Collective rhythmic dynamics from neurons is vital for cognitive functions
such as memory formation but how neurons self-organize to produce such activity
is not well understood. Attractor-based models have been successfully
implemented as a theoretical framework for memory storage in networks of
neurons. Activity-dependent modification of synaptic transmission is thought to
be the physiological basis of learning and memory. The goal of this study is to
demonstrate that using a pharmacological perturbation on in vitro networks of
hippocampal neurons that has been shown to increase synaptic strength follows
the dynamical postulates theorized by attractor models. We use a grid of
extracellular electrodes to study changes in network activity after this
perturbation and show that there is a persistent increase in overall spiking
and bursting activity after treatment. This increase in activity appears to
recruit more "errant" spikes into bursts. Lastly, phase plots indicate a
conserved activity pattern suggesting that the network is operating in a stable
dynamical state
