The Role of Intrinsic Plasticity in Engram Physiology and Temporal Memory Linking

The neuroplastic mechanisms that endow the brain with the capacity to learn and form memories remain a major topic of research in neuroscience and in the development of brain-inspired computational algorithms. Although research into the formation of engrams, the neural assemblies, and codes by which memories are created and stored is primarily focused on synaptic plasticity, a growing body of research is investigating the connection between other forms of plasticity, including intrinsic plasticity, and memory storage.

Intrinsic plasticity, in contrast to synaptic plasticity, is a modification of neuronal excitability. Evidence to support the existence of a relationship between memory formation and intrinsic excitability has existed for nearly half a century (Zhang and Linden, 2003). An early study, conducted by Brons and Woody, of pavlovian conditioning in cats’ sensorimotor cortices found that learned motor performance was reflected in sustained increases of cortical neural excitability recorded via surface electrodes (reviewed in Zhang and Linden, 2003), a landmark observation that motivated thousands of studies. One notable experiment, performed by Moyer, investigated the transience of learning-related changes in rabbits after the animals were conditioned to blink in response to a tone in order to avoid a puff of air to the eye (reviewed in Zhang and Linden, 2003). In electrophysiological recordings of the rabbits’ hippocampal pyramidal neurons, Moyer et al. observed persistent increases in intrinsic excitability for up to 7 d post-training. After which, the conditioned eyeblink response remained strong, despite intrinsic excitability levels returning to their baseline values. Based on this finding, the authors speculated that increases in excitability prime neurons for learning and memory consolidation over a short time period. This led to the hypothesis that neuron priming via intrinsic plasticity makes the network more amenable to changes in synaptic efficacy.

Further efforts to unravel the mechanisms of …

Correspondence should be addressed to Walter Peregrim at peregrim{at}umd.edu or Tim O’Leary at tso24{at}cam.ac.uk.