Environmental enrichment (EE) is known to cause neuroplastic changes in lower-order cortices (e.g., the primary somatosensory area, S1) of the mouse brain. Mice raised in EE conditions (EE-mice) also show increased social ability, as observed in a social interaction test. Because sociality is largely associated with higher brain functions, the increased sociality of EE mice suggests that EE induces neuroplastic changes not only in lower- but also in higher-order cortices. Although some cellular mechanisms have been proposed for the EE-induced neuroplastic changes in lower-order areas, the mechanisms underlying EE-induced changes in higher-order areas are unknown.
Our aim was to examine the effects of EE on neuroplasticity in lower- and higher-order cortices using neuroanatomical, psychophysiological, and electrophysiological approaches. Here, we were specifically interested in examining a reciprocally connected sensory-motor circuit between S1 and a secondary motor area, M2. To understand the effects of EE on the S1-M2 circuit, we raised 2-week-old mice in EE conditions or normal environments (NE) for 3 weeks and observed the cortical activity evoked by hindpaw stimulation with voltage-sensitive dye imaging. Neuronal activity in M2 was significantly increased in EE-mice compared to that in NE-mice, suggesting neural plasticity in the M2 under EE conditions. We hypothesized that some anatomical parameters were changed in EE-mice. To test this hypothesis, we measured the numbers of neurons and glial cells and the density of synapses (excitatory and inhibitory) in EE- and NE-mice using immunohistochemistry and transmission electron microscopy, respectively. We found differences in these parameters between EE- and NE-mice, and these differences varied according to the cortical layer. Next, we hypothesized that the layer-specific changes in these anatomical parameters result in greater M2 activity in EE-mice compared to NE-mice. To test this, we recorded neural firing activity extracellularly from all layers in the S1 and M2 areas during hindpaw stimulation. Here, we report the differences in the various physiological and anatomical parameters between EE- and NE-mice.