Damage incurred by traumatic brain injury is believed to be caused in part by mass depolarization leading to excitotoxicity . One way in which progesterone helps to alleviate some of this excitotoxicity is by blocking the voltage-dependent calcium channels that trigger neurotransmitter release.  It does so by manipulating the signaling pathways of transcription factors involved in this release. Another method for reducing the excitotoxicity is by up-regulating the GABA A , a widespread inhibitory neurotransmitter receptor. 
As indicated above, ACTH is a cleavage product of the pro-hormone, proopiomelanocortin (POMC), which also produces other hormones including α-MSH that stimulates the production of melanin . A family of related receptors mediates the actions of these hormones, the MCR, or melanocortin receptor family. These are mainly not associated with the pituitary - adrenal axis. MC2R is the ACTH receptor . While it has a crucial function in regulating the adrenal, it is also expressed elsewhere in the body, specifically in the osteoblast , which is responsible for making new bone, a continual and highly regulated process in the bodies of air-breathing vertebrates.  The functional expression of MC2R on the osteoblast was discovered by Isales et alia in 2005.  Since that time, it has been demonstrated that the response of bone forming cells to ACTH includes production of VEGF , as it does in the adrenal. This response might be important in maintaining osteoblast survival under some conditions.  If this is physiologically important, it probably functions in conditions with short-period or intermittent ACTH signaling, since with continual exposure of osteoblasts to ACTH, the effect was lost in a few hours.