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Monterey Bay Aquarium
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TVSTRANGERTHINGS
DEAR READER
I'd rather be in outer space 🛸
Mike Driver
let's talk about Bridgerton tea, my ask is open
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PUT YOUR BEARD IN MY MOUTH
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PR's Tumblrdome
2025 on Tumblr: Trends That Defined the Year
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shark vs the universe
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Aqua Utopia｜海の底で記憶を紡ぐ
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Gout: Facts and Information
Gout: Facts and Information
Story at-a-glance Gout is a complex disorder that’s becoming prevalent in the United States and many developed countries. Almost two to five million Americans, 90 percent of them men in their 40s or older, currently suffer from this ailment. Conventional medicine tells you that the only way to treat and relieve gout is to take drugs and painkillers, but I disagree – there are natural ways to…
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i’m so past being a taylor swift fan, i’m like an extreme fan. i’m a non-stop fan. i’m like an air conditioner. a taylor swift air conditioner.
Jay Adams circa 1970 ~ Early 70s “In contests, Jay was simply the most exciting skater to watch. He never skated the same run the same way twice. His routines were wickedly random yet exceedingly tight and beautiful to watch; he even invented tricks during his runs. I’ve never seen any skater destroy convention and expectation better. Watching him skate was something new every second - he was ‘skate and destroy’ personified.” - Stacy Peralta
Thinking about making good use of this blog.
Because reasons.
Oh, just pissin’ in the wind..
Hallucinogens Lecture
NMDA R Antagonists: 3 types
low addiction potential for psychedelics
Phencyclidine (PCP)
dissociative anaesthetics
related to ketamine (“K”)
produce hallucinations → distort reality
noncompetative antagonist @ NMDA R ONLY
Low dose
produces an alcohol-like effect initially (giddy, drunken-like state, disinhibition)
reduces NMDA R function
Moderate dose
produce analgesic effects
distortion of space and time
High dose
model of acute schizo
b/c of acute distortion of reality
Reinforcing effects
readily SA in animal models to point of intoxication
Mechanisms of PCP action
inhibit NMDA R function, doesn’t bind to Glu
is part of NMDA GLuR
Dextromethorphan (DXM)
found in cough medicine
effects similar to PCP, ketamine
b/c DXM inhibits NMDAR
Glutamate Rs: NMDA, Kainate, AMPA
Major excitatory mechanism in brain
Ionotropic subtypes
non-NMDA types
AMPA
Kainate
NMDA
Metabotropic
Endogenous ligand
unknown
Other actions of PCP
enhances DA release, VTA firing → evidence of reinforcing effects
Ketamine as an antidepressant
prozac, ssri = slow acting antidepressants, not helpful b/c of suicide, etc.
ketamine is faster acting
NMDA R antagonist
Hallucinogens
the appearance of something not there
pseudohallucination = distortion of reality
Psychotomimetic = ability to mimic psychosis
psychedelic = pleasurable to the mind
empathogen-entactogen = increase feeling of empathy
3 Major classes
#1 The LSD Family - Indole type
lysergic acid
have endo ring (ring also found in 5-HT)
regid serotonin molecule
binds strongly to 5-HT
structurally similar to 5-HT
reaches serotonin R → action on the brain
no evidence of tolerance
#2 LSD type hallucinogens
DMT
Morning glory seed
bufotenin
PSILOCYBIN + PSILOCIN
magic mushrooms
Mechanisms of action
initial studies: peripheral tissues
5-ht antagonist
LSD + hallucinogens binds to 5-HT-2A Rs = Agonist
#3 The Phenylethylamines
methosyamphetamines
synthetic derivative of mescaline
Mescaline
MDMA (‘Ecstasy’)
loss of 5-HT = up-regulation of 5HT2A Rs
Ecstasy and Brain 5HT
Ecstasy(MDMA) releases 5HT
MDMA causes loss of 5-HT in animals
memory loss
higher levels of 5HT2A Rs in brain
partial recovery of deficits possible over time
1880 mg of DXM, as well as two blunts in honor of 420.
Stacking, proud to see C's used responsibly. :') They DO have their place in certain trips.. Like I know CPM is so bad and killer on the liver... But has anyone else noticed they really do add an extra something to the trip? I have noticed this. After 6 years of DXM use and brain exploration, I am finally realizing this. Thoughts? Opinions? Experiences? Please share with me.
