Phosphodiesterase 10A Inhibition Leads to Brain Region-Specific Recovery Based on Stroke Type.

Stroke is the leading cause of adult disability. Recovery of function after stroke involves signaling events that are mediated by cAMP and cGMP pathways, such as axonal sprouting, neurogenesis, and synaptic plasticity. cAMP and cGMP are degraded by phosphodiesterases (PDEs), which are differentially expressed in brain regions.

Recovery of stress response coincides with responsiveness to voluntary exercise after traumatic brain injury.

We have recently shown that there is a heightened stress response after a mild traumatic brain injury (TBI) during the first 2 post-injury weeks. This corresponds to the same post-injury period when exercise does not increase brain-derived neurotrophic factor (BDNF) and autonomic dysfunction becomes evident with exercise. Here we determined stress and autonomic responses to voluntary and forced exercise at a post-injury time window when exercise has been found to elicit beneficial effects.

Temperature and heart rate responses to exercise following mild traumatic brain injury.

We have previously reported that mild fluid percussion injury (FPI) is associated with a heightening of the hypothalamic-pituitary-adrenal axis response during the first post-injury weeks. This is the same time period when rehabilitative exercise has been strongly suggested to be ineffective. Here, we explored whether cardiac and temperature autonomic function may also be compromised during this early post-injury period.