Neuroscience 2005 Abstract
| Presentation Number: | 1001.8 |
|---|---|
| Abstract Title: | The melanocortin ACTH modulates an electric communication signal by modulating the waveform and timing of action potentials in individual cells. |
| Authors: |
Markham, M. R.*1
; Stoddard, P. K.1
1Dept Biological Sciences, Florida International Univ., Miami, FL |
| Primary Theme and Topics |
Cognition and Behavior - Neuroethology -- Vocal/social communication |
| Secondary Theme and Topics | Neural Excitability, Synapses, and Glia: Cellular Mechanisms<br />- Intrinsic Membrane Properties<br />-- Modulation of neuronal firing properties |
| Session: |
1001. Vocal/Social Communication: Fish and Amphibians Poster |
| Presentation Time: | Wednesday, November 16, 2005 4:00 PM-5:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # NN17 |
| Keywords: | PLASTICITY, EXCITABILITY, ION CHANNEL, NEUROENDOCRINE |
The electric organ discharge (EOD) of gymnotiform electric fish is produced by the simultaneous electric discharges of individual electrocytes (μEODs). In the gymnotiform Brachyhypopomus pinnicaudatus, the EOD and its constituent μEODs are biphasic sinusoids. The biphasic μEOD is produced by the sequential action potentials of the electrocyte’s two excitable membranes. The first action potential (AP1) occurs on the electrocyte’s posterior membrane, and contributes to the positive first phase (P1) of the μEOD. The second action potential (AP2) occurs on the electrocyte’s anterior membrane, producing the negative second phase (P2) of the μEOD. Masculine EODs show greater overall amplitude and greater repolarization time of P2 (tau-P2). In males, the masculinity of the waveform is enhanced on a circadian rhythm, and within minutes in response to stressors and changes in the social environment thus altering the signal’s communication function.
We reported previously (SFN 2004) that in vivo intramuscular injections of the melanocortin peptide adrenocorticotropic hormone (ACTH) increase EOD amplitude and tau-P2 over the course of an hour. Applied to single electrocytes in vitro, ACTH rapidly increases μEOD amplitude and tau-P2. Here we find that ACTH increases P1- and P2-amplitude although he amplitudes of AP1 and AP2 are unchanged. The increase in P1 amplitude results instead from increased AP1-AP2 delay, while increased P2 amplitude and tau-P2 result from a pronounced broadening of only the AP2 spike. Thus, ACTH rapidly increases μEOD amplitude and duration by differentially modulating the spike waveform of the electrocyte’s two excitable membranes, and by changing the timing of these two spikes. Melanocortin peptides appear to serve as the mechanism that couples socially- and stress-regulated brain pathways to unique changes in the intrinsic excitability and spike waveform of excitable membranes in peripheral cells involved in communication.
We reported previously (SFN 2004) that in vivo intramuscular injections of the melanocortin peptide adrenocorticotropic hormone (ACTH) increase EOD amplitude and tau-P2 over the course of an hour. Applied to single electrocytes in vitro, ACTH rapidly increases μEOD amplitude and tau-P2. Here we find that ACTH increases P1- and P2-amplitude although he amplitudes of AP1 and AP2 are unchanged. The increase in P1 amplitude results instead from increased AP1-AP2 delay, while increased P2 amplitude and tau-P2 result from a pronounced broadening of only the AP2 spike. Thus, ACTH rapidly increases μEOD amplitude and duration by differentially modulating the spike waveform of the electrocyte’s two excitable membranes, and by changing the timing of these two spikes. Melanocortin peptides appear to serve as the mechanism that couples socially- and stress-regulated brain pathways to unique changes in the intrinsic excitability and spike waveform of excitable membranes in peripheral cells involved in communication.
Supported by NIMH 1K01MH064550 / NIH S06-GM08205
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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