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[P154]: Characterization of neurogenin 2 ‐regulated transcriptional cascades in the telencephalon
Author(s) -
Mattar P.,
Langevin L.M.,
Klenin N.,
Schuurmans C.
Publication year - 2006
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2006.09.214
Subject(s) - citation , library science , sociology , computer science
opment. We show here that the B2R is differentially expressed during neuronal differentiation of P19 cells, an in vitro model for early neuronal development. Steady state levels of B2R mRNA and protein expression are modulated along the differentiation of embryonal P19 cells to neurons. Following induction to differentiation by retinoic acid, the cells start expressing neuron-specific proteins, reaching highest levels after 7–9 days. At this stage, P19 neurons develop functional synapses and express neurotransmitter receptors. Measurement of [Ca]i in the absence and presence of bradykinin showed that most undifferentiated cells are unresponsive to bradykinin application, but following differentiation, P19 cells express high molecular weight neurofilaments, and respond to bradykinin application with a transient increase in [Ca]i. Induction of gene expression of high molecular weight cininogens in P19 cells and increasing secretion of bradykinin into the culture medium, reaching maximal levels at day 7, suggests the presence of an autocrine loop between bradykinin and its receptor. Specific inhibition of B2R activity by the antagonist HOE-140 on day 5 results in a reduction of the Ca-response to the acetylcholine receptor agonist carbamoylcholine and decreased gene expression levels of M1-M3 muscarinic receptors on day 8, implicating that B2R action is necessary for development of functional synapses during final neuronal maturation (Martins et al., 2005). Despite of the presence of the kinin-B1 agonist des-Argbradykinin together with other metabolites of bradykinin degradation, bradykinin-1–7 and bradykinin-1–5 in the culture medium, there was no evidence for participation of the kinin-B1 receptor in the process of final in vitro-neuronal differentiation of P19 cells.