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Exocytosis of Nonclassical Neurotransmitters
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Xiao Su, Vincent R. Mirabella, Kenneth G. Paradiso, Zhiping P. Pang
Different from three Syts (1, 2 & 9) mentioned above, Syt 7 was suggested to mediate asynchronous neurotransmitter release (Bacaj et al., 2013). Loss of function of Syt 7 in Syt 1-deficient excitatory and inhibitory neurons suppressed asynchronous release. Even in Syt 1 containing neurons, ablation of Syt 7 impaired partially asynchronous release induced by extended high-frequency stimulus trains. However, no major phenotype was detected upon ablation of Syt 7 in wild-type neurons, suggesting Syt 7 function is normally occluded by Syt 1 (Bacaj et al., 2013). Syt 7 exhibits its function selectively via C2A domains whereas Syt 1 requires the C2B domain to exhibit its function. Similarly, Syt 7 KO in calyx synapses has no effect on altering fast release and short-term plasticity in calyx of Held synapses. Syt 7-dependent asynchronous release induces a steady-state, asynchronous postsynaptic current during prolonged Ca2+ influx, sustaining high-fidelity neurotransmission driven by synchronous release during high-frequency stimulus trains (Luo and Südhof, 2017).
The neurosciences at the Max Planck Institute for Biophysical Chemistry in Göttingen
Published in Journal of the History of the Neurosciences, 2023
In Neher’s laboratory, the “Calyx of Held”—a giant synapse from the auditory system in the brain stem—initially served as a model for the release of the neurotransmitter glutamate (Schneggenburger and Neher 2000). Later on, Neher and his colleagues also studied the neurotransmitter release on other synapses of the brain (medial septum, hippocampus) and, in addition to “normal” neurotransmitter release, they studied their plastic changes, which presumably play a role in learning and memory.
Parvalbumin expression affects synaptic development and physiology at the Drosophila larval NMJ
Published in Journal of Neurogenetics, 2018
Tao He, Michael N. Nitabach, Gregory A. Lnenicka
Expression of PV in the motor terminals reduced both the amplitude and decay τ of the single-AP Ca2+ transient; this was observed at both 50 and 500 Hz frame frequencies. Due to its slow action, PV is expected to produce a greater effect on the [Ca2+]i decay than the amplitude of single-AP Ca2+ transients (Lee et al., 2000). For example, the addition of 100 µM PV to the presynaptic terminal at the Calyx of Held did not produce a significant decrease in the Ca2+ transient amplitude but reduced the decay τ (Muller et al., 2007). The Ca2+ transient amplitude may have been reduced in our experiments due to a high level of PV expression. For example, when EGTA, an inorganic Ca2+ buffer that shows similar Ca2+-binding kinetics as PV, was added to granule cells in the rat cerebellum at low concentrations only the decay was affected but at higher concentrations both the Ca2+ transient amplitude and duration were decreased (Atluri & Regehr, 1996). This is consistent with calculations predicting that the mean time for a buffer to capture Ca2+ is inversely related to buffer concentration (Roberts, 1994). For a 5 s AP train delivered at 10 or 20 Hz, the rate of rise and decay of [Ca2+]i was slower for PV-expressing terminals compared to control ones; however, the increase in [Ca2+]i at the plateau was similar for PV-expressing and control terminals. This is consistent with experimental and theoretical studies of the effect of a Ca2+ buffer on an AP train; the Ca2+ buffer binds Ca2+ to slow its buildup; it does not affect the plateau, which occurs when the buffer is saturated and Ca2+ influx is matched by Ca2+ extrusion and it slows the decay due to the release of Ca2+ (Tank, Regehr, & Delaney, 1995).
A cGMP-dependent protein kinase, encoded by the Drosophila foraging gene, regulates neurotransmission through changes in synaptic structure and function
Published in Journal of Neurogenetics, 2021
Jeffrey S. Dason, Marla B. Sokolowski
We found that knockdown of presynaptic for impaired SV endocytosis (Figure 3). We previously used fluorescein-assisted light inactivation of FOR and a temperature-sensitive dynamin mutant, shibirets1, to demonstrate that FOR is necessary for endocytosis of SVs that have undergone exocytosis using a functional FOR protein (Dason et al., 2019). These data show that FOR’s effects on SV endocytosis are not simply a consequence of altered SV exocytosis. These findings are consistent with several studies that propose that PKG plays a key role in balancing SV exocytosis and endocytosis (Collado-Alsina, Ramírez-Franco, Sánchez-Prieto, & Torres, 2014; Dason et al., 2019; Eguchi, Nakanishi, Takagi, Taoufiq, & Takahashi, 2012; Petrov, Giniatullin, Sitdikova, & Zefirov, 2008; Taoufiq, Eguchi, & Takahashi, 2013). During periods of sustained synaptic transmission, SV recycling is upregulated through a retrograde pathway that involves the release of nitric oxide (NO) from the postsynaptic cell and a subsequent increase in presynaptic cGMP and PIP2 in cultured hippocampal neurons and synapses of the rat Calyx of Held (Eguchi et al., 2012; Micheva, Buchanan, Holz, & Smith, 2003). Similarly, application of NO donors at the Drosophila nmj induces cGMP immunoreactivity in presynaptic boutons (Wildemann & Bicker, 1999) and both presynaptic cGMP (Shakiryanova & Levitan, 2008) and PIP2 levels (Dason et al., 2014) were found to be elevated during high frequency stimulation. PKG is activated by cGMP and thought to upregulate PIP2 levels through a Rho-kinase (Eguchi et al., 2012; Taoufiq et al., 2013). PIP2 recruits AP-2 and clathrin to sites of endocytosis (Micheva et al., 2003). Thus, a reduction in PIP2 is likely the cause of the impaired SV endocytosis observed following the inhibition of PKG in mammalian studies or the absence of for in Drosophila studies.