Increased Ca2+ influx through Na+/Ca2+ exchanger during long‐term facilitation at crayfish neuromuscular junctions

Minami, Akira; Xia, Yanfang; Zucker, Robert S.

doi:10.1113/jphysiol.2007.143032

Cited by 12 publications

(9 citation statements)

References 56 publications

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“…Therefore, during a train of synaptic activation, there seems to be some Ca 2+ build‐up in the presynaptic terminal, despite the presence of Cd 2+ , which triggers evoked as well as spontaneous glutamate release. A potential source of such Ca 2+ influx is reverse operation of the Na + –Ca 2+ exchanger (NCX) which may occur in periods of intense neuronal activity (Zhong et al 2001; Minami et al 2007). To ask whether the small STP seen in Cd 2+ is explained by NCX, the reverse‐mode specific blocker KB‐R7943 (50–100 μ m ) was applied in combination with Cd 2+ .…”

Section: Resultsmentioning

confidence: 99%

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca²⁺ channels and mitochondria in the supraoptic nucleus

Quinlan

Alberto

Hirasawa

2008

The Journal of Physiology

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The glutamatergic synapses of the supraoptic nucleus display a unique activity-dependent plasticity characterized by a barrage of tetrodotoxin-resistant miniature EPSCs (mEPSCs) persisting for 5-20 min, causing postsynaptic excitation. We investigated how this short-term synaptic potentiation (STP) induced by a brief high-frequency stimulation (HFS) of afferents was initiated and maintained without lingering presynaptic firing, using in vitro patch-clamp recording on rat brain slices. We found that following the immediate rise in mEPSC frequency, STP decayed with two-exponential functions indicative of two discrete phases. STP depends entirely on extracellular Ca 2+ which enters the presynaptic terminals through voltage-gated Ca 2+ channels but also, to a much lesser degree, through a pathway independent of these channels or reverse mode of the plasma membrane Na + -Ca 2+ exchanger. Initiation of STP is largely mediated by any of the N-, P/Q-or L-type channels, and only a simultaneous application of specific blockers for all these channels attenuates STP. Furthermore, the second phase of STP is curtailed by the inhibition of mitochondrial Ca 2+ uptake or mitochondrial Na + -Ca 2+ exchanger. mEPSCs amplitude is also potentiated by HFS which requires extracellular Ca 2+ . In conclusion, induction of mEPSC-STP is redundantly mediated by presynaptic N-, P/Q-and L-type Ca 2+ channels while the second phase depends on mitochondrial Ca 2+ sequestration and release. Since glutamate influences unique firing patterns that optimize hormone release by supraoptic magnocellular neurons, a prolonged barrage of spontaneous excitatory transmission may aid in the induction of respective firing activities.

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Section: Resultsmentioning

confidence: 99%

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca²⁺ channels and mitochondria in the supraoptic nucleus

Quinlan

Alberto

Hirasawa

2008

The Journal of Physiology

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“…However, NCXs can also contribute to an increase in residual Ca 2+ via their reverse operation depending on Na + gradients. After post-tetanic potentiation, increased Ca 2+ influx through reverse NCXs is involved in residual Ca 2+ accumulation at nerve terminals in neuromuscular junctions (Zhong et al 2001;Minami et al 2007).…”

Section: Ca 2+ Influx Via Reverse Ncxs Leads To a Gradual Rise In Prementioning

confidence: 99%

Mechanisms underlying presynaptic Ca²⁺ transient and vesicular glutamate release at a CNS nerve terminal during in vitro ischaemia

Lee¹,

Kim

2015

The Journal of Physiology

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Key pointsr Here we demonstrate presynaptic responses and mechanisms of increased vesicular glutamate release during in vitro ischaemia in the calyx of Held terminal, an experimentally accessible presynaptic terminal in the CNS. Abstract An early consequence of brain ischaemia is an increase in vesicular glutamate release from presynaptic terminals. However, the mechanisms of this increased glutamate release are not fully understood. Here we studied presynaptic responses and mechanisms of increased glutamate release during in vitro ischaemia, using pre-and postsynaptic whole-cell recordings and presynaptic Ca 2+ imaging at the calyx of Held synapse in rat brainstem slices. Consistent with results from other brain regions, in vitro ischaemia significantly increased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) without affecting their amplitude, suggesting that ischaemia enhances vesicular glutamate release from presynaptic terminals. We found that ischaemia-induced vesicular glutamate release was dependent on a rise in basal Ca 2+ at presynaptic terminals, which resulted from extracellular Ca 2+ influx and Ca 2+ release from intracellular stores. During early ischaemia, increased Ca 2+ influx into presynaptic terminals was due to reverse operation of the plasma membrane Na + /Ca 2+ exchanger (NCX) rather than presynaptic depolarization or voltage-activated Ca 2+ currents. KB-R7943, an inhibitor of NCX, prevented the ischaemia-induced increases in presynaptic Ca 2+ and vesicular glutamate release. In addition, the removal of extracellular Na + completely inhibited the ischaemia-induced Ca 2+ rise. It therefore appears that a link between Na + accumulation and Ca 2+ uptake via NCX underlies the ischaemia-induced Ca 2+ rise and the consequent increase in vesicular glutamate release from presynaptic terminals in the early phase of brain ischaemia.

