Signal Transduction, Plasma Membrane Calcium Movements, and Pigment Translocation in Freshwater Shrimp Chromatophores

Author(s)

Milograna, Sarah Ribeiro ; Bell, Fernanda Tinti ; McNamara, John Campbell

• Document type: Journal article
• Source: JOURNAL OF EXPERIMENTAL ZOOLOGY PART A-ECOLOGICAL AND INTEGRATIVE PHYSIOLOGY; v. 313A, n. 9, p. 13-pg., 2010-11-01.

Abstract

Crustacean color change results from the differential translocation of chromatophore pigments, regulated by neurosecretory peptides like red pigment concentrating hormone (RPCH) that, in the red ovarian chromatophores of the freshwater shrimp Macrobrachium olfersi, triggers pigment aggregation via increased cytosolic cGMP and Ca2+ of both smooth endoplasmatic reticulum (SER) and extracellular origin. However, Ca2+ movements during RPCH signaling and the mechanisms that regulate intracellular [Ca2+] are enigmatic. We investigate Ca2+ transporters in the chromatophore plasma membrane and Ca2+ movements that occur during RPCH signal transduction. Inhibition of the plasma membrane Ca2+-ATPase by La3+ and indirect inhibition of the Na+/Ca2+ exchanger by ouabain induce pigment aggregation, revealing a role for both in Ca2+ extrusion. Ca2+ channel blockade by La3+ or Cd2+ strongly inhibits slow-phase RPCH-triggered aggregation during which pigments disperse spontaneously. L-type Ca2+ channel blockade by gabapentin markedly reduces rapid-phase translocation velocity; N- or P/Q-type blockade by omega-conotoxin MVIIC strongly inhibits RPCH-triggered aggregation and reduces velocity, effects revealing RPCH-signaled influx of extracellular Ca2+. Plasma membrane depolarization, induced by increasing external K+ from 5 to 50 mM, produces Ca2+-dependent pigment aggregation, whereas removal of K+ from the perfusate causes pigment hyperdispersion, disclosing a clear correlation between membrane depolarization and pigment aggregation; K+ channel blockade by Ba2+ also partially inhibits RPCH action. We suggest that, during RPCH signal transduction, Ca2+ released from the SER, together with K+ channel closure, causes chromatophore membrane depolarization, leading to the opening of predominantly N- and/or P/Q-type voltage-gated Ca2+ channels, and a Ca2+/cGMP cascade, resulting in pigment aggregation. J. Exp. Zool. 313A:605-617, 2010. (C) 2010 Wiley-Liss, Inc. (AU)