Glucocorticoids are good and bad for plasticity and learning

Circadian glucocorticoid peaks promote postsynaptic dendritic spine formation in the mouse cortex after motor skill learning, whereas troughs are required for stabilizing newly formed spines that are important for long-term memory retention. Conversely, chronic and excessive exposure to glucocorticoids eliminates learning-associated new spines and disrupts previously acquired memories. Together, these findings indicate that tightly regulated circadian glucocorticoid oscillations are important for learning-dependent synaptic formation and maintenance. 
Circadian glucocorticoid oscillations have dual roles in dendritic spine plasticity, controlling spine formation and elimination through distinct mechanisms important for motor learning.

Nature Neuroscience 

16, 

658–659 

(2013)

How does exercise induces neuroplasticity?

Exercise and Neuroprotection and Neurorestoration in Rodent Models of PD:

Neuroplasticity is a process by which the brain encodes experiences and learns new behaviors and is defined as the modification of existing neural networks by adding or modifying synapses. Evidence is accumulating that both goal directed and aerobic exercise may strengthen and improve motor circuitry through mechanisms that include but are not limited to alterations and glutamate neurotransmission, as well as structural modifications of synapses. In addition, exercise may promote neuroprotection of substantia nigra neurons and their existing connections. Finally, exercise-induced alterations in blood flow and general brain health may promote conditions for neuroplasticity important for facilitating motor skill learning, including cognitive and automatic motor control and overall behavioral performance. While more studies are clearly needed, taken together these findings are supportive of a disease modifying effect of exercise.

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