External Ca<sup>2+</sup>‐Independent Release of Neurotransmitters

Ádám-Vizi, Vera

doi:10.1111/j.1471-4159.1992.tb09736.x

Cited by 161 publications

(54 citation statements)

References 164 publications

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“…The increase in [Na + ] i has been shown to persist and even worsen during reperfusion (Rose et al 1998;Taylor et al 1999). It is well established that a shift in the Na + equilibrium is able to release transmitters via reverse operation of Na + -dependent transmitter carriers (for review see Adam-Vizi 1992). The results of the present study show that when oxidative stress occur in concurrence with an accumulation of Na + in the cytosol, glutamate release induced by the [Na + ] i increase could be significantly enhanced.…”

Section: Discussionmentioning

confidence: 99%

“…Veratridine by blocking the inactivation of voltage dependent Na + channels, allows a continuous Na + entry into cells (Catterall 1980) leading to a rise in [Na Adam-Vizi 1993;Chinopoulos et al 2000). This condition has been known for a long time to result in an increased release of neurotransmitters, including that of glutamate (for review see Adam-Vizi 1992).…”

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confidence: 99%

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Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Tretter

Ádám-Vizi

2002

Journal of Neurochemistry

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Tretter

Ádám-Vizi

2002

Journal of Neurochemistry

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“…Moreover, surface charge effects should have a great influence in experimental conditions in which transmitter release is evoked by smallamplitude graded depolarizations, as for instance, following the application of high K+ concentrations or of various pharmacological agents. It is, in fact, from these studies that the idea of a Ca2+-independent transmitter release has been mainly derived (6,7,35).…”

Section: )mentioning

confidence: 99%

Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.

Piccolino

Byzov

Kurennyi

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

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According to the classical calcium hypothesis of synaptic transmission, the release of neurotransmitter from presynaptic terminals occurs through an exocytotic process triggered by depolarization-induced presynaptic calcium influx. However, evidence has been accumulating in the last two decades indicating that, in many preparations, synaptic transmitter release can persist or even increase when calcium is omitted from the perfusing saline, leading to the notion of a "calcium-independent release" mechanism. Co2+, Ni2+, and Zn2+ is to a large extent accounted for by a depolarizing shift of the Ca2+ current activation curve, by means of an interaction with the negative fixed charges on the photoreceptor presynaptic membrane. Presynaptic depolarization with extrinsic currents, or reduction of extracellular Ca2+, relieves the transmission block because these conditions bring presynaptic transmembrane potential to levels where Ca>2 current can still be activated. Our results may give new insights into the problem of so-called "calcium-independent synaptic transmission" (6, 7). MATERIALS AND METHODSLight Responses in Retinal Eyecups. Eyecups were prepared from the retina of turtles (Pseudemys scripta elegans) or salamanders (Ambystoma tigrinum) and continuously superfused with a modified Ringer saline bubbled continuously with a mixture of 95% 02 and 5% Co2. The composition (in mM) of the saline used in turtle experiments was the following: NaCl, 110; KCI, 2.6; NaHCO3, 22; MgCl2, 2; CaCl2, 2; Dglucose, 10 (pH 7.4). Salamander saline had the followingThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.composition: NaCl, 95; KCI, 2.5; NaHCO3, 30; MgCl2, 2; CaCl2, 2; D-glucose, 10 (pH 7.6). Intracellular recording of the light responses induced by 5-mm-diameter white light spots of variable intensity and duration were made in HCs (and in other retinal neurons) by using fine tip microelectrodes prepared with a Brown-Flaming puller (Sutter Instruments, Novato, CA). The concentration of Ca2> in the nominally zero Ca2> Ringer solution, without EGTA added, was less than 10 ,uM. The pH of the solutions containing EGTA or EDTA was readjusted with NaOH. The concentration of Ca2> in media containing CaCl2 in variable proportions and EGTA (2-10 ,uM) or EDTA (2-5 ,.tM) ranged from 0.45 to 2.4 nM and was estimated by using the computer program SOL i.d. written by Eric Ertel (Hoffmann-La Roche). To keep a normal concentration of Mg2+ in media containing EGTA the proportion of MgCl2 in the perfusing saline was adjusted accordingly. Chemicals were obtained from Sigma. Bicuculline was used as the soluble methobromide salt and added to the perfusing medium just before application to the retina. Picrotoxin was first dissolved in slightly basic, hot distilled water and then added to the Ringer solution. Neutral density filters were used to attenuate light intensity. The flux de...

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“…Rather, the results support the conjecture by Parker and Cubeddu (1986) that amphetamine elevates the cytosolic pool of DA and that subsequent release from this pool is independent of whether the DA is newly synthesized or had previously resided in storage vesicles. Reverse transport of neurotransmitter may occur under physiological conditions (Pin and Bockaert, 1989;Szatkowski et al, 1990;Lonart and Zigmond, 199 1 ;Adam-Vizi, 1992;O'Malley et al, 1992) due to transmitter-dependent increases in sodium flux or anoxia. Such a mechanism could be particularly important for transmitter release from cells in which activity regulates cytosolk versus vesicular transmitter pools (Barasch et al, 1988).…”

Section: Weak Base Mechanism Of Amphetamine Actionmentioning

confidence: 99%

Amphetamine and Other Weak Bases Act to Promote Reverse Transport of Dopamine in Ventral Midbrain Neurons

Sulzer

Maidment²,

Rayport³

1993

Journal of Neurochemistry

267

147

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Amphetamine-like psychostimulants are thought to produce rewarding effects by increasing dopamine levels at mesolimbic synapses. Paradoxically, dopamine uptake blockers, which generally increase extracellular dopamine, inhibit amphetamine-induced dopamine overflow. This effect could be due to either inhibition o f amphetamine uptake or inhibition of dopamine efflux through the transporter (reverse transport). We used weak bases and dopamine uptake blockers in ventral midbrain neuron cultures to separate the effects on blockade of amphetamine uptake from reverse transport ofdopamine. Amphetamine, ammonium chloride, tributylamine, and monensin, at concentrations that produce similar reductions in acidic pH gradients, increased dopamine release. This effect was inhibited by uptake blockers. Although in the case of amphetamine the inhibition of release could have been due to blockade of amphetamine uptake, inhibition also occurred with weak bases that are not transporter substrates. This suggests that reduction of vesicular pH gradients increases cytoplasmic dopamine which in turn promotes reverse transport. Consistent with this model, extracellular 3,4-dihydroxyphenylacetic acid was increased by ammonium chloride and monensin, as would be expected with elevated cytoplasmic dopamine levels. These findings extend the weak base mechanism of amphetamine action, in which amphetamine reduces vesicular pH gradients resulting in increased cytoplasmic dopamine that promotes reverse transport.

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External Ca²⁺‐Independent Release of Neurotransmitters

Cited by 161 publications

References 164 publications

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.

Amphetamine and Other Weak Bases Act to Promote Reverse Transport of Dopamine in Ventral Midbrain Neurons

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External Ca2+‐Independent Release of Neurotransmitters

Cited by 161 publications

References 164 publications

Glutamate release by an Na+ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Glutamate release by an Na+ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.

Amphetamine and Other Weak Bases Act to Promote Reverse Transport of Dopamine in Ventral Midbrain Neurons

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External Ca²⁺‐Independent Release of Neurotransmitters

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion

Glutamate release by an Na⁺ load and oxidative stress in nerve terminals: relevance to ischemia/reperfusion