8993(98)00209-1

Cited by 14 publications

(8 citation statements)

References 15 publications

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“…Previous work has shown that high K + aCSF causes DA release through both vesicular release and reverse transport at monoamine transporters (Yamazaki et al, 1998;Chen et al, 2004). We found that high K + (20 mM) aCSF caused greater DA release in brain slices from F344 rats compared with SD rats (Fig.…”

Section: Discussionsupporting

confidence: 51%

“…We also altered the ionic environment in ways that would be favorable for enhanced reverse transport. In particular, high K + has been shown to be associated with both vesicular and nonvesicular release of DA (Chen et al, 2004;Yamazaki et al, 1998), whereas elevating Zn 2 + levels has been reported to enhance reverse transport of DA through the DAT (Loland et al, 2003;Pifl et al, 2004). As was the case with amphetamine, we also predicted that increased accumulation of cytoplasmic DA in F344 rats would lead to increased nonvesicular release of DA in response to these two ionic challenges.…”

Section: Introductionmentioning

confidence: 81%

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Effects of amphetamine on striatal dopamine release, open-field activity, and play in Fischer 344 and Sprague–Dawley rats

Siviy

McDowell

Eck

et al. 2015

Behavioural Pharmacology

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Previous work from our laboratories has shown that juvenile Fischer 344 (F344) rats are less playful than other strains and also appear to be compromised in dopamine (DA) functioning. To determine whether the dysfunctional play in this strain is associated with deficits in the handling and delivery of vesicular DA, the following experiments assessed the extent to which F344 rats are differentially sensitive to the effects of amphetamine. When exposed to amphetamine, striatal slices obtained from F344 rats showed a small increase in unstimulated DA release when compared with slices from Sprague-Dawley rats; they also showed a more rapid high K+-mediated release of DA. These data provide tentative support for the hypothesis that F344 rats have a higher concentration of cytoplasmic DA than Sprague-Dawley rats. When rats were tested for activity in an open field, F344 rats presented a pattern of results that was consistent with either an enhanced response to amphetamine (3 mg/kg) or a more rapid release of DA (10 mg/kg). Although there was some indication that amphetamine had a dose-dependent differential effect on play in the two strains, play in F344 rats was not enhanced to any degree by amphetamine. Although these results are not consistent with our working hypothesis that F344 rats are less playful because of a deficit in vesicular release of DA, they still suggest that this strain may be a useful model for better understanding the role of DA in social behavior during the juvenile period.

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Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 81%

Effects of amphetamine on striatal dopamine release, open-field activity, and play in Fischer 344 and Sprague–Dawley rats

Siviy

McDowell

Eck

et al. 2015

Behavioural Pharmacology

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“…When reserpine inhibited vesicle transport of NA and reduced NA graduation between the axoplasma and the vesicle, outward efflux of NA (evoked by tyramine) is greater than NA leakage and mobilization from stored NA vesicle. In the previous study, we found that high K + induced carrier‐mediated outward NA transport after the pretreatment with reserpine and ω ‐conotoxin GVIA ( Yamazaki et al . 1998 ).…”

Section: Discussionmentioning

confidence: 94%

“…Electrical stimulation of stellate ganglia or high K + is used to examine whether Ca 2+ ‐dependent exocytotic NA release is intact or impaired ( Yamazaki et al . 1997 , 1998). On the other hand, using locally applied tyramine, it is possible to test whether pathophysiological conditions cause depletion or exhaustion of NA at the sympathetic nerve ending ( Shindo et al .…”

Section: Discussionmentioning

confidence: 99%

Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats

Takauchi

Yamazaki

Akiyama

2000

Acta Physiologica Scandinavica

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With the use of dialysis technique, the effects of tyramine on in situ cardiac sympathetic nerve endings were examined in anaesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and the concentration of dialysate noradrenaline (NA) served as an indicator of NA output at the cardiac sympathetic nerve ending. Locally applied tyramine (600 microM) increased dialysate NA levels from 17 +/- 1 (pg mL-1) to 3466 +/- 209 (pg mL-1). Pretreatment with reserpine (vesicle transport NA blocker 1 microM) did not affect tyramine-induced NA efflux. The tyramine-induced NA efflux was augmented by pretreatment with pargyline (1 mM) but suppressed by pargyline (10 mM). Pretreatment with alpha-methyl-tyrosine suppressed NA efflux evoked by tyramine. These pretreatments did not affect the time course of NA efflux but only altered peak height of NA efflux. The efflux of NA evoked by tyramine was not associated with any reduction of dihydroxyphenylglycol (DHPG). In contrast, in the pretreatment with reserpine, the efflux of NA was associated with a reduction of DHPG. This result suggests that NA graduation between axoplasm and stored vesicle contributes to maintaining the axoplasmic NA level during carrier-mediated outward NA transport. The tyramine-induced NA efflux provides a close reflection of the NA content at the nerve ending. With the use of dialysis, this experimental model is suitable for studying the mechanism of sympathomimetic amine-induced neurotransmitter efflux.

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“…In the previous study, we demonstrated that high K + ‐induced NA release was insensitive to TTX but sensitive to ω‐conotoxin GVIA. Furthermore, high K + caused a marked increase in dialysate NA but little increase in dialysate Ach (Yamazaki et al. 1998, Kawada et al.…”

Section: Discussionmentioning

confidence: 99%

Characterization of ouabain‐induced noradrenaline and acetylcholine release from in situ cardiac autonomic nerve endings

et al. 2007

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Ouabain-induced NA release is attributable to the mechanisms of regional exocytosis and/or carrier-mediated outward transport of NA, from stored NA vesicle and/or axoplasma, respectively, while the ouabain-induced ACh release is attributable to the mechanism of exocytosis, which is triggered by regional depolarization. At both sympathetic and parasympathetic nerve endings, the regional exocytosis is because of opening of calcium channels and intracellular calcium mobilization.

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Norepinephrine efflux evoked by potassium chloride in cat sympathetic nerves: dual mechanism of action

Cited by 14 publications

References 15 publications

Effects of amphetamine on striatal dopamine release, open-field activity, and play in Fischer 344 and Sprague–Dawley rats

Effects of amphetamine on striatal dopamine release, open-field activity, and play in Fischer 344 and Sprague–Dawley rats

Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats

Characterization of ouabain‐induced noradrenaline and acetylcholine release from in situ cardiac autonomic nerve endings

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