Cyclic AMP-dependent modulation of N- and Q-type Ca2+ channels expressed in Xenopus oocytes

Melatonin‐mediated inhibition of Purkinje neuron P‐type Ca2+ channels in vitro induces neuronal hyperexcitability through the phosphatidylinositol 3‐kinase‐dependent protein kinase C delta pathway

“…Similarly, in vestibular afferent neurons, μ ‐opioid receptor‐mediated decreases in I Ba were prevented by the application of PKA inhibitors . By contrast, PKA‐dependent stimulation of P/Q‐type channels has been observed in Xenopus oocytes expressing Cav2.1 . However, in the present study, we found that the inhibitory effect of melatonin on I Ba was PKA independent, which suggests that other non‐cAMP/PKA‐dependent mechanisms are involved in melatonin‐induced I Ba responses.…”

Ghrelin suppresses Purkinje neuron P-type Ca2+ channels via growth hormone secretagogue type 1a receptor, the βγ subunits of Go-protein, and protein kinase A pathway

“…By contrast, in acutely isolated rat basolateral amygdala neurons, pharmacologically isolated P-type channels are potentiated by forskolin, which elevates cAMP to activate PKA [46]. In addition, similar PKA-dependent stimulation of P/Q-type channels has been observed by Fukuda et al [47] in Xenopus oocytes expressing Cav2.1. Although it remains a topic for further investigation, these results together suggest that the PKAregulatory effects on P-type channels can be variable in different tissues expressing P-type channels that are functionally coupled to different Gprotein coupled receptors.…”

Inhibition of Ca2+ channel current by μ‐ and κ‐opioid receptors coexpressed in Xenopus oocytes: desensitization dependence on Ca2+ channel α1 subunits

“…Although second messenger‐regulated protein kinases are thought to be involved in the heterologous desensitization (Huganir & Greengard, 1990), no apparent effects of the agents that alter the phosphorylation state of cellular proteins were observed either on the desensitization of κ‐response during a 10 min or 2 h exposure, or on the initial inhibition by the κ‐agonist. These treatments have been shown to affect other signalling pathways in Xenopus oocytes (Kato et al , 1988; Ito et al , 1988; Kaneko et al , 1994b; Fukuda et al , 1996). Even if the effectiveness of the treatments on the various phosphorylation events is not complete, our results indicate that the heterologous component of μ‐ and κ‐receptor desensitization is resistant to changes in intracellular second messengers and protein kinases.…”

“…Plasmids pSPCBI‐2 (Mori et al , 1991) and pKCRB3 (Fujita et al , 1993) were provided by Dr Y. Mori (National Institute for Physiology, Okazaki, Japan). RNAs for opioid receptors and Ca 2+ channel subunits were synthesized by in vitro transcription by use the recombinant plasmids pSPCBI‐2 (rabbit P/Q‐type, α 1A ), pKCRB3 (rabbit N‐type, α 1B ), pHCaB (human β 2 ; Fukuda et al , 1996), pKOPR (rat κ‐opioid receptor; Minami et al , 1993), and pMOPR (rat μ‐opioid receptor; Minami et al , 1994). Oocytes of Xenopus laevis were defolliculated by collagenase and injected with 50 nl of RNA solution including N‐ or Q‐type α 1 subunit (2.5 ng), β subunit (2.5 ng), and μ‐and/or κ‐opioid receptor (2 ng for μ‐receptor, 4 ng for κ‐receptor).…”