Kappa Opioid & Schizophrenia

[theAsparagus]

Taking a look around on this forum, I did not seem to find any discussions of a possible cause or trigger of schizophrenia being within kappa opioid receptors.

I'll assume at this point that people who respond to this thread will already be educated on the basic workings of the kappa opioid system, to save myself the finger power. Anyone else interested in this topic that is not familiar with this receptor might want to read the basic wikipedia article found here; en.wikipedia.org/wiki/Kappa_Opioid_receptor

k-receptor agonists have recently been known to help correct psychological addictions to drugs, but it's also briefly realized that they help the mind hold a grip on reality. Proving this, there's Salvinorin A - the most common, receptor-specific agonist that has been known to both; induce visual, auditory, and tactile hallucinations, and completely corrupt the brains understanding of reality. Knowing this intrigued me, so delving further into the subject I came to understand that Salvinorin A did indeed produce effects that mimic the effects of schizophrenia.

With this information, it is possible to hypothesize that the effects are centralized (and spread from) the kappa opioid receptor.

Does anyone else have any more information they can toss down to build on the concept? How about to break the concept?

Mason

 

[David Baxter PhD]

I think when all the data is in (whenever or if ever that occurs) we're going to find that schizophrenia has multiple causes, not just one, and that searching for the cause of schizophrenia is therefore futile. What may be more profitable is to look at all of the pieces of the puzzle - genetic/chromosomal, receptor level impairment, neurotransmitter issues, brain damage or malformation, etc., etc., and eventually try to figure out the commonality in all of these.

One of the problems withj research into schizophrenia is that, because it's so debilitating a disease, often sufferers will have serious impairment of functioning in all areas and will manifest signs of obsessive-compulsive personality disorder (i.e., OCPD, not OCD). As a result, their diets and other habits may be unusual, and often they will spend lengthy or repeated periods of time instituionalized. As well, the medications and the doses of those medications needed to treat schizophrenia have a powerful effect on the brain and body in several ways.

That presents a problem of interpretation in simple comparisons of schizophrenia vs. non-schizophrenia control subjects: Which of the observed differences are causes of schizophrenia? and which are effects of having developed and having been treated for schizophrenia?

 

[theAsparagus]

Perhaps "cause" was the incorrect word. In dealing with the kappa receptor, many kinds of social interactions, upbringings, beliefs, drugs, can influence the way everyone views life and reality - each one of those kinds and instances could be a cause itself, but the way that the cause turns into the manifestation could be looked at in this way.

Theres research to suggest that it develops and occurs more frequently at the point of late adolescence, when theres is a newly presented view of everything. For me, when I remember childhood, I remind myself how mainly care-free, very imaginative and fun-oriented everything was. I still often think about how this newly accepted life could be what I viewed it as before, and sometimes even wish that it was all the same view as before, however it is not. Coming into late adolescence today more or less means the stress of accepting a new way of living your life hits pretty hard for some people, especially because kappa isn't directly activated in a conscious manner day to day. Sure it doesn't hit everyone in this way, which could have been because their upbringing was in a small bit less "care-free" way. Maybe something just didn't blast their ideas out of the world out of proportion before they hit late adolescence and therefore not everything was blown out of proportion.

It points some pretty hefty fingers at this mechanism of action, and I recall having read that there are studies being done by use of drugs such as Salvinorin A, promoting development of new schizophrenic drugs based on the kappa-oriented compound. But it's more the exact method of action that is the question in this point and as you said, there really is not an exact mode from a psychological stand-point. Perhaps there is a way to see if this is an accurate hypothesis by multiple communicative tests that could be handled directly by kappa receptors.

 

[David Baxter PhD]

I'm really not sure those fingers are any heftier than a hundred others. I've been following schizophrenia research since the 1960s and in that time I've seen a number of seemingly promising leads fizzle out. By now, I'm a little skeptical.

I don't want to burst your balloon. I find all of these lines of research interesting, but I haven't seen a whole lot to single out one more than the others.

There's research to suggest that it develops and occurs more frequently at the point of late adolescence

If by "it develops" you mean schizophrenia, while it's true that it most commonly emerges in terms of identifiable symptoms of schizophrenia of "first episode" during adolescence or the early adult years (most commonly in the 17 or 18 to 25 year old range), I think there's almost always evidence of "ecentricity" and behavioral oddities long before that. The best evidence from current genetic research would suggest that the vulnerability at least is there from birth for most schizophrenias.