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Gene Expression Profiling of Rat Brain Neurons Reveals Angiotensin II-Induced Regulation of Calmodulin and Synapsin I: Possible Role in Neuromodulation¹

Department of Physiology, College of Medicine, and McKnight Brain Institute, University of Florida, Gainesville, Florida 32610

Address all correspondence and requests for reprints to: Colin Sumners, Ph.D., Department of Physiology, University of Florida, P.O. Box 100274, 1600 SW Archer Road, Gainesville, Florida 32610. E-mail: csumners{at}phys.med.ufl.edu

Angiotensin (Ang II) activates neuronal AT₁ receptors located in the hypothalamus and the brainstem and stimulates noradrenergic neurons that are involved in the control of blood pressure and fluid intake. In this study we used complementary DNA microarrays for high throughput gene expression profiling to reveal unique genes that are linked to the neuromodulatory actions of Ang II in neuronal cultures from newborn rat hypothalamus and brainstem. Of several genes that were regulated, we focused on calmodulin and synapsin I. Ang II (100 nM; 1–24 h) elicited respective increases and decreases in the levels of calmodulin and synapsin I messenger RNAs, effects mediated by AT₁ receptors. This was associated with similar changes in calmodulin and synapsin protein expression. The actions of Ang II on calmodulin expression involve an intracellular pathway that includes activation of phospholipase C, increased intracellular calcium, and stimulation of protein kinase C. Taken together with studies that link calmodulin and synapsin I to axonal transport and exocytotic processes, the data suggest that Ang II regulates these two proteins via a Ca²⁺-dependent pathway, and that this may contribute to longer term or slower neuromodulatory actions of this peptide.

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