Short communicationPotentiation of transmitter release from NMB human neuroblastoma cells by kappa-opioids is mediated by N-type voltage-dependent calcium channels
Section snippets
Acknowledgements
This study was supported by a grant from the Anti-Drug Authority of Israel.
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Contribution of G inhibitory protein alpha subunits in paradoxical hyperalgesia elicited by exceedingly low doses of morphine in mice
2011, Life SciencesCitation Excerpt :Depending on the type of cell used and dose applied, opioids can induce hyperpolarization or depolarization and either inhibit or stimulate neuronal cells. On the basis of electrophysiological studies, it was suggested that either stimulatory or inhibitory influence on neurones by opioid agonists depends on the dose applied (North and Uchimura, 1989; Crain and Shen, 1990; Smart and Lambert, 1996; Keren et al., 1999). Studies in primary dorsal root ganglion cultures showed that neuronal stimulation occurred at nanomolar concentrations of opioids whereas inhibition occurred at micromolar concentrations.
G-protein-independent modulation of P-type calcium channels by μ-opioids in Purkinje neurons of rat
2010, Neuroscience LettersDifferent stimulatory opioid effects on intracellular Ca<sup>2+</sup> in SH-SY5Y cells
2000, Brain ResearchCitation Excerpt :However, from the middle of the 1970s, experiments began to show opioid might also take excitatory roles as well. For example, opiate were found to increase cAMP production [8,25], to enhance both L- and N-typed VOC channel [7,20], to elevate [Ca2+]i in NG108-15 cells (either through mobilization of Ca2+ store or through membrane depolarization) [10,11,30,36], to prolong action potential duration of DRG neuron [3,27–29], and finally to enhance transmitter release from SK-N-SH and NMB cells [15,16,23]. Some of the stimulatory effects are pertussis toxin (PTX) sensitive while others are cholera toxin (CTX) sensitive [3,28,29].
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2003, Journal of Bioenergetics and Biomembranes