Elsevier

Brain Research

Volume 880, Issues 1–2, 13 October 2000, Pages 198-201
Brain Research

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Tetanus-induced asynchronous GABA release in cultured hippocampal neurons

https://doi.org/10.1016/S0006-8993(00)02746-3Get rights and content

Abstract

Asynchronous GABA release was studied in cultured hippocampal neurons using paired whole-cell recordings. Tetanization of the presynaptic GABAergic neuron was accompanied by a train of IPSCs which showed tetanic depression. Asynchronous IPSCs (asIPSCs) also developed during the train and continued for 1.85±0.3 s after the stimulation. The threshold frequency for evoking asIPSCs was 10 Hz, while maximal asynchronous activity was achieved at 40 Hz. Perfusion with EGTA-AM blocked asIPSCs. The elevation of [Ca2+]i that accompanies presynaptic action potential firing triggers asynchronous release of GABA vesicles, thereby counteracting tetanic depression of synchronous IPSCs.

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Acknowledgements

We thank the Danish Medical Research Council, Aarhus Universitets Forsknings Fond, and Glaxo/Wellcome for financial support. We thank K. Kandborg for preparation of the cultures and S. Kristensen for technical help.

References (20)

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Cited by (12)

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    On the other hand, asynchronous release of GABA vesicles is correlated to the size and duration of the rise in intraterminal [Ca2+]i, (Jensen et al., 2000b; Kirischuk and Grantyn, 2003). This asynchronous activity is readily blocked by EGTA (Jensen et al., 2000b) in accordance with the strong acceleration of Ca2+ decay in the presence of EGTA (Chen and Regehr, 1999). In summary, the process underlying PTP is triggered by the activation of L-type channels, and does not require the maintained presence of elevated [Ca2+]i.

  • Post-tetanic potentiation of GABAergic IPSCs in cultured hippocampal neurons is exclusively time-dependent

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    Moreover, we have found that the time course of the decline in intrabouton [Ca2+]i is markedly shorter than the time course of PTP (Lambert et al., 2002). On the other hand, the wave of increased [Ca2+]i during and following stimulation is more closely correlated to asynchronous vesicle release seen during and following the tetanic stimulation (Jensen et al., 2000a,b). PTP is also related to the number of pulses in the train, rather than the frequency at which they are delivered (Jensen et al., 1999a).

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    When action potentials fire at high frequency, release becomes largely asynchronous (Barrett and Stevens, 1972; Goda and Stevens, 1994; Cummings et al., 1996; Atluri and Regehr, 1998; Lu and Trussell, 2000; Hagler and Goda, 2001; Otsu et al., 2004; reviewed in Atwood and Karunanithi, 2002). Synchronous release is triggered by brief localized Ca2+ waves induced by action potentials (Llinas et al., 1995), whereas asynchronous release is triggered by increased bulk “residual” Ca2+ (Atluri and Regehr, 1998; Jensen et al., 2000; Kirischuk and Grantyn, 2003). Asynchronous release induced by high-frequency stimulation consists of two types: (1) release during the stimulus train when synchronous release still operates but is outcompeted by asynchronous release, and (2) release after the stimulus train (“delayed release”) when residual Ca2+ remains sufficiently high to trigger synaptic vesicle exocytosis.

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