Haven't slept for more than two hours in last few days

The_Golden_Turd · August 22, 2016, 8:54pm

No, I mostly blame lives’ problems on philosophers who didn’t try hard enough to resolve issues at hand.

And given your solution to everything is to smoke weed, I’m not going to hold your prescriptive descriptions on the common ailes of life as too serious.

anand_droog · August 23, 2016, 7:07am

Your prejudice, your loss, Turd.

Also, I recommend vaping or ingesting, not smoking…

solution to EVERYthing? Nah. Weed, the good depressant, just calms down an overheated, stressed-out mind & body. It’s a medicine to be taken only if such things are going out of hand.
Some like it recreationally too, but in the rat race regular, recreational use imparts a competitive disadvantage in the quantitative walks of life, but at the same time also a theoretical advantage, boosted nonlinear thinking.
Given the beauty of nonlinear insight, true philosophers might not care about this disadvantage, especially if they live in a utopia

You’re right to blame the mainstream theoretically stunted “philosophers” though, who probably all hate weed. High on dopamine, they verbosely trick themselves into believing in their “philosophical genius”, although most of the times they are merely being syllogical, plausibly recycling and rearranging high amounts of low-quality information, not logical, mostly.

The_Golden_Turd · August 23, 2016, 8:28am

It isn’t my prejudice, it’s my consciousness, something you fail to see. I simply can’t and won’t, should be self evident why.

You keep pushing the dopamine aspect.

In order to understand the circuitry of the basal ganglia, one has to first understand the important participants in this circuit. Parts of the basal ganglia are in direct communication with the thalamus and the cortex. The cortex, thalamus, and the basal ganglia are, therefore, the three main participants in a circuit created by the basal ganglia.

At the top of the hierarchy lies the cerebral cortex. The cortex has many different areas with different functions. One such cortical area is called the primary motor cortex (along the pre-central gyrus). Specialized neurons from the primary motor cortex extend their axons all the way to the striatum portion of the basal ganglia. These cortical neurons release the neurotransmitter glutamate, which is excitatory in nature. Once excited by glutamate, the cells in the striatum project in two different directions giving rise to two major pathways: the “direct” and the “indirect” pathways:

In the direct pathway, cortical cells project excitatory inputs to the striatum, which in turn projects inhibitory neurons onto the cells of the SNr-GPi complex. The SNr-GPi complex projects directly onto the thalamus through the inhibitory ansa lenticularis pathway. The striatal inhibition of the SNr-GPi complex coupled with SNr-GPi inhibition of the thalamus therefore results in a net reduction of inhibition of the thalamus via the striatum. The thalamus projects excitatory glutamatergic neurons to the cortex itself. The direct pathway, therefore, results in the excitation of the motor cortex by the thalamus. Once stimulated, the cortex projects its own excitatory outputs to the brain stem and ultimately muscle fibers via the lateral corticospinal tract. The following diagram depicts the direct pathway:

Cortex (stimulates) → Striatum (inhibits) → “SNr-GPi” complex (less inhibition of thalamus) → Thalamus (stimulates) → Cortex (stimulates) → Muscles, etc. → (hyperkinetic state)
The indirect pathway also starts from neurons in the striatum. Once stimulated by the cortex, striatal neurons in the indirect pathway project inhibitory axons onto the cells of the globus pallidus externa (GPe), which tonically inhibits the subthalamic nucleus (STN). This inhibition (by the striatum) of the inhibitory projections of the GPe, results in the net reduction of inhibition of the STN. The STN, in turn, projects excitatory inputs to the SNr-GPi complex (which inhibits the thalamus). The end-result is inhibition of the thalamus and, therefore, decreased stimulation of the motor cortex by the thalamus and reduced muscle activity. The direct and indirect pathways are therefore antagonist in their functions. Following is a diagram of the indirect pathway:

Cortex (stimulates) → Striatum (inhibits) → GPe (less inhibition of STN) → STN (stimulates) → “SNr-GPi” complex (inhibits) → Thalamus (is stimulating less) → Cortex (is stimulating less) → Muscles, etc. → (hypokinetic state)

