#dopamine agonists

[helenwhiteart-blog]

When the dopamine wears off...avoiding the next crash

I’ve been busy clocking the important effect dopamine has on pain and symptomatology since I first started noticing its close relationship to PEM (post exertional malaise) in ME/CFS. To recap, when you have ME/CFS, you have a fairly limited “energy envelope” in which you can safely operate without causing another crash back into fatigue, pain and other symptoms. However, the dopamine theory I…

[deinheilpraktiker]

Gefahren des Freizeit-/medizinischen Cannabiskonsums Laut dem Büro der Vereinten Nationen für Drogen- und Verbrechensbekämpfung ist Cannabis die am häufigsten konsumierte illegale Droge der Welt. Während Cannabis neben seiner medizinischen Verwendung zur Behandlung chronischer Schmerzen zunehmend als Freizeitdroge verwendet wird, gibt es kaum Beweise für seine Sicherheit. Einige Daten deuten darauf hin, dass die neurokognitiven Funktionen durch den Cannabiskonsum beeinträchtigt werden, wobei anatomische Verschlechterunge... #Abstinenz #Adenosin #Agonist #Amygdala #Analgesie #Antiphlogistikum #B_Zelle #Bipolare_Störung #Cannabidiol #Cannabinoid #Cannabis #chronisch #Chronischer_Schmerz #Depression #Dopamin #Drogen #Epilepsie #Forschung #Frequenz #Gehirn #Genetisch #Hippocampus #Kehle #Kehlkopfkrebs #Kopf_Hals_Krebs #Kortex #Krebs #Limbisches_System #Mikrobiom #Multiple_Sklerose #Nacken #Nervöses_System #Neuroimaging #Noradrenalin #Operation #Opioide #Placebo #Rauchen #Rausch #Rezeptor #Schizophrenie #Schmerz #Schmerztherapie #Sklerose #Sucht #Tabak #Tetrahydrocannabinol #Toxine #Verbindung #Wachstumsfaktor #Zelle #Zentrales_Nervensystem #Zunge

[bonefall]

if something is an agonist to glutamate receptors, that means a clan cat would think it tastes good, right?

Oh no, honey, that's not taste buds that's neurotransmitter stuff. That's brains

You're thinking of glucose. Glucose is sugar. Glutamate is from glutamic acid and related to "umami" flavors, but in the form you said, you're talking about its use in biochemistry

An agonist is a chemical that binds to a receptor and produces a similar response. Like.... ADHD meds! If you're taking an agonist to dopamine receptors, the medication will act LIKE dopamine. Even though it is not dopamine.

Glutamate is used in a ton of nervous system processes, so if you're talking about a glutamate agonist, you're talking about memory, nerve processes, motor functions, etc. Not taste buds.

That's where my knowledge ends tho, I know basic medicinal chemistry just enough for funny cat herb guides but not to give you an in-depth lecture on glutamate. A chemist is what you're looking for! But no, glutamate doesn't work that way.

[pro-birth]

While cabergoline (and other dopamine agonists) are not the only drugs that can inhibit angiogenesis, the Boston and Brigham researchers believe that cabergoline has a better safety profile compared to other drugs with the same effect. They are currently enrolling more women in a new clinical trial to attempt to increase their sample size and glean more information about the potential benefits of cabergoline for endometriosis-related pain (this time, compared to a placebo). 

With a larger sample size, the researchers can also measure how (or if) cabergoline helps reduce other symptoms of endometriosis, like infertility or irregular bleeding, plus whether cabergoline shrinks endometriosis lesions or prevents or slows existing lesion growth. A tiny 2011 study of just nine women found that another dopamine agonist, quinagolide, decreased endo lesions by 69.5% over the course of 20 weeks [7]. Might cabergoline do the same? 

[luxe-pauvre]

Rather than thinking of it as a disease of the same kind as schizophrenia, I tend to think of addiction as the result of a mismatch between our evolved brain and our modern environment. In chapter 7 we discussed the brain's system for making choices, and the central role of dopamine in creating habits. All forms of addiction seem to involve dopamine; in fact, many of the most powerful drugs of addiction are those that directly affect the dopamine system in the brain. Cocaine causes a flood of dopamine in the synapses between neurons by turning off a chemical pump that usually sucks extra dopamine from the synapse back into the cell so that it can be recycled and used again. Amphetamines can actually cause these pumps to go in reverse, spewing out even more dopamine into the synapse. Other drugs of abuse (including alcohol and nicotine) have more indirect effects on dopamine, but ultimately it seems that dopamine is the key to all forms of addictive behaviour. The fact that dopamine agonist medication for Parkinson's disease can cause strange addictions (as I mentioned in chapter 7) provides even stronger evidence for this idea. All of this is due to two of dopamine's main effects: it causes us to be motivated to obtain rewards ("wanting") and it increases the likelihood that any action that results in dopamine release will be repeated in the future, turning behaviours into habits. Our brains evolved in a world where the strongest stimulation that our dopamine system ever received was probably from sexual intercourse. The foods that our hunter/gatherer ancestors ate were almost certainly healthier than those that most humans eat today, but it's doubtful that they were particularly tasty given that there was little access to salt, sugar, or spices, and whatever fruits they scavenged had not been bred for flavour like the supersweet strawberries and apples that we eat today. Fast-forward to modern society, and we now have access to an enormous number of ways to stimulate our dopamine system that go far beyond what evolution had prepared us for, from highly palatable junk foods to both legal and illegal drugs that stimulate dopamine release in ways that were unprecedented in our evolutionary history.

