Posted by SLS on September 17, 2005, at 15:17:20
In reply to effexor and remeron with opioid activity?, posted by iforgotmypassword on September 16, 2005, at 22:58:16
When operating properly, an opioid system in the brain helps regulate the state of the HPA axis by inhibiting the release of CRF when opioid receptors are stimulated, thereby preventing the synthesis of too much cortisol. In depression, this balance goes awry, leaving the HPA axis dysregulated. In the most severe of depressions where psychomotor retardation is prominent, the HPA axis seems to be most often hyperactive. A reduced opioid tone might contribute to this. The abstract you cited indicates that increasing the responsiveness of opioid receptors by certain antidepressants could reverse the HPA axis hyperactivity, thereby enhancing these drugs' effectiveness. The question is, how is this done? I have read that NE pathways might be the route by which these antidepressants modulate the opioid system. SSRI drugs might not be as robust here because they don't directly manipulate NE synapses. One must be careful, however, not to treat the vast complexity of the brain as simplistically as I have done here.
HPA = hypothalamus pituitary adrenal
CRF = corticotropin releasing factor (sometimes referred to as CRH)
NE = norepinephrine
SSRI = selective serotonin reuptake inhibitor
- Scott
poster:SLS
thread:555898
URL: http://www.dr-bob.org/babble/20050914/msgs/556006.html