arXiv subjects

Brandon R. Munn

Publications and source records attributed to Brandon R. Munn.

3 recordsLinked to original sources

arXiv2025

A Minimal Quantitative Model of Perceptual Suppression and Breakthrough in Visual Rivalry

When conflicting images are presented to either eye, binocular fusion is disrupted. Rather than experiencing a blend of both percepts, often only one eye's image is experienced, whilst the other is suppressed from awareness. Importantly, suppression is transient - the two rival images compete for dominance, with stochastic switches between mutually exclusive percepts occurring every few seconds with law-like regularity. From the perspective of dynamical systems theory, visual rivalry offers an experimentally tractable window into the dynamical mechanisms governing perceptual awareness. In a recently developed visual rivalry paradigm - tracking continuous flash suppression (tCFS) - it was shown that the transition between awareness and suppression is hysteretic, with a higher contrast threshold required for a stimulus to breakthrough suppression into awareness than to be suppressed from awareness. Here, we present an analytically-tractable model of visual rivalry that quantitatively explains the hysteretic transition between periods of awareness and suppression in tCFS. Grounded in the theory of neural dynamics, we derive closed-form expressions for the duration of perceptual dominance and suppression, and for the degree of hysteresis (i.e. the depth of perceptual suppression), as a function of model parameters. Finally, our model yields a series of novel behavioural predictions, the first of which - distributions of dominance and suppression durations during tCFS should be approximately equal - we empirically validate in human psychophysical data.

q-bio.NC↗

arXiv2025

The role of gain neuromodulation in layer-5 pyramidal neurons

Biological and artificial learning systems alike confront the plasticity-stability dilemma. In the brain, neuromodulators such as acetylcholine and noradrenaline relieve this tension by tuning neuronal gain and inhibitory gating, balancing segregation and integration of circuits. Fed by dense cholinergic and noradrenergic projections from the ascending arousal system, layer-5 pyramidal neurons in the cerebral cortex offer a relevant substrate for understanding these dynamics. When distal dendritic signals coincide with back-propagating action potentials, calcium plateaus turn a single somatic spike into a high-gain burst, and interneuron inhibition sculpts the output. These properties make layer-5 cells gain-tunable amplifiers that translate neuromodulatory cues into flexible cortical activity. To capture this mechanism we developed a two-compartment Izhikevich model for pyramidal neurons and single-compartment somatostatin (SOM) and parvalbumin (PV) interneurons, linked by Gaussian connectivity and spike-timing-dependent plasticity (STDP). The soma and apical dendrite are so coupled that somatic spikes back-propagate, while dendritic plateaus can switch the soma from regular firing to bursting by shifting reset and adaptation variables. We show that stronger dendritic drive or tighter coupling raise gain by increasing the likelihood of calcium-triggered somatic bursts. In contrast, dendritic-targeted inhibition suppresses gain, while somatic-targeted inhibition raises the firing threshold of neighboring neurons, thus gating neurons output. Notably, bursting accelerates STDP, supporting rapid synaptic reconfiguration and flexibility. This suggests that brief gain pulses driven by neuromodulators could serve as an adaptive two-timescale optimization mechanism, effectively modulating the synaptic weight updates.

q-bio.NC↗

arXiv2023

Noradrenergic neuromodulation of nonlinear bursting neurons controls critical dynamics

In order to remain adaptable to a dynamic environment, neural activity must be simultaneously both sensitive and stable. To solve this problem, the brain has been hypothesised to sit near a critical boundary. Yet, precisely how criticality and these opposing information processing modes are implemented in the brain remains elusive. A potential solution to this problem involves modulating intrinsically nonlinear neurons within the cerebral cortex with neuromodulatory neurotransmitters such as noradrenaline, a highly-conserved chemical released from the pontine locus coeruleus. Here we confirm that neuronal spiking in mice is poised close to the critical point of a branching process and that time-varying signatures of criticality fluctuate with neuromodulatory tone, as assessed by dynamic alterations in pupil diameter. We explore these results theoretically by creating a dual-compartment model of non-linear pyramidal neurons - capable of both regular spike and bursting modes - that replicates our main empirical findings of slightly subcritical dynamics. We then probe our model at a resolution impossible in vivo to demonstrate that noradrenaline differentially alters spiking- and bursting-criticality to facilitate sensitive and stable dynamics following an inverted-U profile that peaks at intermediate noradrenergic tone. Finally, we demonstrate that this intermediate noradrenergic regime displays burst avalanches with power-law size and duration distributions and scaling relationship belonging to the universality class of self-organized criticality. Our results confirm that the noradrenergic ascending arousal system acts as a control parameter for emergent critical dynamics in the brain. This methodology could be extended to explore other neuromodulators as control parameters of the brain.

q-bio.NC↗