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Davey, C. E.

Publications and source records attributed to Davey, C. E..

3 recordsLinked to original sources

Modelling Predictive Coding in the Primary Visual Cortex (V1): Layer 2/3 Circuits for Prediction Error Computation through Compartmentalized Spiking Neurons

Cortical Layer 2/3 has been consistently implicated as the locus of prediction-error signalling in hierarchical models of cortical sensory processing. However, the circuit mechanisms that generate biologically plausible prediction-error (PE) signals remain elusive. A spiking network model is presented here in which two-compartment excitatory pyramidal neurons interact with three inhibitory subtypes: parvalbumin-expressing (PV), somatostatin-expressing (SOM), and vasoactive-intestinal-peptide-expressing (VIP) interneurons, to compute sign-specific prediction errors (positive and negative PEs). Feedforward input targets the soma, whereas top-down feedback reaches the distal apical dendrite, enabling a local somato-dendritic comparison. A PE emerges whenever the balance between excitation and inhibition is selectively disrupted within one compartment, recruiting either positive-error (PE+) or negative-error (PE-) subpopulations of pyramidal neurons. Unlike prior learning-dependent, rate-based accounts, this fixed-weight spiking circuit shows that bidirectional PE signals (PE+ and PE-) can arise online from compartment-specific balance without any synaptic weight updates. The model reproduces key experimental observations, including sparse mismatch responses, compartment-specific inhibition, and VIP-mediated disinhibition. Across four canonical sensory-prediction configurations, the circuit maintains a tight balance during matched input and generates bidirectional PE signals only under mismatch. By routing sensory drive from Layer 4 into Layer 2/3 and allowing the resulting PE activity to project toward deeper feedback generators, the model situates Layer 2/3 as a dedicated, feature-specific mismatch detector within a hierarchical inference network. These results provide a mechanistic bridge from dendritic computation to laminar predictive coding, demonstrating how realistic spiking dynamics can implement fast, sign-specific PE signaling without learning. Author summaryIn this study, we present a biologically grounded spiking model of layer 2/3 in primary visual cortex within the predictive coding framework. Our goal is to explain how superficial cortical circuits compute fast, sign-specific prediction errors when sensory input does not match top-down expectations. The model uses two-compartment pyramidal neurons whose somata receive feedforward drive from layer 4 while apical dendrites receive feedback, together with three key inhibitory interneuron classes, parvalbumin-expressing (PV), somatostatin-expressing (SOM), and vasoactive-intestinal-peptide-expressing (VIP), that provide compartment-specific inhibition and disinhibition. When input and prediction match, excitation and inhibition remain tightly balanced and activity is sparse; when they differ, this balance is transiently broken in the appropriate compartment, and distinct populations signal either a positive error (unexpected presence) or a negative error (unexpected absence). The circuit reproduces several in vivo observations in layer 2/3, including sparse mismatch responses, compartment-specific inhibition, and VIP-mediated disinhibition, and it does so without requiring synaptic weight changes. By routing feature-selective signals from layer 4 into layer 2/3 and relaying the resulting errors toward deeper layers, the model positions layer 2/3 as a local, feature-specific mismatch detector in a hierarchical system. This work provides a concrete, testable mechanism linking dendritic computation, inhibitory diversity, and predictive coding in the cortex.

neuroscience↗

A neural framework for spontaneous development of orientation selectivity in the primary visual cortex

The mechanism or microcircuitry behind orientation selectivity in primary visual cortex (V1), and the means by which it develops without supervision or visual input, both remain unresolved questions. Work on the developmental question has assumed the prevalent spatial convergence model of orientation selectivity as the target mechanism. Encouraged by growing evidence challenging both the completeness of this model and its developmental viability, we investigated an alternative scheme. Accordingly, we demonstrate computationally how a scheme in which orientation selectivity originates from the orientation biases already in the retina and lateral geniculate nucelus (LGN) can answer both the mechanistic and developmental questions. In this scheme, the divergence of outputs from the retina allows retinal spontaneous activity to create correlations within the LGN. These correlations in turn allow a Hebbian plasticity mechanism to strengthen those LGN inputs to V1 which carry similar orientation biases and thus provide an orientation tuned excitatory input.

neuroscience↗

Sites of Circadian Clock Neuron Plasticity Mediate Sensory Integration and Entrainment.

Networks of circadian timekeeping in the brain display marked daily changes in neuronal morphology. In Drosophila melanogaster, the striking daily structural remodeling of the dorsal medial termini of the small ventral lateral neurons has long been hypothesized to mediate endogenous circadian timekeeping. To test this model, we have specifically abrogated these sites of daily neuronal remodeling through the reprogramming of neural development and assessed the effects on circadian timekeeping and clock outputs. Remarkably, the loss of these sites has no measurable effects on endogenous circadian timekeeping or on any of the major output functions of the small ventral lateral neurons. Rather, their loss reduces sites of glutamatergic sensory neurotransmission that normally encodes naturalistic time-cues from the environment. These results support an alternative model: structural plasticity in critical clock neurons is the basis for proper integration of light and temperature and gates sensory inputs into circadian clock neuron networks.

neuroscience↗