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“…A recent experiment performed on the crayfish neuromuscular junction corroborates this statement. It was observed that a long-term facilitation-inducing tetanus (20 Hz for 10 min) caused a substantial (manifold) increase in Ca 2+ influx through reverse mode operation of NCX probably by Ca 2+ -dependent modulation of Na + ⁄ Ca 2+ transporters (Minami et al, 2007). Such modulations of NCX could be important for the dendritic segments and could help to cope better with, and recover faster from, excess Ca 2+ loads.…”

Section: Altered Ca 2+ Decay Kinetics In Epileptic Neuronsmentioning

confidence: 99%

Epileptiform activity induces distance‐dependent alterations of the Ca²⁺ extrusion mechanism in the apical dendrites of subicular pyramidal neurons

Srinivas

Sikdar

2008

Eur J of Neuroscience

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The cellular and molecular mechanisms that underlie acquired changes in Ca(2+) dynamics of different neuronal compartments are important in the induction and maintenance of epileptiform activity. Simultaneous electrophysiology and Ca(2+) imaging techniques were used to understand the basic properties of dendritic Ca(2+) signaling in rat subicular pyramidal neurons during epileptiform activity. Distance-dependent changes in the Ca(2+) decay kinetics locked to spontaneous epileptiform discharges and back-propagating action potentials were observed in the apical dendrites. A decrement in the mean tau value of Ca(2+) decay was observed in distal parts (95-110 mum) of the apical dendrites compared with proximal segments (30-45 mum) in in-vitro epileptic conditions but not in control. Pharmacological agents that block Ca(2+) transporters, i.e. Na(+)/ Ca(2+) exchangers (Benzamil), plasma membrane Ca(2+)-ATPase pumps (Calmidazolium) and smooth endoplasmic reticulum Ca(2+)-ATPase pumps (Thapsigargin), were applied locally to the proximal and distal part of the apical dendrites in both experimental conditions to understand the molecular aspects of the Ca(2+) extrusion mechanisms. The relative contribution of Na(+)/Ca(2+) exchangers in Ca(2+) extrusion was higher in the distal apical dendrites in the in-vitro epileptic condition and this property modulated the excitability of the neuron in simulation. The Ca(2+) homeostatic mechanisms that restore normal Ca(2+) levels could play a major neuroprotective role in the distal dendrites that receive synaptic inputs.

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Increased Ca²⁺ influx through Na⁺/Ca²⁺ exchanger during long‐term facilitation at crayfish neuromuscular junctions

Abstract: Intense motor neuron activity induces a long-term facilitation (LTF

Cited by 12 publications

References 56 publications

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca²⁺ channels and mitochondria in the supraoptic nucleus

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca²⁺ channels and mitochondria in the supraoptic nucleus

Mechanisms underlying presynaptic Ca²⁺ transient and vesicular glutamate release at a CNS nerve terminal during in vitro ischaemia

Epileptiform activity induces distance‐dependent alterations of the Ca²⁺ extrusion mechanism in the apical dendrites of subicular pyramidal neurons

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Increased Ca2+ influx through Na+/Ca2+ exchanger during long‐term facilitation at crayfish neuromuscular junctions

Abstract: Intense motor neuron activity induces a long-term facilitation (LTF

Cited by 12 publications

References 56 publications

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca2+ channels and mitochondria in the supraoptic nucleus

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca2+ channels and mitochondria in the supraoptic nucleus

Mechanisms underlying presynaptic Ca2+ transient and vesicular glutamate release at a CNS nerve terminal during in vitro ischaemia

Epileptiform activity induces distance‐dependent alterations of the Ca2+ extrusion mechanism in the apical dendrites of subicular pyramidal neurons

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Resources

About

Increased Ca²⁺ influx through Na⁺/Ca²⁺ exchanger during long‐term facilitation at crayfish neuromuscular junctions

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca²⁺ channels and mitochondria in the supraoptic nucleus

Short‐term potentiation of mEPSCs requires N‐, P/Q‐ and L‐type Ca²⁺ channels and mitochondria in the supraoptic nucleus

Mechanisms underlying presynaptic Ca²⁺ transient and vesicular glutamate release at a CNS nerve terminal during in vitro ischaemia

Epileptiform activity induces distance‐dependent alterations of the Ca²⁺ extrusion mechanism in the apical dendrites of subicular pyramidal neurons