HORMONAL MODULATION OF A COMMUNICATION SIGNAL

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In communication systems it is important for the signal and receiver to be matched in the frequency domain to maximize information transfer. Thus, the frequency sensitivity of a species' sensory systems are often matched to the spectrum of that species' communication signal. Nevertheless, little is known about the developmental mechanisms by which output and sensory structures come to be matched or whether they have any capacity for plasticity in mature animals. The match between signal and receiver are extremely precise in those animals that have "active" sensory systems like echolocating bats and electrolocating weakly electric fish. Weakly electric fish are intriguing because the frequency sensitivity of the sensory receptors and the frequency output of the emitter, the electric organ, are not only well matched but both effector and receptor pathways show hormone-mediated plasticity. of prime interest is how the ion currents of the cells in this communication pathway are modulated by hormones. In this proposal we concentrate on hormone induced plasticity of the emitter, the electric organ, where our preliminary data suggest that, variation in and plasticity of a Na+ current is the major determinant of the waveshape properties of its output and the locus of hormone-mediated plasticity. In this proposal we wish to 1) measure additional properties of the Na+ currents (i.e.--I-V curves, steady state inactivation, recovery from inactivation, dissociation constants for TTX and mu conotoxin) to determine if other parameters also vary with electrocyte (a single electric organ cell) spike duration 2) determine whether the kinetics of the delayed rectifying K+ current in electrocytes from fish with a range of EOD frequencies also show individual variation 3) record Na+ currents and K+ currents before and after fish have been treated with androgens or gonadotropin to determine whether the kinetics of these currents can be altered by these hormones 4) determine whether Na+ current kinetics are altered by treatment of the electrocytes with agents that induce phosphorylation of the Na+ channel in other preparations.