Topic: CA3

In understanding circuit operations, a key issue is the extent to which neuronal spiking reflects local computation or responses to upstream inputs. Because pyramidal cells in CA1 do not have local recurrent projections, it is currently assumed that firing in CA1 is inherited from its inputs – thus, entorhinal inputs provide communication with the rest of the neocortex and the outside world, whereas CA3 inputs provide internal and past memory representations. Several studies have attempted to prove this hypothesis, by lesioning or silencing either area CA3 or the entorhinal cortex and examinin

The hippocampal formation plays a key role in learning and memory, with CA3 thought to be the substrate of pattern completion [1]. However, its underlying computational and synaptic mechanisms are not yet understood. Here we analyze the mechanisms behind sequence replay through simulations of spiking neurons and a time-discrete model of moving membrane potential distributions. First, we simulated spiking networks of excitatory leaky integrate-and-fire cells forming a sequence of assemblies. The sequence contains both recurrent and feedforward connections (within and across assemblies, respect

Creating place fields in place cells is crucial for forming spatially dependent episodic memories in the brain, with the hippocampus playing a central role. Specifically, we focus on CA1 pyramidal neurons, which receive inputs from the CA3 and entorhinal cortex (EC). No widely accepted network-based theory for place field formation exists, but many models offer mechanisms for place-field firing. One type of hypotheses proposes that it results from summated output of spatially tuned cells, like grid cells or boundary vector cells. Another suggests CA1 place fields are replicate of CA3 place fie