Neuroscience 2005 Abstract
| Presentation Number: | 752.21 |
|---|---|
| Abstract Title: | Sensory regulation of rhythmic motor activity via presynaptic inhibition. |
| Authors: |
DeLong, N. D.*1
; Nadim, F.2,3
; Nusbaum, M. P.1
1Dept Neurosci, Univ. of Pennsylvania School of Medicine, Phila, PA 2NJ, 215 Stemmlar Hall, 19104, 3USA, 215 Stemmlar Hall, 19104, |
| Primary Theme and Topics |
Sensory and Motor Systems - Pattern Generation and Locomotion -- Invertebrate pattern generation |
| Secondary Theme and Topics | Sensory and Motor Systems<br />- Invertebrate Sensory and Motor Systems<br />-- Invertebrate motor systems |
| Session: |
752. Invertebrate Pattern Generation II Poster |
| Presentation Time: | Tuesday, November 15, 2005 1:00 PM-2:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # DD25 |
| Keywords: | STOMATOGASTRIC, NETWORK, SENSORIMOTOR, CRUSTACEA |
We are elucidating a novel cellular mechanism underlying sensorimotor integration as part of our characterization of how the gastropyloric receptor (GPR), an identified proprioceptor neuron, influences the gastric mill (chewing) CPG in the stomatogastric ganglion of the crab Cancer borealis. We elicit the gastric mill rhythm by selective stimulation of MCN1, a projection neuron that excites the reciprocally inhibitory neurons (LG, Int1) that form the core of the gastric mill CPG (Bartos et al, J Neurosci 1999). Rhythmic GPR stimulation that mimics its in vivo activity pattern selectively prolongs the retractor (Int1 active; LG inactive) phase of the gastric mill rhythm. Our previous work suggested that this effect is likely mediated either by GPR excitation of Int1 or by its presynaptic inhibition of MCN1 (Beenhakker & Nusbaum, SFN Abstract 2004). We tested the ability of each of these two synaptic actions to selectively prolong the retractor phase by using both computational modeling (Nadim et al, J Neurosci 1998) and physiological manipulations that include Dynamic Clamp-introduced synaptic or ionic currents. We found that GPR excitation of Int1 is theoretically and functionally unable to selectively regulate the retractor phase. Instead, its manipulation coordinately changes the duration of both phases of the rhythm. Conversely, GPR regulation of MCN1 transmitter release via presynaptic inhibition accurately replicates the GPR actions on the gastric mill rhythm in both our model and our Dynamic Clamp experiments. The increased duration of the retractor phase results from the reduced (but not eliminated) MCN1 excitation of LG, which slows the LG escape from Int1 inhibition. Thus, the presynaptic inhibition of MCN1 appears to be responsible for the selective regulation of the gastric mill retractor phase by GPR. The function of the GPR excitation of Int1 is instead to ensure maintenance of the retractor phase by replacing the reduced level of excitation from MCN1 to Int1.
Supported by NIH NS42813 (MPN)
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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