Calcium-independent release of amino acid neurotransmitters: Fact or artifact?
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Multiple functions of neuronal plasma membrane neurotransmitter transporters
2015, Progress in NeurobiologyPresynaptic CaMKIIα modulates dopamine D3 receptor activation in striatonigral terminals of the rat brain in a Ca<sup>2+</sup> dependent manner
2013, NeuropharmacologyCitation Excerpt :In this study we evaluated whether procedures that markedly enhance cytoplasmic Ca2+ modify the effects of activating D3Rs in the striatal projections to the SNr via a CaMKIIα-mediated process. We concentrated, mostly, on the effects of K+-induced depolarization because this procedure triggers Ca2+-dependent transmitter release that is akin to the naturally occurring process (Bernath, 1992). Furthermore, K+ depolarization of neuronal cultures leads to CaMKIIα accumulation near active zones (AZs) (Tao-Cheng et al., 2006).
GABA<inf>B</inf> receptors modulate depolarization-stimulated [<sup>3</sup>H]glutamate release in slices of the pars reticulata of the rat substantia nigra
2010, European Journal of PharmacologyCitation Excerpt :The depolarization caused by the high K+ concentration releases glutamate from the nerve terminals and glial cells (Bernath, 1992). Because the release of the glutamate from the glial cells is not Ca2+-dependent (Bernath, 1992), the strong Ca2+ dependency (Fig. 1) suggests that, under the present conditions, the [3H]glutamate was released mainly from the nerve terminals. The presence of dihydrokainic acid during incubation of the slices would have reduced the uptake of the [3H]glutamate into the glial cells (Kawahara et al., 2002; Bernardinelli and Chatton, 2008), thereby reducing the release from glial cells caused by the high K+ solution.