The influence of sensory experience on the glutamatergic synapse

The ability of glutamatergic synaptic strength to change in response to prevailing neuronal activity is believed to underlie the capacity of animals, including humans, to learn from experience. This learning better equips animals to safely navigate challenging and potentially harmful environments, while reinforcing behaviours that are conducive to survival. Early descriptions of the influence of experience on behaviour were provided by Donald Hebb who showed that an enriched environment improved performance of rats in a variety of behavioural tasks, challenging the widely-held view at the time that psychological development and intelligence were largely predetermined through genetic inheritance. Subsequent studies in a variety of species provided detailed cellular and molecular insights into the neurobiological adaptations associated with enrichment and its counterparts, isolation and deprivation. Here we review those experience-dependent changes that occur at the glutamatergic synapse, and which likely underlie the enhanced cognition associated with enrichment. We focus on the importance of signalling initiated by the release of BDNF and a prime downstream effector, MSK1, in orchestrating the many structural and functional neuronal adaptations associated with enrichment. In particular we discuss the MSK1-dependent expansion of the dynamic range of the glutamatergic synapse, which may allow enhanced information storage or processing, and the establishment of a genomic homeostasis that may both stabilise the enriched brain, and may make it better able to respond to novel experiences.

Automated summary

The ability of glutamatergic synaptic strength to change in response to neuronal activity is believed to underlie animal learning from experience. BDNF signaling and MSK1 play a crucial role in the structural and functional adaptations associated with enrichment, potentially allowing for enhanced information storage and establishment of genomic homeostasis.