Pitutary adenylate cyclase-activating polypeptide (PACAP) and nerve growth factor (NGF) have been shown to promote neurite outgrowth and inhibit proliferation of rat pheochroocytoma (PC12) cells. PACAP- and NGF-mediated neuritogenesis is related to the activation of variety of downstream processes involving stimulation of specific kinases and kinases-dependent pathways. PACAP and NGF regulate common and distinct mechanisms to control PC12 cell differentiation suggesting their complementary role. The activity of plasma membrane calcium pump (PMCA) controls the intracellular Ca²⁺ and its role is prominent in neurite outgrowth. PMCA exists in 4 isoforms, with various distribution among tissues from neuron-specific PMCA2 and 3 to PMCA1 and 4 broadly distributed in nearly all tissues. Our previous research showed that neuronal differentiation of PC12 may be induced by signals other than extracellular. The neuron-specific isoforms mRNA’s antisense treatment affected the basal level of Ca²⁺, generating the metamorphosis of PC12 into pseudo-neuronal phenotype. The level of Ca²⁺ in cell lines carrying desired antisense was increased, as detected previously. The aim of this study was to examine the activity changes of p38 MAPK, ERK1/2 and JNK under the condition of altered calcium homeostasis generated by specific blocking of PMCA2, PMCA3 or both isoforms expression. We observed differences in the activity of examined kinases as well as alteration in kinases-dependent pathways. This may suggest that increase in Ca²⁺ level can serve as a switcher of kinases activity in a different manner than under calcium homeostasis. In the absence of upstream signals the regulation of kinases activity may also be altered, however this requires further study.

Supported by the grants No: PBZ-MIN-012/P04/2004 and 2/P05A/03529 from the Ministry of Education and Science, and 503-6086-02 from the Medical University of Lodz.

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