Input normalization by global feedforward inhibition expands cortical dynamic range
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The cortex is sensitive to weak stimuli, but responds to stronger inputs without saturating. The mechanisms that enable this wide range of operation are not fully understood. We found that the amplitude of excitatory synaptic currents necessary to fire rodent pyramidal cells, the threshold excitatory current, increased with stimulus strength. Consequently, the relative contribution of individual afferents in firing a neuron was inversely proportional to the total number of active afferents. Feedforward inhibition, acting homogeneously across pyramidal cells, ensured that threshold excitatory currents increased with stimulus strength. In contrast, heterogeneities in the distribution of excitatory currents in the neuronal population determined the specific set of pyramidal cells recruited. Together, these mechanisms expand the range of afferent input strengths that neuronal populations can represent.
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Feedforward inhibition participates in gain modulation through input normalization.
“Feedforward inhibition has also been shown to participate in gain modulation through input normalization (Pouille et al., 2009).”
From GABAergic Interneurons in the Neocortex: From Cellular Properties to Circuits (2016) · cites this paper as Pouille et al., 2009
This pattern creates a compound synaptic event that drives spiking with greater temporal precision than excitation alone.
“This pattern of activity creates a compound synaptic event that drives spiking with much greater temporal precision than could be achieved by excitation alone (Pouille et al., 2009; Pouille and Scanziani, 2001).”
From Unifying Views of Autism Spectrum Disorders: A Consideration of Autoregulatory Feedback Loops (2016) · cites this paper as Pouille et al., 2009
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- Authors
- Pouille, F., Marin-Burgin, A., Adesnik, H., Atallah, B. V., & Scanziani, M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Scanziani, Massimo
- Venue
- Nature Neuroscience
- Published
- 2009-11-01
- Volume
- 12
- Issue
- 12
- Pages
- 1577-1585
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2124909604
- Cited by
- 306
- References
- 45
- Citations by year
- 2026: 8 · 2025: 17 · 2024: 15 · 2023: 28 · 2022: 16 · 2021: 11 · 2020: 18 · 2019: 19 · 2018: 16 · 2017: 18 · 2016: 21 · 2015: 19 · 2014: 22 · 2013: 22 · 2012: 24
- FWCI
- 9.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- CONICET Digital (CONICET) (submittedVersion, cc-by-nc-sa)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health
- National Institute of Mental Health (MH71401, R01MH071401)
- National Institute of Neurological Disorders and Stroke (F31NS061521, NS061521)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- feedforward inhibition, input normalization, pyramidal neurons, stimulus sensitivity, population coding, rodent cortex
- MeSH terms
- Action Potentials, Animals, Interneurons, Models, Neurological, Neural Inhibition, Neural Pathways, Rodentia, Somatosensory Cortex, Synapses, Pyramidal Cells, Excitatory Postsynaptic Potentials, Feedback, Physiological, CA1 Region, Hippocampal
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