Previous multi-parameter bifurcation analyses of the Pinsky–Rinzel neuron model have elucidated a mechanistic explanation for the complex interplay between the membrane potentials of CA3 pyramidal cells and their intracellular dendritic calcium levels. By coupling this neuron model with the Li–Rinzel-type model of astrocytic Ca \(^{2+}\) dynamics, we demonstrate how astrocytic calcium signaling dynamically modulates neuronal activity. We present a classification of potential dynamical transients, including transitions to epileptiform activity. Furthermore, we identify a bidirectional role of astrocytes where they may not only facilitate the emergence of high-frequency oscillations associated with epileptiform activity but may also contribute to their attenuation. Additionally, we propose a mechanism that prolongs the bursting duration of pyramidal cells, which may be associated with synaptic plasticity. Finally, we validate our modeling framework by replicating experimental paradigms that link astrocytic Ca \(^{2+}\) dynamics with neuronal hyperexcitability, demonstrating that astrocytes may drive neurons toward the seizure threshold. These findings enhance our understanding of integrated neural circuit dynamics, particularly the role of neuron–astrocyte interactions in modulating bursting behavior, neural signaling, and their potential contribution to both the generation and suppression of epileptiform ripples.
