Blockade of presynaptic K ATP channels reduces the zinc-mediated posttetanic depression at hippocampal mossy fiber synapses

Matias, Carlos M.; Saggau, Peter; Quinta‐Ferreira, Mário

doi:10.1016/j.brainres.2010.01.021

Cited by 13 publications

(6 citation statements)

References 35 publications

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“…This in turn leads to the closing of VDCCs and K ATP channels, and to a decrease in presynaptic calcium entry and of glutamate and zinc co-release. This sequence of events explains the observed zinc depression, in agreement with previous findings, from combined LTP and zinc experiments (Bancila et al 2004;Quinta-Ferreira and Matias 2005;Matias et al 2010). Upon TEA removal the field potentials become po-…”

Section: Discussionsupporting

confidence: 91%

Sulfamethoxazole induces zinc changes at hippocampal mossy fiber synapses from pregnant rats

Corceiro

Bastos²,

Matias³

et al. 2018

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The accumulation of intracellular ionic zinc and pharmaceutical compounds, like the antibiotic sulfamethoxazole, may contribute to various neuropathologies. Sulfamethoxazole and the drug trimethoprim, are inhibitors of enzymes involved in the synthesis of tetrahydrofolate and also of carbonic anhydrases. The inhibition of the latter enzymes, which are localized both intra- and extracellularly and have a key role in pH regulation, causes alkalinization that is associated with higher spontaneous transmitter release. Intense synaptic stimulation causes the entry of released zinc into postsynaptic neurons, through glutamate receptor channels or voltage dependent calcium channels. The aim of this study was to evaluate the effect of sulfamethoxazole (180 μM) on basal postsynaptic zinc and to compare it with that caused by two depolarizing media, containing high potassium or tetraethylammonium, which may induce long term synaptic plasticity. The studies were performed in brain slices from gestating rats, at the mossy fiber synapses from hippocampal CA3 area, using the zinc indicator Newport Green. In the presence of KCl (20 mM) and sulfamethoxazole (180 μM) the zinc signals were enhanced, unlike in tetraethylammonium (25 mM). After sulfamethoxazole the tetraethylammonium evoked zinc signal had reduced amplitude. Thus, the data suggests that sulfamethoxazole enhances transmitter release affecting synaptic zinc physiology.

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Section: Discussionsupporting

confidence: 91%

Sulfamethoxazole induces zinc changes at hippocampal mossy fiber synapses from pregnant rats

Corceiro

Bastos²,

Matias³

et al. 2018

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“…As seen in Figure 4A, 20 mM of TEA (tetraethylammonium), which blocks many types of K + channel including one activated by FSP (Guerrero and Darszon, 1989), did not inhibit the Zn 2+ -induced hyperpolarization. It was reported that Zn 2+ activates K ATP channels in pancreatic beta cells and brain nerve terminals (Bancila et al, 2005; Bloc et al, 2000; Matias et al, 2010; Prost et al, 2004), but two K ATP channel blockers, either tolbutamide (Fig. 4B) or glibenclamide (Fig.…”

Section: Resultsmentioning

confidence: 94%

Zn2+ induces hyperpolarization by activation of a K+ channel and increases intracellular Ca2+ and pH in sea urchin spermatozoa

Beltrán

Rodríguez‐Miranda

Granados-González

et al. 2014

Developmental Biology

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Zinc (Zn2+) has been recently recognized as a crucial element for male gamete function in many species although its detailed mechanism of action is poorly understood. In sea urchin spermatozoa, Zn2+ was reported as an essential trace ion for efficient sperm motility initiation and the acrosome reaction by modulating intracellular pH (pHi). In this study we found that submicromolar concentrations of free Zn2+ change membrane potential (Em) and increase the concentration of intracellular Ca2+ ([Ca2+]i) and cAMP in Lytechinus pictus sperm. Our results indicate that the Zn2+ response in sperm of this species mainly involves an Em hyperpolarization caused by K+ channel activation. The pharmacological profile of the Zn2+-induced hyperpolarization indicates that the cGMP-gated K+ selective channel (tetraKCNG/CNGK), which is crucial for speract signaling, is likely a main target for Zn2+. Considering that Zn2+ also induces [Ca2+]i fluctuations, our observations suggest that Zn2+ activates the signaling cascade of speract, except for an increase in cGMP, and facilitates sperm motility initiation upon spawning. These findings provide new insights about the role of Zn2+ in male gamete function.

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“…Thus, zinc plays significant modulatory roles in synaptic activity and possibly also in long-term potentiation (LTP) [2,[9][10][11][12]. A negative feedback action at presynaptic sites seems also to occur, when released zinc activates the ATP-sensitive K + (K ATP ) channels [13,14], besides inhibiting VDCCs [15,16] on the boutons. These processes are thought to protect synapses from excessive neurotransmitter release and, consequently, too much postsynaptic activity.…”

Section: Introductionmentioning

confidence: 99%

FAD-Linked Autofluorescence and Chemically-Evoked Zinc Changes at Hippocampal Mossy Fiber-CA3 Synapses

Bastos¹,

Matias²,

Lopes³

et al. 2022

Hippocampus - Cytoarchitecture and Diseases

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Glutamatergic vesicles in hippocampal mossy fiber presynaptic boutons release zinc, which plays a modulatory role in synaptic activity and LTP. In this work, a fluorescence microscopy technique and the fluorescent probe for cytosolic zinc, Newport Green (NG), were applied, in a combined study of autofluorescence and zinc changes at the hippocampal mossy fiber-CA3 synaptic system. In particular, the dynamics of flavoprotein (FAD) autofluorescence signals, was compared to that of postsynaptic zinc signals, elicited both by high K+ (20 mM) and by tetraethylammonium (TEA, 25 mM). The real zinc signals were obtained subtracting autofluorescence values, from corresponding total NG-fluorescence data. Both autofluorescence and zinc-related fluorescence were raised by high K+. In contrast, the same signals were reduced during TEA exposure. It is suggested that the initial outburst of TEA-evoked zinc release might activate ATP-sensitive K+ (KATP) channels, as part of a safeguard mechanism against excessive glutamatergic action. This would cause sustained inhibition of zinc signals and a more reduced mitochondrial state. In favor of the “KATP channel hypothesis”, the KATP channel blocker tolbutamide (250 μM) nearly suppressed the TEA-evoked fluorescence changes. It is concluded that recording autofluorescence from brain slices is essential for the accurate assessment of zinc signals and actions.

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Blockade of presynaptic K ATP channels reduces the zinc-mediated posttetanic depression at hippocampal mossy fiber synapses

Cited by 13 publications

References 35 publications

Sulfamethoxazole induces zinc changes at hippocampal mossy fiber synapses from pregnant rats

Sulfamethoxazole induces zinc changes at hippocampal mossy fiber synapses from pregnant rats

Zn2+ induces hyperpolarization by activation of a K+ channel and increases intracellular Ca2+ and pH in sea urchin spermatozoa

FAD-Linked Autofluorescence and Chemically-Evoked Zinc Changes at Hippocampal Mossy Fiber-CA3 Synapses

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