Neural network complexity allows for diverse neuronal population dynamics and realizes higherorder brain functions such as cognition and memory. Complexity is enhanced through chemical synapses with exponentially decaying conductance and greater variation in the neuronal connection strength due to synaptic plasticity. However, in the macroscopic neuronal population model, synaptic connections are often described by spike connections, and connection strengths within the population are assumed to be uniform. Thus, the effects of synaptic connections variation on network synchronization remain unclear. Based on recent advances in mean field theory for the quadratic integrate-and-fire neuronal network model, we introduce synaptic conductance and variation of connection strength into the excitatory and inhibitory neuronal population model and derive the macroscopic firing rate equations for faithful modeling. We then introduce a heuristic switching rule of the dynamic system with respect to the mean membrane potentials to avoid divergences in the computation caused by variations in the neuronal connection strength. We show that the switching rule agrees with the numerical computation of the microscopic level model. In the derived model, variations in synaptic conductance and connection strength strongly alter the stability of the solutions to the equations, which is related to the mechanism of synchronous firing. When we apply physiologically plausible values from layer 4 of the mammalian primary visual cortex to the derived model, we observe event-related desynchronization at the alpha and beta frequencies and event-related synchronization at the gamma frequency over a wide range of balanced external currents. Our results show that the introduction of complex synaptic connections and physiologically valid numerical values into the low-dimensional mean field equations reproduces dynamic changes such as eventrelated (de)synchronization, and provides a unique mathematical insight into the relationship between synaptic strength variation and oscillatory mechanism.

Gamma oscillations are thought to play a role in information processing in the brain. Bursting neurons, which exhibit periodic clusters of spiking activity, are a type of neuron that are thought to contribute largely to gamma oscillations. However, little is known about how the properties of bursting neurons affect the emergence of gamma oscillation, its waveforms, and its synchronized characteristics, especially when subjected to stochastic fluctuations. In this study, we proposed a bursting neuron model that can analyze the bursting ratio and the phase response function. Then we theoretically analyzed the neuronal population dynamics composed of bursting excitatory neurons, mixed with inhibitory neurons. The bifurcation analysis of the equivalent Fokker-Planck equation exhibits three types of gamma oscillations of unimodal firing, bimodal firing in the inhibitory population, and bimodal firing in the excitatory population under different interaction strengths. The analyses of the macroscopic phase response function by the adjoint method of the Fokker-Planck equation revealed that the inhibitory doublet facilitates synchronization of the high-frequency oscillations. When we keep the strength of interactions constant, decreasing the bursting ratio of the individual neurons increases the relative high-gamma component of the populational phase-coupling functions. This also improves the ability of the neuronal population model to synchronize with faster oscillatory input. The analytical frameworks in this study provide insight into nontrivial dynamics of the population of bursting neurons, which further suggest that bursting neurons have an important role in rhythmic activities.

The free-energy principle is a candidate unified theory for learning and memory in the brain that predicts that neurons, synapses, and neuromodulators work in a manner that minimizes free energy. However, electrophysiological data elucidating the neural and synaptic bases for this theory are lacking. Here, we propose a novel theory bridging the information-theoretical principle with the biological phenomenon of spike-timing dependent plasticity (STDP) regulated by neuromodulators, which we term mSTDP. We propose that by integrating an mSTDP equation, we can obtain a form of Friston’s free energy (an information-theoretical function). Then we analytically and numerically show that dopamine (DA) and noradrenaline (NA) influence the accuracy of a principal component analysis (PCA) performed using the mSTDP algorithm. From the perspective of free-energy minimization, these neuromodulatory changes alter the relative weighting or precision of accuracy and prior terms, which induces a switch from pattern completion to separation. These results are consistent with electrophysiological findings and validate the free-energy principle and mSTDP. Moreover, our scheme can potentially be applied in computational psychiatry to build models of the faulty neural networks that underlie the positive symptoms of schizophrenia, which involve abnormal DA levels, as well as models of the NA contribution to memory triage and posttraumatic stress disorder.

Connection strength estimation is widely used in detecting the topology of neuronal networks and assessing their synaptic plasticity. A recently proposed model-based method using the leaky integrate-and-fire model neuron estimates membrane potential from spike trains by calculating the maximum a posteriori (MAP) path. We further enhance the MAP path method using variational Bayes and dynamic causal modeling. Several simulations demonstrate that the proposed method can accurately estimate connection strengths with an error ratio of less than 20%. The results suggest that the proposed method can be an effective tool for detecting network structure and synaptic plasticity.