| Abstract No.: | A-D1152 |
| Country: | Canada |
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| Title: | FEEDBACK MODULATION OF FIRING DYNAMICS RESTORES FEATURE DETECTION IN ELECTROSENSORY PROCESSING |
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| Authors/Affiliations: | 1 W. Hamish Mehaffey*; 1 Ray W. Turner; 2 Louis-Philippe Bernier; 2 Gary Mo, 2 Ariel Ase, 2 Stephanie Chevallier, 2 Dominique Blais, 2 Xinkang Tong, 2 Edith Hamel, 2 Eric Boue-Grabot, 2 Philippe Seguela,
1 Hotchkiss Brain Institute, Calgary, AB, Canada; 2 McGill University, Montreal, QC, Canada
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| Content: | Objectives: Neurons are almost invariably embedded in complex feedback networks that can significantly change their firing behaviours. Here, we study the feedback regulation of individual neurons in the context of sensory coding in the electrosensory lobe (ELL) of weakly electric fish. This simple and well understood feedback network is known to be recruited under specific social conditions. Further, recent work has delineated the mechanism(s) by which bursting, and thus sensory coding with bursts, can be regulated in real time by synaptic inputs via this feedback network. By using a previous model of burst regulation in ELL pyramidal cells placed into a network context, we examined burst regulation in a more realistic model of sensory processing.
Materials and Methods: We use a computational approach to study the behaviour of a small network of neurons with known and thus realistic firing dynamics to gain a better understanding of possible behaviours of the network. We model a simple network based on the known neuroanatomical architecture underlying sensory processing in the ELL of Apteronotus leptorhynchus. This consists of a network of 100 biophysically plausible ELL neurons embedded in an inhibitory closed loop consisting of excitatory ELL pyramidal cell output and reciprocal and atopographical inhibitory feedback in the form of GABAA and GABAB mediated conductances.
Results: We have previously shown an interaction between the GABAB portion of inhibitory feedback and the burst dynamics intrinsic to ELL pyramidal cells. Briefly, sufficient dendritic inhibition is capable of delaying the timing of a dendritic spike and thereby causing a dramatically increased somatic excitability. By incorporating the intrinsic bursting dynamics into a network model we were able to replicate specific in vivo results relating to the regulation of bursting by this feedback network, and able to examine its regulation of sensory coding. The GABAA component of inhibition is able to create a network mediated oscillation which significantly deteriorates coding. We show that the GABAB inputs neither contribute to this oscillation nor ameliorate its deleterious consequences on stimulus encoding. Instead, the GABAB feedback component improves the ability of pyramidal cells to accurately detect specific low frequency components of stimulus features.
Conclusion: We have shown that distinct elements of a feedback pathway (e.g. GABAA, GABAB) are able to differentially regulate sensory processing in a network model of the ELL, and improve the detection of low frequency components of an input signals. As these stimuli are usually indicative of prey or environmental signals, this may represent a mechanism for improving the detection of prey-like stimuli in the presence of conspecifics.
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