Russell Poldrack, The New Mind Readers: What Neuroimaging Can and Cannot Reveal About Our Thoughts

[dorianbrightmusic]

New Antipsychotic FDA Approval – Cobenfy

Cobenfy (xanomeline/trospium chloride) has just been approved for schizophrenia treatment in the US. This is huge. It's the first antipsychotic in decades to not target dopamine directly. It's got a much, much better side-effect profile, and it might work for negative and cognitive symptoms.

FOR MORE READING – news report/patient-centred plain language overview: See here.

FOR MORE READING – scientific evidence report: See here (note: the drug is referred to as 'KarXT' in this report).

I couldn't be happier right now. People with psychosis go through so, so much trying to find medications that are both useful and tolerable, and psychiatry has historically neglected psychotic people's needs so, so awfully. (Not to mention how little there is that actually helps with anything other than positive symptoms.) So I'm really, really hoping that with the proof that we can, in fact, make antipsychotics that aren't based on the same old pharmacological things we've tried before. Cobenfy is a muscarinic agonist/antagonist in fixed combination – and it also indirectly regulates dopamine and glutamate. And given that we know both dopamine and NMDA are probably involved in schizophrenia somehow – AND that treating things to do with either is hard – this is so, so, so exciting.

This isn't to say Cobenfy doesn't have side-effects (the most common ones being nausea, constipation, dyspepsia, vomiting, hypertension, dry mouth, and tachycardia. We also know that there is a small risk of extrapyramidal symptoms, and that prolactin-related side-effects do happen, unfortunately). We don't know much about how it affects folks in the long-term, or much about the long-term tardive dyskinesia risk. But even so, it's progress compared to some of the worse antipsychotic side-effects.

Moreover, there is a possibility it might be useful for negative and cognitive symptoms. Holy crap.

I'm really really really excited. I hope this is the start of a shift in psychiatry towards better standards of patient-centred care for psychosis. Y'all have deserved better for far too long – here's hoping this is the start of more ethical, effective treatment.

[detentiontrack]

Cartoons are my only normal interests. I have two things I’m currently reading and they are an amphibia fanfiction on ao3 and an APA PsycNet journal article entitled “indirect and direct cannabinoid agonists differentially affect mesolimbic dopamine release and related behaviors”

[covid-safer-hotties]

SARS-CoV-2 spike protein acts as a β-adrenergic receptor agonist: A potential mechanism for cardiac sequelae of long COVID - Published July 29, 2024

Abstract Background Currently, pathophysiological mechanisms of post-acute sequelae of coronavirus disease-19-cardiovascular syndrome (PASC-CVS) remain unknown.

Methods and results Patients with PASC-CVS exhibited significantly higher circulating levels of severe acute respiratory syndrome-coronavirus-2 spike protein S1 than the non-PASC-CVS patients and healthy controls. Moreover, individuals with high plasma spike protein S1 concentrations exhibited elevated heart rates and normalized low frequency, suggesting cardiac β-adrenergic receptor (β-AR) hyperactivity. Microscale thermophoresis (MST) assay revealed that the spike protein bound to β1- and β2-AR, but not to D1-dopamine receptor. These interactions were blocked by β1- and β2-AR blockers. Molecular docking and MST assay of β-AR mutants revealed that the spike protein interacted with the extracellular loop 2 of both β-ARs. In cardiomyocytes, spike protein dose-dependently increased the cyclic adenosine monophosphate production with or without epinephrine, indicating its allosteric effects on β-ARs.

Conclusion Severe acute respiratory syndrome-coronavirus-2 spike proteins act as an allosteric β-AR agonist, leading to cardiac β-AR hyperactivity, thus contributing to PASC-CVS.

[neuroticboyfriend]

daily reminder that seroquel (quetiapine) is not just an antipsychotic. it is also a potent:

antihistamine (for example, benadryl is an antihistamine)

dopamine antagonist (blocker)

alpha blocker (blocks adrenaline)

anticholinergic (blocks acetylcholine, another very important brain chemical)

serotonin... partial agonist, antagonist, and receptor ligand. alright then.

these are not even all the other drug functions it has. you may not know what all these words mean but basically this means seroquel (and antipsychotics in general) really plays with your nervous and endocrine system. inherently.

they do not tell us this kind of thing when they prescribe these medications, despite the far reaching negative effects antipsychotics can have on us. i feel like we have a right to know what is being put into our body. so. yeah.

