Bose:
Dynamics of Neuronal Oscillators
The primary goal of the research of Amitabha Bose is to derive and analyze
mathematical models of neuronal activity. Primary applications include
studies of the crustacean stomatogastric ganglion (STG).
In particular, Bose and collaborators have developed models which explain how
neurons in the pyloric network of the STG maintain phase relationships with
one another as the frequency of network oscillations change (Manor, Bose, Booth
and Nadim, 2003; Bose, Manor, Nadim, 2004). Other models explain how
the frequency of the gastric mill rhythm is controlled by modulatory inputs to
the STG (Ambrosio, Nadim, Bose; 2005). Bose is also interested in
understanding the various roles that short-term synaptic plasticity can play in
neruonal networks. He has shown how plasticity can give rise to bi-stability in
oscillator-follower networks (Bose, Manor, Nadim; 2001) and how it can be used
to explain the phenomena of episodic bursting in the context of frog
ventilatory rhythmogenesis (Bose, Lewis, Wilson; 2005).
A second and developing interest is to understand how localized patterns of
activity can arise in excitatory networks.
In the figures below, two different activity patterns from a 1-dimensional
array of neural oscillators coupled only be excitatory synapses are shown.
In one, a wave of excitation spreads through the entire network causing
all cells to eventually oscillate (time on vertical axis, neurons 1-20
on horizontal axis). Alternatively, in the other for a slightly smaller
value of coupling strength, the excitation does not spread to the entire
network and a stable bump solution is obtained in which only 7 neurons
oscillate. Both simulations have the same initial conditions. Neurons
9, 10 and 11 were initially given a 50 msec jolt of excitation to initiate
activity. Stable bumps are thought to be important in modeling working
memory in which a bump would correspond to a recalled memory.
The existence of stable bumps in excitatory networks has recently been
reported, but the mechanism by which the spread of excitation is stopped
remained a mystery. Jonathan Rubin and I show that the spread of excitation
can be curtailed due to slow passage near a saddle-node bifurcation (Rubin,
Bose; 2004). The
results show that the timing of synaptic inputs, and not just the strength of
inputs, to a particular neuron determine whether or not it will fire. Thus
while two adjacent neurons may receive excitatory inputs of equal strength,
only one of the two may fire thereby stopping the spread of the excitatory
wave.