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Jones, M. W.

Publications and source records attributed to Jones, M. W..

2 recordsLinked to original sources

Locus Coeruleus tracking of prediction errors optimises cognitive flexibility: an Active Inference model.

The locus coeruleus (LC) in the pons is the major source of noradrenaline (NA) in the brain. Two modes of LC firing have been associated with distinct cognitive states: changes in tonic rates of firing are correlated with global levels of arousal and behavioural flexibility, whilst phasic LC responses are evoked by salient stimuli. Here, we unify these two modes of firing by modelling the response of the LC as a correlate of a prediction error when inferring states for action planning under Active Inference (AI).\n\nWe simulate a classic Go/No-go reward learning task and a three-arm foraging task and show that, if LC activity is considered to reflect the magnitude of high level state-action prediction errors, then both tonic and phasic modes of firing are emergent features of belief updating. We also demonstrate that when contingencies change, AI agents can update their internal models more quickly by feeding back this state-action prediction error - reflected in LC firing and noradrenaline release - to optimise learning rate, enabling large adjustments over short timescales. We propose that such prediction errors are mediated by cortico-LC connections, whilst ascending input from LC to cortex modulates belief updating in anterior cingulate cortex (ACC).\n\nIn short, we characterise the LC/ NA system within a general theory of brain function. In doing so, we show that contrasting, behaviour-dependent firing patterns are an emergent property of the LCs crucial role in translating prediction errors into an optimal mediation between plasticity and stability.\n\nAuthor SummaryThe brain uses sensory information to build internal models and make predictions about the world. When errors of prediction occur, models must be updated to ensure desired outcomes are still achieved. Neuromodulator chemicals provide a possible pathway for triggering such changes in brain state. One such neuromodulator, noradrenaline, originates predominantly from a cluster of neurons in the brainstem - the locus coeruleus (LC) - and plays a key role in behaviour, for instance, in determining the balance between exploiting or exploring the environment.\n\nHere we use Active Inference (AI), a mathematical model of perception and action, to formally describe LC function. We propose that LC activity is triggered by errors in prediction and that the subsequent release of noradrenaline alters the rate of learning about the environment. Biologically, this describes an LC-cortex feedback loop promoting behavioural flexibility in times of uncertainty. We model LC output as a simulated animal performs two tasks known to elicit archetypal responses. We find that experimentally observed phasic and tonic patterns of LC activity emerge naturally, and that modulation of learning rates improves task performance. This provides a simple, unified computational account of noradrenergic computational function within a general model of behaviour.

neuroscience

Defining the synaptic mechanisms that tune CA3-CA1 reactivation during sharp-wave ripples.

During non-REM sleep, memory consolidation is driven by a dialogue between hippocampus and cortex involving the reactivation of specific neural activity sequences ( replay). In the hippocampus, replay occurs during sharp-wave ripples (SWRs), short bouts of excitatory activity in area CA3 which induce high frequency oscillations in the inhibitory interneurons of area CA1. Despite growing evidence for the functional importance of replay, its neural mechanisms remain poorly understood. Here, we develop a novel theoretical model of hippocampal spiking during SWRs. In our model, noise-induced activation of CA3 pyramidal cells triggered an excitatory cascade capable of inducing local ripple events in CA1. Ripples occurred stochastically, with Schaffer Collaterals driving their coordination, so that localized sharp waves in CA3 produced consistently localized CA1 ripples. In agreement with experimental data, the majority of pyramidal cells in the model showed low reactivation probabilities across SWRs. We found, however, that a subpopulation of pyramidal cells had high reactivation probabilities, which derived from fine-tuning of the network connectivity. In particular, the excitatory inputs along synaptic pathway(s) converging onto cells and cell pairs controlled emergent single cell and cell pair reactivation, with inhibitory inputs and intrinsic cell excitability playing differential roles in CA3 vs. CA1. Our model predicts (1) that the hippocampal network structure driving the emergence of SWR is also able to generate and modulate reactivation, (2) inhibition plays a particularly prominent role in CA3 reactivation and (3) CA1 sequence reactivation is reliant on CA3-CA1 interactions rather than an intrinsic CA1 process.

neuroscience