(if anything here is wrong, someone feel free to correct me)

[transmutationisms]

i'm generally on the same page as you about addiction adhd etc but there's pretty good evidence that dopamine agonist drugs (often used to treat parkinson's) have the common side effect of inducing compulsive behaviors such as gambling addiction in people who previously had no trouble with those behaviors, which seems like the clearest example i could imagine of addictive behavior with a "purely chemical" basis

inb4 someone starts saying this about ozempic

[ordinarytalk]

Dopamine, migraines, and ADHD

Y'all.

I had a bad migraine today, pain 8/10, and I noticed I was yawning constantly all day. Out of curiosity, once I had recovered enough that I could take off the blindfold, I looked up "do migraines make you yawn."

Yeah. Migraines can make you yawn. They make you yawn because it's a dopaminergic symptom. Migraines involve fluctuations in dopamine, and people who have more of the dopaminergic symptoms (yawning, drowsiness, fatigue, nausea, mood swings, and increased urination) also tend to have migraines that are longer and worse.[1]

Not only that, it turns out that migraines are much more common in people with low dopamine.

"ADHD is caused by low dopamine," thought, so I looked up ADHD and migraine. Yeah! ADHD and migraine are correlated.[2] Low dopamine levels can increase the risk of ADHD, migraine, sleep disorders, and pain disorders. Dopamine-signaling cells are part of neural pathway for perceiving pain.

Here's how low dopamine makes migraines worse:

If you naturally have a low level of dopamine in your body, your body will try to adjust by increasing the amount or sensitivity of your dopamine receptors.

Dopamine levels rise during the migraine prodrome (the part before the pain hits).

The dopamine receptors will start firing at a lower dopamine level than normal, because they're all super-sensitive to deal with chronic low dopamine.

Now everything hurts for no damn reason.

Outside of me realizing that the low dopamine is, yet again, my personal villain, I also learned something else kind of cool: Dopamine antagonists (meds that lower dopamine activity) can help stop a migraine once it's started, but dopamine agonists (meds that increase dopamine activity) can prevent migraines from happening.[3]

That makes sense, if you think about it. If you're already mid-migraine, you need the dopamine turned off so your pain receptors can reset. And if you don't have chronic low dopamine to start with, your body won't make your dopamine receptors super sensitive.

My point for this entire post: There's evidence that taking ADHD meds can help prevent migraines.[4]

All I could find was one single preliminary study looking at this, but the results were very promising. I know that I personally have noticed less frequent migraines since I got on Adderall.

The fact that no one is studying this is driving me bonkers. I might actually try to email some college professors out of the blue to look at this. Hey! If you're in neuroscience and you're reading this, maybe study dopamine agonists as a method of preventing migraine!

(sources below cut)

[1] Barbanti et al. (2020). Dopaminergic symptoms in migraine: A cross-sectional study on 1148 consecutive patients. International Headache Society. https://journals.sagepub.com/doi/10.1177/0333102420929023

[2] Hansen et al. (2018). Comorbidity of migraine with ADHD in adults. BMC Neurology. https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-018-1149-6

[3] Gelfand, A.A., Goadsby, P.J. (2012) A Neurologists's Guide to Acute Migraine Therapy in the Emergency Room. Neurohospitalist. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3737484/

[4] Haas, D., Sheehe, P. (2004) Dextroamphetamine pilot crossover trials and n of 1 trials in patients with chronic tension-type and migraine headache. Headache. https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/j.1526-4610.2004.04199.x

[brightlotusmoon]

Masturbation to Orgasm Stimulates the Release of the Endocannabinoid 2-Arachidonoylglycerol in Humans | The Journal of Sexual Medicine | Oxford Academic

Endocannabinoids are critical for rewarding behaviors such as eating, physical exercise, and social interaction. The role of endocannabinoids in mammalian sexual behavior has been suggested because of the influence of cannabinoid receptor agonists and antagonists on rodent sexual activity. However, the involvement of endocannabinoids in human sexual behavior has not been studied.

_

This is from 2017. As of 2024, we definitely know that there's endocannabinoids in our blood after an orgasm, whether masturbation or partnered sex.

This is probably why so many stoners feel like their minds become clear and free and uninhibited - because the cannabinoids are sparking surges of dopamine, serotonin, oxytocin, endorphins. No wonder G Gordon Liddy tried so hard to shut down cannabis use. You cannot control a free mind.

