Oxidation induces autonomous activation of protein kinase C Apl I, but not protein kinase C Apl II in homogenates of Aplysia neurons.
The Ca(2+)-independent protein kinase C (PKC) Apl II, but not the Ca(2+)-activated PKC Apl I, becomes autonomously active during intermediate periods of facilitation in Aplysia neurons. We examined the ability of superoxide formed by the enzymatic reaction of xanthine with xanthine oxidase (X/XO) to induce autonomous activity of PKCs in Aplysia. X/XO stimulated autonomous PKC activity in Aplysia nervous system homogenates, but this activity resulted solely from activation of PKC Apl I. PKC Apl I is also more sensitive to activation by X/XO when expressed in insect cells. Our results suggest that oxidation can autonomously activate PKC Apl I in the Aplysia nervous system, but that the activation of PKC Apl II during synaptic facilitation is not due to oxidation of the enzyme.
Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Room 776, 3801 University Street, Montreal, Quebec H3A 2B4, Canada.
Nawal
N
Zabouri
Wayne S
WS
Sossin
D000818:Animals; D001048:Aplysia; D003213:Conditioning, Psychological / Q000502:physiology; D007527:Isoenzymes / Q000378:metabolism*; D008568:Memory / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000201:enzymology*; D010084:Oxidation-Reduction; D011493:Protein Kinase C / Q000378:metabolism*; D013481:Superoxides / Q000378:metabolism
D007527:Isoenzymes; D013481:Superoxides; D011493:Protein Kinase C