Burst firing in sensory systems

Krahe, Rüdiger; Gabbiani, Fabrizio

doi:10.1038/nrn1296

Cited by 421 publications

(363 citation statements)

References 119 publications

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“…Delayed feedback-It is well known that neurons in cortical areas of the nervous system are the target of massive descending projections (Cajal 1909;Hollander 1970;Ostapoff et al 1990;Maler et al 1991;Guillery 2002, 2006) and that such pathways can give rise to interesting dynamics such as bursting (Krahe and Gabbiani 2004;Chacron and Bastian 2008;Toporikova and Chacron 2009;). In particular, Doiron et al (2003) showed that neurons with intrinsic renewal spike train statistics could display nonrenewal spike train statistics simply by introducing coupling between them through global delayed inhibitory feedback.…”

Section: Mechanisms That Give Rise To a Single Negative Isi Correlatimentioning

confidence: 99%

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Ávila-Ǻkerberg

Chacron

2011

Exp Brain Res

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Many neurons display significant patterning in their spike trains (e.g. oscillations, bursting), and there is accumulating evidence that information is contained in these patterns. In many cases, this patterning is caused by intrinsic mechanisms rather than external signals. In this review, we focus on spiking activity that displays nonrenewal statistics (i.e. memory that persists from one firing to the next). Such statistics are seen in both peripheral and central neurons and appear to be ubiquitous in the CNS. We review the principal mechanisms that can give rise to nonrenewal spike train statistics. These are separated into intrinsic mechanisms such as relative refractoriness and network mechanisms such as coupling with delayed inhibitory feedback. Next, we focus on the functional roles for nonrenewal spike train statistics. These can either increase or decrease information transmission. We also focus on how such statistics can give rise to an optimal integration timescale at which spike train variability is minimal and how this might be exploited by sensory systems to maximize the detection of weak signals. We finish by pointing out some interesting future directions for research in this area. In particular, we explore the interesting possibility that synaptic dynamics might be matched with the nonrenewal spiking statistics of presynaptic spike trains in order to further improve information transmission.

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Section: Mechanisms That Give Rise To a Single Negative Isi Correlatimentioning

confidence: 99%

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Ávila-Ǻkerberg

Chacron

2011

Exp Brain Res

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“…Neuronal burst firing is thought to play an important role in information processing by enhancing synaptic transmission via increased neurotransmitter release and synaptic plasticity. Furthermore, it is hypothesized that information conveyed by bursts is qualitatively different from that of single spike firing (Cooper, 2002), such that certain burst firing parameters may mediate selective communication between neurons (Krahe and Gabbiani, 2004). Burst firing in mPFC is diminished by systemic administration of NMDA receptor antagonists, drugs which also disrupt working memory (Homayoun et al, 2005;Jackson et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Burst firing in mPFC is diminished by systemic administration of NMDA receptor antagonists, drugs which also disrupt working memory (Homayoun et al, 2005;Jackson et al, 2004). Given that NMDA receptor hypofunction and FG-7142 treatment have similar effects on mPFC bursting and working memory (Birnbaum et al, 1999;Murphy et al, 1996), burst firing in mPFC may play a critical role in mediating cognitive functions such as attention and vigilance (Krahe and Gabbiani, 2004). Similarly, amygdaloid bursts occur in response to affectively relevant stimuli (Nishijo et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

Stevenson

Halliday

Marsden

et al. 2007

Synapse

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The medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) coordinate various stress responses. Although the effects of stressors on mPFC and BLA activity have been previously examined, it remains unclear to what extent stressors affect functional interactions between these regions. In vivo electrophysiology in the anesthetized rat was used to examine mPFC and BLA activity simultaneously in response to FG-7142, a benzodiazepine receptor partial inverse agonist that mimics various stress responses, in an attempt to model the effects of stressors on corticolimbic functional connectivity. Extracellular unit and local field potential (LFP) recordings, using multielectrode arrays positioned in mPFC and BLA, were conducted under basal conditions and in response to systemic FG-7142 administration. This drug increased mPFC and BLA unit firing at the lowest dose tested, whereas higher doses of FG-7142 decreased various burst firing parameters in both regions. Moreover, LFP power was attenuated at lower (<1 Hz) and potentiated at higher frequencies in mPFC (1-12 Hz) and BLA (4-8 Hz). Interestingly, FG-7142 diminished synchronized unit firing, both within and between mPFC and BLA. Finally, FG-7142 decreased LFP synchronization between these regions. In a separate group of animals, pretreatment with the selective benzodiazepine receptor antagonist flumazenil blocked the changes in burst firing, LFP power and synchronized activity induced by FG-7142, confirming direct benzodiazepine receptor-mediated effects. These results indicate that FG-7142 disrupts corticolimbic network interactions via benzodiazepine receptor partial inverse agonism. Perturbation of mPFC-BLA functional connectivity induced by FG-7142 may provide a useful model of corticolimbic dysfunction induced by stressors.

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“…An example of such dynamics consists of those that give rise to burst firing (i.e. the firing of packets of action potentials followed by quiescence) which is seen ubiquitously in the CNS (Krahe and Gabbiani 2004). Although the intrinsic and network mechanisms that give rise to burst firing are generally well understood (Izhikevich 2000;Sherman and Guillery 2002;Krahe and Gabbiani 2004), the functional role of burst firing is less well understood.…”

Section: Introductionmentioning

confidence: 99%

“…the firing of packets of action potentials followed by quiescence) which is seen ubiquitously in the CNS (Krahe and Gabbiani 2004). Although the intrinsic and network mechanisms that give rise to burst firing are generally well understood (Izhikevich 2000;Sherman and Guillery 2002;Krahe and Gabbiani 2004), the functional role of burst firing is less well understood. In particular, it has been proposed that bursts, when treated as a single event, can signal the presence of particular stimulus features Metzner et al 1998;Sherman 2001;Sherman and Guillery 2002;Chacron et al 2004a;Lesica and Stanley 2004;Oswald et al 2004).…”

Section: Introductionmentioning

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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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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Burst firing in sensory systems

Cited by 421 publications

References 119 publications

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Systemic administration of the benzodiazepine receptor partial inverse agonist FG‐7142 disrupts corticolimbic network interactions

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

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