Short communicationTetanus-induced asynchronous GABA release in cultured hippocampal neurons
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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.
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Imaging of Ca<sup>2+</sup> responses mediated by presynaptic L-type channels on GABAergic boutons of cultured hippocampal neurons
2009, Brain ResearchCitation Excerpt :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
2007, Brain ResearchCitation Excerpt :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).
Autonomous function of synaptotagmin 1 in triggering synchronous release independent of asynchronous release
2005, NeuronCitation Excerpt :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.
Different types of retinal inhibition have distinct neurotransmitter release properties
2015, Journal of NeurophysiologyMolecular mechanisms for synchronous, asynchronous, and spontaneous neurotransmitter release
2014, Annual Review of Physiology