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. Author manuscript; available in PMC: 2010 Dec 28.
Published in final edited form as: Neuromolecular Med. 2008 Feb 14;10(2):118–127. doi: 10.1007/s12017-008-8027-0

Figure 4.

Figure 4

Integrating voluntary physical activity into the framework of stress circuitry. Voluntary exercise has been demonstrated using a number of functional and structural assays to enhance the capacity for excitatory synaptic transmission in the hippocampus. Output from hippocampal area CA1 ultimately reaches the paraventricular nucleus of the hypothalamus (PVN), via excitatory projections from the subiculum. These projections terminate on inhibitory neurons in the PVN, thereby reducing HPA axis activity at this level. The hippocampus projects to the prefrontal cortex (PFC) via the subiculum, and the PFC sends excitatory projections to the PVN, also terminating on inhibitory neurons to reduce HPA axis output. Increased HPA axis activation likely occurs through increased activity in the central nucleus of the amygdala with voluntary running (AMY; Burghardt et al., 2006). This region sends inhibitory projections to inhibitory neurons of the PVN, increasing HPA axis drive. The balance between HPA axis activation and inhibition with voluntary running is likely to be shifted, and the consequences of such a shift could determine the response to other, heterotypic stressors.