Modulation of vertebrate neuronal calcium channels by transmitters
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Cited by (157)
Quantitative aspects of L-type Ca<sup>2+</sup> currents
2012, Progress in NeurobiologyCitation Excerpt :For an introduction to fundamentals about ion channels see, for example, Levitan and Kaczmarek (1997). Additional reviews on voltage-dependent Ca2+-channels pertaining to their molecular structure, nomenclature and function, including modulation and regulation are contained in, for example, in chronological order, Tsien et al. (1988), Bean (1989), Tsien and Tsien (1990), Anwyl (1991), Catterall (1995), De Waard et al. (1996), Jones (1998), Hofmann et al. (1999), Catterall (2000), Ertel et al. (2000), Kamp and Hell (2000), Lacinová (2005), Zamponi (2005) and Catterall (2010). Reviews addressing specific related topics include those on synaptic transmission (Meir et al., 1999; Neher and Sakaba, 2008), T-type currents (Perez-Reyes, 2003; Cueni et al., 2009), calcium-dependent inactivation in neurons (Budde et al., 2002), dynamics of calcium signaling in neurons (Augustine et al., 2003), models of calcium sparks and waves (Coombes et al., 2004), L-type currents in the heart (Bodi et al., 2005), the role of calcium currents in circadian rhythms (Brown and Piggins, 2007), calcium release and the roles of ryanodine receptors in heart and skeletal muscle diseases (Zalk et al., 2007), Ca2+ channels in chromaffin cells (Marcantoni et al., 2008) and calcium dynamics in relation to absence epilepsy (Weiergräber et al., 2010).
Role of periaqueductal grey prostaglandin receptors in formalin-induced hyperalgesia
2006, European Journal of PharmacologyFK962, a novel enhancer of somatostatin release, exerts cognitive-enhancing actions in rats
2005, European Journal of PharmacologyThe involvement of glutamate-gated channels in negative feedback from horizontal cells to cones
2005, Progress in Brain ResearchCitation Excerpt :Therefore, it is important to reflect on other mechanisms. It has been proposed that glutamate (Anwyl, 1991), GABA (Kaneko et al., 1986), and nitric oxide (NO) (Savchenko et al., 1997) are the feedback neurotransmitters. Furthermore, changes in the concentration of divalent cations (Piccolino et al., 1999), and protons (Barnes et al., 1993) can shift the Ca2+-current activation function to more negative potentials.