Abstract
AbstractCell assemblies are believed to represent the substrate of memory. Although long-term plasticity likely enables the formation of cell assemblies, how other factors, such as astrocytes and short-term plasticity (STP), affect their properties is poorly understood. To close this gap, we investigated cell assembly dynamics in a recurrent network model mimicking the hippocampal area CA3. As shown in experiment, recurrent connections in our model obey a symmetric spike-timing-dependent plasticity (STDP), in which weight change may or may not depend on the releasable amount of neurotransmitter. The former case involves an interplay between STDP and STP. In addition, we implicitly modeled the effect of astrocyte NMDA receptors by manipulating the breadth of the distribution of neurotransmitter release probability in STP. Both STP-dependent and STP-independent STDP enabled spontaneous cell assembly formation. Under the former, however, cell assemblies tend to be smaller and more responsive to external stimulation, improving the network’s memory capacity and enabling flexible network restructuring. Furthermore, astrocyte regulation of the STP-dependent STDP facilitates stimulus-driven reorganization of neural networks without destroying existing assembly structure, thus balancing cell assemblies’ flexibility and robustness. Our findings elucidate the computational advantages of interaction between STP and STDP and highlight astrocytes’ possible regulatory role in memory formation.
Publisher
Cold Spring Harbor Laboratory