Primate neocortex performs balanced sensory amplification

The sensory cortex amplifies relevant features of external stimuli. This sensitivity and selectivity arise through the transformation of inputs by cortical circuitry. We characterize the circuit mechanisms and dynamics of cortical amplification by making large-scale simultaneous measurements of sing...

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Veröffentlicht in:Neuron (Cambridge, Mass.) Mass.), 2024-02, Vol.112 (4), p.661-675.e7
Hauptverfasser: Pattadkal, Jagruti J., Zemelman, Boris V., Fiete, Ila, Priebe, Nicholas J.
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Sprache:eng
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Zusammenfassung:The sensory cortex amplifies relevant features of external stimuli. This sensitivity and selectivity arise through the transformation of inputs by cortical circuitry. We characterize the circuit mechanisms and dynamics of cortical amplification by making large-scale simultaneous measurements of single cells in awake primates and testing computational models. By comparing network activity in both driven and spontaneous states with models, we identify the circuit as operating in a regime of non-normal balanced amplification. Incoming inputs are strongly but transiently amplified by strong recurrent feedback from the disruption of excitatory-inhibitory balance in the network. Strong inhibition rapidly quenches responses, thereby permitting the tracking of time-varying stimuli. •Population dynamics in area MT reveal the mechanisms of cortical amplification•Cortical amplification models can be differentiated using their distinct dynamics•The dynamics of area MT are consistent with a balanced amplification model•Balanced amplification increases sensitivity while maintaining fast dynamics Sensory circuits show high sensitivity to signals of interest even in noisy, changing environments. Pattadkal et al. place constraints on the circuitry for amplification using calcium imaging and electrophysiology in marmoset area MT. Different circuits for amplification are characterized by distinct dynamics. Area MT dynamics match a balanced amplification circuit.
ISSN:0896-6273
1097-4199
DOI:10.1016/j.neuron.2023.11.005