Main circuits of the basal ganglia. This diagram shows 2 coronal slices that have been superimposed to include the involved basal ganglia structures. The + and – signs at the point of the arrows indicate whether the pathway is excitatory or inhibitory, respectively, in effect. Green arrows refer to excitatory glutamatergic pathways, red arrows refer to inhibitory GABAergic pathways and turquoise arrows refer to dopaminergic pathways that are excitatory on the direct pathway and inhibitory on the indirect pathway.
The antagonistic functions of the direct and indirect pathways are modulated by the substantia nigra pars compacta (SNc), which produces dopamine. In the presence of dopamine, D1-receptors in the basal ganglia stimulate the GABAergic neurons, favoring the direct pathway, and thus increasing movement. The GABAergic neurons of the indirect pathway are stimulated by excitatory neurotransmitters acetylcholine and glutamate. This sets off the indirect pathway that ultimately results in inhibition of upper motor neurons, and less movement. In the presence of dopamine, D2-receptors in the basal ganglia inhibit these GABAergic neurons, which reduces the indirect pathways inhibitory effect. Dopamine therefore increases the excitatory effect of the direct pathway (causing movement) and reduces the inhibitory effect of the indirect pathway (preventing full inhibition of movement). Through these mechanisms the body is able to maintain balance between excitation and inhibition of motion. Lack of balance in this delicate system leads to pathologies such as Parkinson’s disease. Parkinson’s disease involves the loss of dopamine which means the direct pathway is less able to function (so no movement is initiated) and the indirect pathway is in overdrive (causing too much inhibition of movement).

My personality type is based on the indirect pathway. I’m naturally strongly averse to messing with it. Drugs don’t make me happy or lossen me up, they make me go numb. I don’t like doing, leads to reduced sensory integration. I go dumber as a result. It is a breakdown of self. A aspect very, very important in modern civilization.

Serotonin inhibits dopamine in the striosomal path.

It isn’t my prejudice that causes me to lose in this case, but what identifies me. I would lose myself if I followed your advice. An entire strata of personality types exists down this pathway, and your recommendations are akin to a sledge hammer being brought upon us. You don’t destroy the self of the patient/subject to treat a symptom causing duress. That’s barbaric.

anand_droog · August 23, 2016, 10:53am

Though i don’t understand the exact part of the human spectrum that you’re talking about,… still, i identify with you, if only because I’d put forth exactly the same argument as above when a shrink hired by my mom who worried for my style of quitting stupid (imo) jobs – offered me some shady dopamine boosting nostrums: Hey, i’m an inherently low dopamine kind of guy, i think it’s a pretty cool way of life, i’d rather choose this than stress, depression, baldness etc.

i hope you get back your sleep through some other means, then.
But you should still respect the necessity of quasi-anandamide in the body system. As the ancient Chinese medicine men said, it’s only when the right pulse gets stronger than the left pulse, not the other way around, that the human is in a disease state (lack of Chi energy/Norepi).

The_Golden_Turd · August 23, 2016, 11:46am

The Serotonin Receptor
Jose Alexandre Crippa and his colleagues at the University of San Paulo in Brazil and at the King’s College in London have conducted pioneering research into CBD and the neural correlates of anxiety.

At high concentrations, CBD directly activates the 5-HT1A (hydroxytryptamine) serotonin receptor, thereby conferring an anti-depressant effect. This receptor is implicated in a range of biological and neurological processes, including (but not limited to) anxiety, addiction, appetite, sleep, pain perception, nausea and vomiting.

5-HT1A is a member of the family of 5-HT receptors, which are activated by the neurotransmitter serotonin. Found in both the central and peripheral nervous systems, 5-HT receptors trigger various intracellular cascades of chemical messages to produce either an excitatory or inhibitory response, depending on the chemical context of the message.

CBD triggers an inhibitory response that slows down 5-HT1A signaling. In comparison, LSD, mescaline, magic mushrooms, and several other hallucinogenic drugs activate a different type of 5-HT receptor that produces an excitatory response.

projectcbd.org/how-cbd-works

Bad idea.

It is important to do a wide range typographical personality type of a person before administering any medication that effects neural transmitters, because personality types are heavily dependent on set configurations. It can lead to unintended consequences in one case, and seemingly none in another. I’m deeply reliant on these pathways, whereas only a few percents of the average population has a personality based in these areas. It wouldn’t be noticeable to most, but the few thinking in this mode, very very important to modern civilization. They are the top intellectuals, I’m not merely talking about philosophy… in science, engineering, architecture, business.