Abstract
The classical mode of action of ecdysteroids (ES) is the receptor-mediated control of gene activity, influencing transcription, and, subsequently, protein synthesis. Most of these actions occur after a lag phase of 10 min or more, usually after several hours. During the last three decades evidence has accumulated that ES also operate independently of genomic action. The nongenomic effects have short latencies, sometimes in the range of a few seconds. This renders possible their semiochemical effects as pheromones and feeding deterrents. The favoured target sites of nongenomic ES effects are presumably plasma membrane associated proteins. ES interact with Na+-K+ATPase, carrier proteins, adenylyl cyclase, GABAA receptor channels, Na+-H+ exchangers, and K+ channels, having impact on ES transport, electrolyte transport (Na+, K+, H+, Ca++, Cl–) or on second messengers (cAMP, Ca++). A new concept of ES action includes both genomic and nongenomic pathways. Furthermore, it seems as if ES can act by both mechanisms simultaneously, modulating their own genomic effects by nongenomic actions.Arch. Insect Biochem. Physiol. 41:89–98, 1999. © 1999 Wiley-Liss, Inc.
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