MindStream 1

 

This is an experimental style post. I will research and show my research in a way that reveals my actual thought processes. Raw brain-data. If I/you like this, there will be a series of these posts, perhaps anytime I am lazy and researching minimalistic-style, as opposed to writing some fully coherent post.

What is psychotic depression?

So I searched it

Does Wikipedia Know?

wikipedia

No, this answer is incomplete, although, it is very interesting that it doesn’t mention schizophrenia as a possible context, only bipolar and depressive disorder.

Does Google Scholar Know?

Oh, I’ve decided red hypothesis text means it’s a failed hypothesis. For faster reading.

Hypothesis:

censored

This bothered me so much I had to shredder-censor it.

My recent fetish has been dynorphin. Interestingly, that could mean something on many levels, if you know what I mean ;). Joking aside, I am frustrated that my search seemed to not even bring up any results actually referring to this concept of psychotic depression. But don’t fret, Google scholar does produce results for psychotic depression, in general.

This means we must do some. . .

digging.

First Hypothesis

abstract 1

Link To Above Study Here

 

Hypothesis

Second hypothesis

A team of scientists abusively handled rats but found out  that both 8-OH-DPAT and DOI may be capable of stimulating corticosterone secretion through an ACTH-independent mechanism. (Endocrinology126: 1888–1894,1990) << You must read the abstract.

I know that low densities of 5HT2a in the DorsoLateral Prefrontal Cortex (DLPFC) receptors is correlated to depression and bipolar disorder, while schizophrenics aren’t affected by changes to DLPFC 5HT2a receptors. This could theoretically be due to downregulation by serotonin or DMT overstimulating the receptors.

Important Question

Do the effects of high densities of a receptor mimic receptor agonism effects, specifically due to increased tendency to be bound by endogenous ligands of the receptor type?

If the answer is yes, then we might expect that high density of receptors due to less binding of endogenous ligands might mimic the effects of high amounts of the same endogenous ligand, because the chance of binding might be higher, despite less of the neurotransmitter to bind to it, and also we should expect that the under-activated receptors, as well as their downstream mechanisms, to be more reactive.

F A C T ?

This means that both high receptor density and low receptor density of a specific receptor type could signify hyperactivity of the effects linked to that receptor type.

Hypothesis

The corticosteroid/dopamine hypothesis for psychotic depression could involve endogenous 5HT2a agonist mechanisms.

-Not Relevant, But These Sort Of Blew My Mind-

1

The in vitro identification of dimethyltryptamine (DMT) in mammalian brain and its characterization as a possible endogenous neuroregulatory agent

Random 1

2

Hypothesis: DMT could function as an endogenous degree-of-abstraction synchronizing agent for humans to reach the same level of abstraction, as each other, in order to facilitate language development and aide in communication, sociability, and also play a crucial role in domestication. There is evidence in theories about domestication and schizophrenia, which involves correlations to adrenocortical changes, across species, which alter working memory function, across species. These theories propose that schizophrenia evolved from sociability and is essentially a condition of hyper-domestication, where autism is consider hypo-domestication. Adrenocortical changes are linked to changes in working memory within our species as well. Now we have found a link between 5HT2a agonists and corticosteroid function, giving rise to the possibility of a social function of endogenous DMT. Directionality of these correlations between  will be found. It would be even more fascinating if 5HT2a ‘tunes’ time-perception and attention sharpness/diffusion via heteromeric interactions with D2 dopamine receptors. There could be a mechanism here that allows for increased mirror neuron reactivity, or enhanced similarity between members of our species that allows for better functioning of our theory-of-mind processing, simply due to increased overlapping of similarities, and less information to process. This concept could even explain this dichotomy between autism and schizophrenia that seems to exist along an axis of hypo-domestication to hyper-domestication. Mirror neurons could be the basis for hive-minding. 

Evidence

Serotonin and MAO A implicated in domestication

Domestication alters 5-HT1A receptor binding in rat brain

Increased 5HT1a in schizophrenics

5HT1a and 5HT2a alterations in schizophrenia

Social behavior and 5HT2a and 5HT1a

5HT2a and autism

5HT1a and autism

Multiple neurotransmitters and autism

Seasons and neuroendocrinology – bipolar relevant

Chicken domestication, D2 receptors, and motivation for food

D2 and D3 modulate sociability

These findings will be explored and added to my post on domestication, seen below.

 

Dog Infant
 

A Case For Animal Cognition

 

 

 

-Now Moving Back To Our Main Plot-

To Be Continued. . .

 

 

 

 

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