Reviving drugs with anti-stroke potential, minus side effects
In the 1990s, neuroscientists identified a class of drugs that showed promise in the area of stroke. NMDA receptor antagonists could limit damage to the brain in animal models of stroke. But one problem complicated testing the drugs in a clinical setting: the side effects included disorientation and hallucinations.
(Image caption: Schematic representation of the NMDA receptor complex. NMDA receptor antagonists can have beneficial effects in animal models of stroke, but also have pronounced side effects such as disorientation and hallucinations)
Now researchers have found a potential path around this obstacle. The results were published in Neuron.
“We have found neuroprotective compounds that can limit damage to the brain during ischemia associated with stroke and other brain injuries, but have minimal side effects,” says senior author Stephen Traynelis, PhD, professor of pharmacology at Emory University School of Medicine.
“These compounds are most active when the pH is lowered by biochemical processes associated with injury of the surrounding tissue. This is a proof of concept study that shows this mechanism of action could potentially be exploited clinically in several conditions, such as stroke, traumatic brain injury and subarachnoid hemorrhage.”
In a mouse model of ischemic stroke, a NMDA receptor antagonist called 93-31 can reduce the volume of damaged brain tissue by more than half, researchers found. At the same time, giving mice 93-31 does not seem to lead to the side effects seen with other NMDA receptor antagonists.
The drugs phencyclidine (also known as PCP) and ketamine are NMDA receptor antagonists; their ability to block all subtypes of NMDA receptors is thought to account for their psychoactive side effects. NMDA receptors are abundant on the surfaces of brain cells and play key roles in healthy processes such as memory formation.
In brain tissue affected by stroke or traumatic injury, the environment becomes more acidic because of the lack of oxygen and the buildup of metabolites such as lactic acid. In addition, NMDA receptors get overstimulated by an increase in the neurotransmitter glutamate – enough to kill cells. Researchers reasoned that NMDA receptor antagonists whose activity is dependent on acidic conditions should, at the right dose, be active only in the injured areas of the brain.
To identify the new pH-dependent drugs, Emory pharmacologists led by Traynelis and Ray Dingledine, PhD collaborated with chemists Dennis Liotta, PhD and James Snyder, PhD. The co-first authors of the Neuron paper are pharmacology instructor Hongjie Yuan PhD, chemistry postdoctoral fellow Gordon Wells, PhD and Scott Myers, PhD, director of drug discovery at Atlanta-based pharmaceutical company NeurOp.
In medicinal chemistry terms, 93-31 is ten times more potent at pH 6.9, typical for ischemic tissue with an insufficient blood supply, than at pH 7.6, close to the value for healthy brain tissue.
In collaboration with Katherine Nicholson, PhD at Virginia Commonwealth University, the researchers tested 93-31 on mice trained to press a lever when they detect low levels of PCP. When researchers substituted 93-31 for PCP, the mice did not perceive 93-31’s subjective effects to be similar enough to PCP’s to respond by pressing levers in the same way.
Doses of 93-31 that had a positive effect in the stroke model did not seem to impair coordination or motor function. The mice could still hold onto a turning rod, in contrast with mice dosed with other NMDA receptor antagonists.
The research that led to 93-31’s identification has been a platform for further drug discovery efforts by NeurOp, according to the company’s CEO, Barney Koszalka, PhD. However, 93-31’s pharmaceutical profile may not be optimal for further development, he says. In mouse experiments in the Neuron paper, 93-31 was either injected directly into the brain or into the body cavity.
NeurOp is developing a related candidate drug as a potential preventive measure for people who experience subarachnoid hemorrhage, because they have a high risk of a secondary stroke-like event for days after the initial hemorrhage. NeurOp is completing safety studies and is planning to file an Investigational New Drug application with the FDA later in 2015.
“We are taking an analogue of the compound identified in the Neuron paper forward as a post-surgical treatment for individuals that have suffered a subarachnoid hemorrhage,” Koszalka says. “The pH boost we see with this series of subunit specific NMDA modulators is expected to provide an additional safety advantage.”
My absolute favorite class of drugs. NMDA receptor antagonists. DXM, memantine, MXE, and Ketamine specifically. (In that order) I have yet to get wet, but not ruling that out in the future.
Yessss
About that life.
