Question:
Chronic, severe exposure to stress or an innate vulnerability to stress causes
destructive biochemical reactions in the body that may lead to a variety of
illnesses, including depression.
Now, researchers from Northwestern University Medical School and San Diego
State University have published the first study to show that a peptide found in
the brain and in the body can reduce both hormonal and behavioral
manifestations of stress. The study was published in a recent issue of the
Journal of Neuroscience.
Answer:
This is patently false. This is precisely what opioid agonists
and endogenous opioid peptides do. Particularly in rodents. Of
course, this statement may be presented as though it were true
by adding the qualification that opioids are not classified as
'anxiety-reducing agents' (no matter what their effects on
anxiety may be.)
you know, one could also say that cars and bicycles do the same
thing (ie getting you from point A to point B), but they still may have
their own particular utilities.
if you get right down to it, "this" (that the peptide decreased fear
and anxiety-related behaviors while simultaneously promoting arousal) is
also "precisely" what metyrapone (a cortisol synthesis inhibitor) and a
host of other drugs do. and YET, their subjective and reinforcing
effects are nothing like opioid agonists. for that matter, not even
opioid agonists are the same (eg delta v. kappa v. mu) in their ability
to inhibit pain response, inhibit cortisol, and produce euphoria.
preproTRH cannot be directly compared to opioid agonists or endogenous
peptides.
OK, i withdraw the "poorly informed" bit (unless you've truly mastered
the cut and paste from Medline). Nonetheless, preproTRH (ps4) certainly
does not produce the same profile of neuroadaptation as mu opioid
agonists. Whereas you get acute and chronic tolerance at the cellular
level in the LC and dysphoria/stereotypical opiate withdrawal at the
behavioral level with u-agonists, there are no reports indicating any
such maladaptive responses to ps4.
Moreover, the differences between ps4 and opioid ligands are more
manifest in their ability to be regulated by antidepressant treatments.
Opioid ligands have little or no antidepressant efficacy, while there's
at least some evidence for ps4's involvement in the neuroplastic
response to ECT. Granted, this is far from "proof" and falls more under
the category of "possible lead", but i think you're a bit too quick to
dismiss these findings based on some surface similarities to opioid
peptide research.
