Reversible caging of Zn2+

INOR 614

H. M. Dhammika Bandara, h.bandara@uconn.edu and Shawn C. Burdette, shawn.burdette@uconn.edu. Department of Chemistry, University of Connecticut, 55, North Eagleville Road, Storrs, CT 06269
Zinc is known to be present in pre-synaptic vesicles of certain neurons of the central nervous system and is believed to play a vital role in neurotransmission. During neurotransmission, Zn2+ is released in to the synaptic cleft along with other neurotransmitters and is believed to modulate the action of neurotransmitter-receptors on the post-synaptic membrane. There is evidence that Zn2+ also causes the release of Ca2+ in receptor neurons, thereby acting as an ionic signal between neurons. Many proposed Zn2+ signaling pathways involve sinusoidal fluctuations in the concentration of the metal ion. Reversible uncaging of Zn2+ will allow these processes to be mimicked. In reversible uncaging, the release of Zn2+ is brought about by a reversible process such as the cis-trans photoisomerization of an azobenzene. We have synthesized and characterized several compounds that may reversibly cage Zn2+. At present we are investigating their metal binding properties.