Extracellular receptor kinase and cAMP response element binding protein activation in the neonatal rat heart after perinatal cocaine exposure.

Prenatal exposure to cocaine has been shown to induce an increase in the myocardial expression and activation of the cAMP response binding protein (CREB), a transcriptional factor that has been shown to regulate gene expression. Several different kinases, including protein kinase A, calcium calmodulin kinase II, and mitogen-activated protein kinase can induce phosphorylation of CREB at serine 133, a necessary step for CREB activation. We examined whether the mitogen-activated protein kinase-extracellular receptor kinase (ERK) pathway may be involved in mediating the serine 133 CREB phosphorylation in cardiac nuclei after perinatal cocaine exposure.

Cardiac memory is associated with decreased levels of the transcriptional factor CREB modulated by angiotensin II and calcium.

Cardiac memory (CM) has short- (STCM) and long-term (LTCM) components modulated by calcium and angiotensin II. LTCM is associated with reduced Ito and Kv4.3 mRNA levels.

Perinatal cocaine exposure stimulates the expression and activation of CREB in the neonatal rat heart.

cAMP response binding protein (CREB) is a transcriptional factor known to regulate gene expression. Phosphorylation of CREB at serine 133 is necessary for CREB activation, and quantification of phospho-CREB (p-CREB) expression is an index of CREB activation. Because CREB expression and activation in specific brain regions are modified after chronic cocaine administration, we sought to determine whether chronic perinatal cocaine exposure affects the expression of CREB and p-CREB in the postnatal rat heart.