The functional role of burst firing (i.e. the firing of packets of action potentials followed by quiescence) in sensory processing is still under debate. Should bursts be considered as unitary events that signal the presence of a particular feature in the sensory environment or is information about stimulus attributes contained within their temporal structure? We compared the coding of stimulus attributes by bursts in vivo and in vitro of electrosensory pyramidal neurons in weakly electric fish by computing correlations between burst and stimulus attributes. Our results show that, while these correlations were strong in magnitude and significant in vitro, they were actually much weaker in magnitude if at all significant in vivo. We used a mathematical model of pyramidal neuron activity in vivo and showed that such a model could reproduce the correlations seen in vitro, thereby suggesting that differences in burst coding were not due to differences in bursting seen in vivo and in vitro. We next tested whether variability in the baseline (i.e. without stimulation) activity of ELL pyramidal neurons could account for these differences. To do so, we injected noise into our model whose intensity was calibrated to mimic baseline activity variability as quantified by the coefficient of variation. We found that this noise caused significant decreases in the magnitude of correlations between burst and stimulus attributes and could account for differences between in vitro and in vivo conditions. We then tested this prediction experimentally by directly injecting noise in vitro through the recording electrode. Our results show that this caused a lowering in magnitude of the correlations between burst and stimulus attributes in vitro and gave rise to values that were quantitatively similar to those seen under in vivo conditions.While it is expected that noise in the form of baseline activity variability will lower correlations between burst and stimulus attributes, our results show that such variability can account for differences seen in vivo. Thus, the high variability seen under in vivo conditions has profound consequences on the coding of information by bursts in ELL pyramidal neurons. In particular, our results support the viewpoint that bursts serve as a detector of particular stimulus features but do not carry detailed information about such features in their structure.
Many neurons display intrinsic interspike interval correlations in their spike trains. However, the effects of such correlations on information transmission in neural populations are not well understood. We quantified signal processing using linear response theory supported by numerical simulations in networks composed of two different models: One model generates a renewal process where interspike intervals are not correlated while the other generates a nonrenewal process where subsequent interspike intervals are negatively correlated. Our results show that the fractional rate of increase in information rate as a function of network size and stimulus intensity is lower for the nonrenewal model than for the renewal one. We show that this is mostly due to the lower amount of effective noise in the nonrenewal model. We also show the surprising result that coupling has opposite effects in renewal and nonrenewal networks: Excitatory (inhibitory coupling) will decrease (increase) the information rate in renewal networks while inhibitory (excitatory coupling) will decrease (increase) the information rate in nonrenewal networks. We discuss these results and their applicability to other classes of excitable systems.
Abstract. The interplay between intrinsic and network dynamics has been the focus of many investigations. Here we use a combination of theoretical and numerical approaches to study the effects of delayed global feedback on the information transmission properties of neural networks. Specifically, we compare networks of neurons that display intrinsic interspike interval correlations (nonrenewal) to networks that do not (renewal). We find that excitatory and inhibitory delays can tune information transmission by single neurons but not by the entire network. Most surprisingly, addition of a delay can change the dependence of the information on the coupling strength for renewal neurons and not for nonrenewal neurons. Our results show that intrinsic ISI correlations can have nontrivial interactions with network-induced phenomena.
Understanding how sensory information is encoded by populations of neurons is complicated by the fact that neurons display variability in their responses to repeated presentations of the same stimulus. A further complication comes from the fact that these variabilities can be correlated. In fact, the role of correlations in neural variabilities (noise correlations) has been the focus of much debate in recent years as even a small amount of correlation between a pair of neurons can have dramatic effects on information transmission by neural populations [1]. Recent experimental evidence has shown that burst firing can modulate the amount of noise correlations displayed by neural populations [2]. Here we investigate the role of intrinsic bursting dynamics in model neurons receiving correlated input. These model neurons transition from a tonic firing regime to a bursting regime as the amount of depolarizing current is varied. We find that, given an input correlation c, the output correlation R between neural pairs in the network is less when both neurons are in bursting regime than when they are in the tonic regime. Our theoretical results are supported by experimental results obtained from a slice preparation. We show that intrinsic burst dynamics can decorrelate neural populations and therefore regulate their information transmission properties.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.