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Blackman, R. K.

Publications and source records attributed to Blackman, R. K..

2 recordsLinked to original sources

Monkey Prefrontal Cortex Learns to Minimize Sequence Prediction Error

In this study, we develop a novel recurrent neural network (RNN) model of pre-frontal cortex that predicts sensory inputs, actions, and outcomes at the next time step. Synaptic weights in the model are adjusted to minimize sequence prediction error, adapting a deep learning rule similar to those of large language models. The model, called Sequence Prediction Error Learning (SPEL), is a simple RNN that predicts world state at the next time step, but that differs from standard RNNs by using its own prediction errors from the previous state predictions as inputs to the hidden units of the network. We show that the time course of sequence prediction errors generated by the model closely matched the activity time courses of populations of neurons in macaque prefrontal cortex. Hidden units in the model responded to combinations of task variables and exhibited sensitivity to changing stimulus probability in ways that closely resembled monkey prefrontal neurons. Moreover, the model generated prolonged response times to infrequent, unexpected events as did monkeys. The results suggest that prefrontal cortex may generate internal models of the temporal structure of the world even during tasks that do not explicitly depend on temporal expectation, using a sequence prediction error minimization learning rule to do so. As such, the SPEL model provides a unified, general-purpose theoretical framework for modeling the lateral prefrontal cortex.

neuroscience↗

A prefrontal network model operating near steady and oscillatory states links spike desynchronization and synaptic deficits in schizophrenia

Schizophrenia results in part from a failure of prefrontal networks but we lack full understanding of how disruptions at a synaptic level cause failures at the network level. This is a crucial gap in our understanding because it prevents us from discovering how genetic mutations and environmental risks that alter synaptic function cause prefrontal network to fail in schizophrenia. To address that question, we developed a recurrent spiking network model of prefrontal local circuits that can explain the link between NMDAR synaptic and spike timing deficits we recently observed in a pharmacological monkey model of prefrontal network failure in schizophrenia. We analyze how the balance between AMPA and NMDA components of recurrent excitation and GABA inhibition in the network influence spike timing to inform the biological data. We show that reducing recurrent NMDAR synaptic currents prevents the network from shifting from a steady to oscillatory state in response to extrinsic inputs such as might occur during behavior. This explains how NMDAR synaptic deficits, implicated by genetic evidence as causal in schizophrenia, could prevent the emergence of 0-lag synchronous spiking in prefrontal local circuits during behavior, potentially disconnecting those circuits via spike-timing dependent mechanisms in the human disease.

neuroscience↗