Co-activation of PKA and PKC in cerebrocortical nerve terminals synergistically facilitates glutamate release
作者： Carmelo Millán , Magdalena Torres , José Sánchez-Prieto
DOI: 10.1046/J.1471-4159.2003.02065.X
关键词:
摘要: Protein kinase A and protein kinase C are involved in processes that enhance glutamate release at glutamatergic nerve terminals. However, it is not known whether these two kinases co-exist within the same terminal, nor clear what impact their simultaneous activation may have on neurotransmitter release. In cerebrocortical terminals, co-application of forskolin, which increases cAMP levels activates kinase A, 4β-phorbol dibutyrate, a direct activator kinase C, synergistically enhanced spontaneous glutamate. This enhancement exhibited both tetrodotoxin-sensitive tetrodotoxin-resistant components. Interestingly, component was observed when cyclic AMP-dependent kinase (PKA) calcium- phospholipid-dependent (PKC) were activated separately, but developed slowly after co-activation kinases, accounting for 50% facilitated dependent voltage-dependent Ca2+ channels opened spontaneously PKA PKC occurred absence Na+ channel firing. These data provide functional evidence co-existence PKA- PKC-signalling pathways subpopulation
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