Why don't you first identify the neurochemical interaction determining the binding sites on the molecule and its mechanism for delivering the psychological impact you are desiring. I remember there has been some study of this but it certainly requires more anyway.
My point is then you might be able to synthesize an 'analog' that is both more absorbed and able to better pass the blood brain barrier. However that would only begin the process of identifying detrimental side effects but after all this is how the pharaceuticals make the big bucks.
I typed this response up to somebody in the past and would like to add it to this thread since it may be interestingn in regards to answering more on how these chemicals work...
There's a chapter in this book that I have ("Cognitive Enhancement Drugs" edited by J.J. Buccafisco) that gives some general insight in the chapter that starts on pg.115 on oxytocine and vasopressin...
http://books.google.com/books?id=OfFoTzKQr...lt&resnum=3It appears both these peptides are produced by neurons within the posterior pituitary area where:
Vasopressin is released as a hormone triggered by a feedback mechanism telling the body to increase blood pressure and for the kidneys to absorb more water (anti-diuretic hormone).
Oxytocine is released as a hormone triggered by a feedback mechanism (in females) for contraction.
Here's where it gets interesting:
Vasopressin:
The nuerotransmitter effect of both peptides seem to be seperate (but sometimes connected) from the hormonal mechanism of release and action.
It appears that Vasopressin's (AVP) central nueral systems where "they and their breakdown products have nueromodulatory (possibly meaning influencing both the post-synaptic as well as pre-synaptic receptor in indirect ways) roles independent of "neurohypophysis" (whatever that means). It appears that various receptors distributed throughout the hippocampus, amygdala, and Septum are implicated in learning and memory. The 2 central pathways seem to be the AVP type 1 receptors (these "activate protein kinase C+" and increase cytosolic Ca2+). Also, there are AVP type 2 receptors (these simulate adenylate cyclase
and oxytocine receptors). Also, it appears both types of receptors have a sort of nueromodulatory connection to "Acetylcholine".
AVP as well as it's analogues (that have no hormonal effect) help restore learning and memory according to various studies (specifically in rats with diabetes insipidus). The analogues (not sure if these are administerable or not) include:
AVP (4-9)-this is devoid of hormonal activity and enhances radial maze performance (tester for aquisition and work memory)
AVP (4-8)-improves concept learning (win-stay and loose shift) in rats with hippocampal lesion (not in rats with PFC lesions)
NC-1900-enhances place learning in rats with "Cyclohexamide" caused hippocampus lesions
Overall, this seems to mean that AVP and it's analogues seem to counteract with lesions (chemically or physically induced) and be seperate from the hormonal (pressor) actions of AVP. Also, tt's effect on learning and memory could account for some companies like Antiaging Systems marketing the product for post-traumatic amnesia among other things.
I'm not sure to what extent the analogues mentioned above target AVP 2 receptors or not (the effects cited in the 2 senteces above seem to be mainly tied to AVP 1 receptors but I'm not sure); if they do judging by what's mentioned above, they could effect oxytocine receptors as well.
Oxy
Based on what I've read on oxytocine, it appears that it's transmitter effect impairs memory retention in inhibitory avoidance
(in contrast to AVP), which happens as a result of modulating the acetylcholine system
(AVP appears to increase memory retention in inhibitory avoidance thru modulating the acetylcholine system so there appears to be a sort of oppisite effect at least in this regard).
While Oxytocine may impair memory retention in inhibitory avoidance, it appears that oxytocine increases the acquisition and consolidation phase of memory, which accounts for the increase in "social memory". Vasopressin does this as well but just thru different pathways.
It appears that both Vasopressin and Oxytocine act via fast nueral pathways (due to both peptides having a dual role as both a hormone and a nuerotransmitter) by "altering the permeability of pre+post ion channels. Both these peptides can also have release mechanisms (tied to transmitter) that are seperate from the hormonal release mechanisms.
However, the hormonal action of oxytocine seems to still be tied pretty strongly to it's nuerotransmitter action. For instance, I read that females seem to have increased spatial memory during periods of lactation or pregnancy when more oxytocine is released, which leads to a "MAP kinase cascade"+CREB phosphorylation that leads overtime to increased hippocampus plasticity and LTP (this supposedly helps mothers remember where their offspring is and accounts for increased social memory). This neurological effect is mainly due to oxytocine acting as a modulator and not due to inducing a specific receptor expression. This has lead many researchers into trying to develop therapies to induce oxytocine in the brain along with other seperate studies not tied to oxytocine such as how estrogen seems to have an effect on NMDA receptors.
Very interesting stuff. Hopefully, this doesn't seem to confusing. Alot of this stuff is crammed into like 2 pages of this article that I found in that book I mentioned. I'm not sure what it all means really but hopefully this is some help.
I'm thinking some of the vasopressin analogues may be worth looking into...