Conditional Spike Backpropagation Generates Burst Discharge in a Sensory Neuron

Lemon, Neal; Turner, Ray W.

doi:10.1152/jn.2000.84.3.1519

Cited by 90 publications

(128 citation statements)

References 61 publications

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“…Indeed, bursting in ELL pyramidal neurons is intrinsic and relies on a somatodendritic interaction (Turner et al 1994;Lemon and Turner 2000). Somatic action potentials back-propagate into the proximal apical dendrites where they trigger a dendritic spike that propagates back to the soma, leading to a depolarizing afterpotential (DAP) and promotes the firing of another somatic action potential.…”

Section: Modeling Differences In Burst Coding Seen In Vitro and In Vivomentioning

confidence: 99%

“…Somatic action potentials back-propagate into the proximal apical dendrites where they trigger a dendritic spike that propagates back to the soma, leading to a depolarizing afterpotential (DAP) and promotes the firing of another somatic action potential. This DAP grows in size throughout the burst, which leads to a progressive depolarization and a shortening of the inter-spike interval (ISI) throughout the burst (Lemon and Turner 2000). The burst terminates with a characteristic doublet when the ISI becomes shorter than the dendritic refractory period (Noonan et al 2003), which leads to dendritic failure characterized by the absence of a dendritic spike and terminates the burst.…”

Section: Modeling Differences In Burst Coding Seen In Vitro and In Vivomentioning

confidence: 99%

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In vivo conditions influence the coding of stimulus features by bursts of action potentials

Akerberg

Chacron

2011

J Comput Neurosci

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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.

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Section: Modeling Differences In Burst Coding Seen In Vitro and In Vivomentioning

confidence: 99%

Section: Modeling Differences In Burst Coding Seen In Vitro and In Vivomentioning

confidence: 99%

In vivo conditions influence the coding of stimulus features by bursts of action potentials

Akerberg

Chacron

2011

J Comput Neurosci

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“…Pyramidal cells have a well-characterized intrinsic burst mechanism that relies on a somatodendritic interaction (Fernandez et al, 2005b;Lemon and Turner, 2000). Burst firing is driven by a depolarizing afterpotential (DAP) generated by current flowing back to the soma from actively back-propagating dendritic Na + spikes.…”

Section: Regulation Of Pyramidal Cell Burstingmentioning

confidence: 99%

Ionic and neuromodulatory regulation of burst discharge controls frequency tuning

Mehaffey

Ellis

Krahe

et al. 2008

Journal of Physiology-Paris

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Sensory neurons encode natural stimuli by changes in firing rate or by generating specific firing patterns, such as bursts. Many neural computations rely on the fact that neurons can be tuned to specific stimulus frequencies. It is thus important to understand the mechanisms underlying frequency tuning. In the electrosensory system of the weakly electric fish, Apteronotus leptorhynchus, the primary processing of behaviourally relevant sensory signals occurs in pyramidal neurons of the electrosensory lateral line lobe (ELL). These cells encode low frequency prey stimuli with bursts of spikes and high frequency communication signals with single spikes. We describe here how bursting in pyramidal neurons can be regulated by intrinsic conductances in a cell subtype specific fashion across the sensory maps found within the ELL, thereby regulating their frequency tuning. Further, the neuromodulatory regulation of such conductances within individual cells and the consequences to frequency tuning are highlighted. Such alterations in the tuning of the pyramidal neurons may allow weakly electric fish to preferentially select for certain stimuli under various behaviourally relevant circumstances.

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“…It has been shown that the DAP is generated within a few ms after an action potential is initiated. 22,23 The amplitude of the DAP is expressed either as percentage of the peak of the CAP amplitude or in absolute value (mV).…”

Section: Isolation Of Spinal Cordmentioning

confidence: 99%

Electrophysiological changes in isolated spinal cord white matter in response to oxygen deprivation

Pryor

Lee

2006

Spinal Cord

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Methods: The hypoxic injury was induced by reducing the oxygen tension of the perfused solution by 80%. Compound action potentials (CAPs) were monitored before, during, and after oxygen deprivation. Results: We have found that 60 min of hypoxia reduced the conduction to 30% of preinjury level and recovered to approximately 60% of the preinjury level upon reoxygenation. Larger axons appeared to be more vulnerable to oxygen deprivation. We noted a significant decrease and recovery of the depolarizing afterpotential (DAP). Likewise, there was a delay and recovery of absolute and relative refractory period. Concomitantly, the ability of axons to follow repetitive stimuli was suppressed following oxygen deprivation but recovered upon reoxygenation. Conclusion: Following 60 min of oxygen deprivation and 30 min of reoxygenation, mammalian spinal cord white matter can partially recover electrical impulse conduction. However, within the same period, cords gained a complete recovery of other electrical properties, such as the depression of DAP, the delaying of refractory period, and the decreased ability to respond to repetitive stimuli. Compared to previous findings when both oxygen and glucose were deprived, we conclude that glucose plays a relatively minor role during the acute stage of oxygen deprivation in mammalian spinal cord white matter.

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Conditional Spike Backpropagation Generates Burst Discharge in a Sensory Neuron

Cited by 90 publications

References 61 publications

In vivo conditions influence the coding of stimulus features by bursts of action potentials

In vivo conditions influence the coding of stimulus features by bursts of action potentials

Ionic and neuromodulatory regulation of burst discharge controls frequency tuning

Electrophysiological changes in isolated spinal cord white matter in response to oxygen deprivation

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