Modeling the dynamic interaction of Hebbian and homeostatic plasticity.
Hebbian and homeostatic plasticity together refine neural circuitry,
but their interactions are unclear. In most existing models, each form
of plasticity directly modifies synaptic strength. Equilibrium is
reached when the two are inducing equal and opposite changes. We show
that such models cannot reproduce ocular dominance plasticity (ODP)
because negative feedback from the slow homeostatic plasticity
observed in ODP cannot stabilize the positive feedback of fast Hebbian
plasticity. We propose a model in which synaptic strength is the
product of a synapse-specific Hebbian factor and a
postsynaptic-cell-specific homeostatic factor, with each factor
separately arriving at a stable inactive state. This model captures
ODP dynamics and has plausible biophysical substrates. We confirm
model predictions experimentally that plasticity is inactive at stable
states and that synaptic strength overshoots during recovery from
visual deprivation. These results highlight the importance of multiple
regulatory pathways for interactions of plasticity mechanisms
operating over separate timescales.
T. Toyoizumi, M. Kaneko, M. P. Stryker, and K. D. Miller, Neuron 84,
497-510 (2014).
