Neuroscience 2003 Abstract
| Presentation Number: | 604.12 |
|---|---|
| Abstract Title: | Hormonal modulation of neuronal modulation. |
| Authors: |
Kirby, M. S.*1
; Nusbaum, M. P.1
1Dept. Neurosci, Univ. of Penn Sch. of Med, Phila, PA |
| Primary Theme and Topics |
Motor Systems - Pattern Generation and Locomotion |
| Secondary Theme and Topics | Motor Systems<br />- Invertebrate Motor Systems |
| Session: |
604. Pattern Generation: Small Circuits Poster |
| Presentation Time: | Tuesday, November 11, 2003 11:00 AM-12:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # H62 |
| Keywords: | Central Pattern Generator, Motor Control, Stomatogastric, Projection Neurons |
We are testing the hypothesis that peptide hormones modulate the actions of modulatory projection neurons onto rhythmic motor circuits both presynaptically (projection neuron level) and postsynaptically (circuit level). To this end, we are studying the influence of the hormone crustacean cardioactive peptide (CCAP) on the gastric mill (chewing) circuit in the stomatogastric ganglion (STG) of the crab Cancer borealis. In the crab, the STG is situated in the ophthalmic artery. CCAP is pumped into this artery from the heart to bathe the STG after it is released by the pericardial organs into the lumen of the heart. We showed previously that CCAP superfusion influences the actions of the projection neuron MCN1 (which does not contain CCAP) in several ways (Kirby and Nusbaum, SFN 2002). For example, during the MCN1-elicited gastric mill rhythm (GMR), CCAP (10-6–10-7M) increases the GMR cycle period (~20%) as well as the burst duration (~35%) and number of action potentials/burst (>50%) of the pattern generator neuron LG. Here we show that these CCAP effects persist at lower doses (10-8M, n=3 and 10-9M, n=3). For example, CCAP increases the GMR cycle period by 10-15% plus the LG burst duration by ~15% and the number of LG action potentials/burst by 15-25%. Focal application of CCAP [10-5M, 5psi, 0.5sec duration] to the STG during superfusion of reduced Ca2+ (0.1X)/added Mn2+ saline to block transmitter release excited a subset of gastric mill neurons, including the reciprocally inhibitory neurons (LG, Int1) that are the core of this pattern generator. The CCAP-excited neurons included LG (n=16/16), Int1 (n=2/4), MG (n=9/9) and AM (n=6/6). The other gastric mill circuit neurons, including GM (n=15/15) and DG (n=10/10), showed no response either at rest or when depolarized. CCAP appears to have no effect on MCN1 in either its ganglion of origin (n=7/8) or in the STG (n=2/2). We are continuing to study CCAP actions on this system, including how its actions modify the MCN1-elicited GMR.
Supported by NIH NS29436 (MPN), NSF DGE9616278 (MSK)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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