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Autaptic excitation contributes to bistability and rhythmicity in the neural circuit for feeding in Aplysia

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POSTER PRESENTATION

Open Access

Autaptic excitation contributes to bistability and

rhythmicity in the neural circuit for feeding

in

Aplysia

Douglas A Baxter

1*

, Enrico Cataldo

2

, John H Byrne

1

From Nineteenth Annual Computational Neuroscience Meeting: CNS*2010

San Antonio, TX, USA. 24-30 July 2010

The feeding circuit in

Aplysia is a useful model system

for studying the neuronal bases of cognitive functions

such as sensory processing, generation of behavior,

motivation, decision making, learning, and memory

[1,2]. The goals of the present study are to develop a

biologically-realistic model of the feeding circuit and to

investigate the ways in which component processes

con-tribute to circuit function. To begin, we developed a

model of the central pattern generator (CPG) that

mediates rhythmicity in the feeding circuit (Fig. 1A).

Simulations indicated that two positive-feedback loops

(the B31 autapse and the synaptic interactions between

B31 and B63) introduced bistability into the membrane

potential of the B31 soma (Figures 1B, 1C1). In addition,

simulations indicated that this plateau-like potential was

the

‘deciding factor’ for initiating rhythmic activity (Fig.

1C). Simulations also helped identify features of the

model that warrant further empirical investigation; e.g.,

* Correspondence: [email protected]

1Department of Neurobiology and Anatomy, The University of Texas Medical

School at Houston, Houston, TX 77030, USA

Figure 1 Bistability and rhythmicity in the feeding circuit. A: Circuit diagram of the feeding CPG. We expanded our previous ten-cell model [3] by representing B31 and B63 with two-compartments (soma and axon compartments), incorporating a modulatory synapse from B63 to B31, and implementing an autapse in B31 (new elements in red). See Panel B for additional details. The circuit was implemented in SNNAP [4]. Cellular and synaptic properties matched empirical data. Fill colors indicate cells that fire in phase. B: Hurwitz et al. [5] characterized and modeled membrane currents in the nonspiking soma of B31. We expanded that model by including a second-messenger system, which activated an inward current (new elements in red). C1: A 1-s depolarization of B63 (not shown) elicited a plateau-like potential in B31, which drove rhythmic activity (e.g., bursting in B64). C2: Without the autapse, B31 failed to manifest a plateau-like potential and rhythmic activity was blocked.

Baxteret al. BMC Neuroscience 2010, 11(Suppl 1):P58 http://www.biomedcentral.com/1471-2202/11/S1/P58

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the simulated amplitude of the plateau-like potential was

less than empirical observations.

Acknowledgements

This work was supported by NIH grant P01 NS038310. Author details

1

Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, TX 77030, USA.2Department of Biology,

General Physiology Unit, University of Pisa, Italy. Published: 20 July 2010

References

1. Baxter DA, Byrne JH: Feeding behavior ofAplysia: a model system for comparing cellular mechanisms of classical and operant conditioning. Learn Mem 2006, 13:669-680.

2. Cropper EC, Evans CG, Hurwitz I, Jing J, Proekt A, Romero A, Rosen SC: Feeding neural networks in the -molluscAplysia. Neurosignals 2004, 13(z):70-86.

3. Cataldo E, Byrne JH, Baxter DA: Computational model of a central pattern generator. Lec Not Comput Sci 2006, 4210:242-256.

4. Baxter DA, Byrne JH: Simulator for neural networks and action potentials. Methods Mol Biol 2007, 401:127-154, (SNNAP is available at http://www. snnap.uth.tmc.edu).

5. Hurwitz I, Ophir A, Korngreen A, Koester J, Susswein AJ: Currents contributing to decision making in neurons B31/32 ofAplysia. J Neurophysiol 2008, 99:814-830.

doi:10.1186/1471-2202-11-S1-P58

Cite this article as: Baxter et al.: Autaptic excitation contributes to bistability and rhythmicity in the neural circuit for feeding inAplysia. BMC Neuroscience 2010 11(Suppl 1):P58.

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Baxteret al. BMC Neuroscience 2010, 11(Suppl 1):P58 http://www.biomedcentral.com/1471-2202/11/S1/P58

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