[compneuropapers]

Interesting Papers for Week 31, 2023

Abnormal evidence accumulation underlies the positive memory deficit in depression. Cataldo, A. M., Scheuer, L., Maksimovskiy, A. L., Germine, L. T., & Dillon, D. G. (2023). Journal of Experimental Psychology: General, 152(1), 139–156.

Internal neural states influence the short-term effect of monocular deprivation in human adults. Chen, Y., Gao, Y., He, Z., Sun, Z., Mao, Y., Hess, R. F., … Zhou, J. (2023). eLife, 12, e83815.

Mesolimbic dopamine adapts the rate of learning from action. Coddington, L. T., Lindo, S. E., & Dudman, J. T. (2023). Nature, 614(7947), 294–302.

Sensorimotor feedback loops are selectively sensitive to reward. Codol, O., Kashefi, M., Forgaard, C. J., Galea, J. M., Pruszynski, J. A., & Gribble, P. L. (2023). eLife, 12, e81325.

Multiphasic value biases in fast-paced decisions. Corbett, E. A., Martinez-Rodriguez, L. A., Judd, C., O’Connell, R. G., & Kelly, S. P. (2023). eLife, 12, e67711.

Hippocampal–cortical coupling differentiates long-term memory processes. Dahal, P., Rauhala, O. J., Khodagholy, D., & Gelinas, J. N. (2023). Proceedings of the National Academy of Sciences, 120(7), e2207909120.

The visual encoding of graspable unfamiliar objects. Federico, G., Osiurak, F., Brandimonte, M. A., Salvatore, M., & Cavaliere, C. (2023). Psychological Research, 87(2), 452–461.

Complex economic decisions from simple neurocognitive processes: the role of interactive attention. He, L., & Bhatia, S. (2023). Proceedings of the Royal Society B: Biological Sciences, 290(1992), 20221593.

Behavioral encoding across timescales by region-specific dopamine dynamics. Jørgensen, S. H., Ejdrup, A. L., Lycas, M. D., Posselt, L. P., Madsen, K. L., Tian, L., … Gether, U. (2023). Proceedings of the National Academy of Sciences, 120(7), e2215230120.

Olfactory receptor neurons generate multiple response motifs, increasing coding space dimensionality. Kim, B., Haney, S., Milan, A. P., Joshi, S., Aldworth, Z., Rulkov, N., … Stopfer, M. A. (2023). eLife, 12, e79152.

Local memory allocation recruits memory ensembles across brain regions. Lavi, A., Sehgal, M., de Sousa, A. F., Ter-Mkrtchyan, D., Sisan, F., Luchetti, A., … Silva, A. J. (2023). Neuron, 111(4), 470-480.e5.

D2/3 Agonist during Learning Potentiates Cued Risky Choice. Mortazavi, L., Hynes, T. J., Chernoff, C. S., Ramaiah, S., Brodie, H. G., Russell, B., … Winstanley, C. A. (2023). Journal of Neuroscience, 43(6), 979–992.

Coordinated drift of receptive fields in Hebbian/anti-Hebbian network models during noisy representation learning. Qin, S., Farashahi, S., Lipshutz, D., Sengupta, A. M., Chklovskii, D. B., & Pehlevan, C. (2023). Nature Neuroscience, 26(2), 339–349.

Distinct early and late neural mechanisms regulate feature-specific sensory adaptation in the human visual system. Rideaux, R., West, R. K., Rangelov, D., & Mattingley, J. B. (2023). Proceedings of the National Academy of Sciences, 120(6), e2216192120.

Single spikes drive sequential propagation and routing of activity in a cortical network. Riquelme, J. L., Hemberger, M., Laurent, G., & Gjorgjieva, J. (2023). eLife, 12, e79928.

Testing, explaining, and exploring models of facial expressions of emotions. Snoek, L., Jack, R. E., Schyns, P. G., Garrod, O. G. B., Mittenbühler, M., Chen, C., … Scholte, H. S. (2023). Science Advances, 9(6).

Distinct replay signatures for prospective decision-making and memory preservation. Wimmer, G. E., Liu, Y., McNamee, D. C., & Dolan, R. J. (2023). Proceedings of the National Academy of Sciences, 120(6), e2205211120.

A dopaminergic reward prediction error signal shapes maternal behavior in mice. Xie, Y., Huang, L., Corona, A., Pagliaro, A. H., & Shea, S. D. (2023). Neuron, 111(4), 557-570.e7.

A discipline-wide investigation of the replicability of Psychology papers over the past two decades. Youyou, W., Yang, Y., & Uzzi, B. (2023). Proceedings of the National Academy of Sciences, 120(6), e2208863120.

Development of dynamic attention: Time-based visual selection for objects in motion between 6–12 years of age. Zupan, Z., Blagrove, E. L., & Watson, D. G. (2023). Developmental Psychology, 59(2), 312–325.

[justkidneying]

from the previous ask

antipsychotics like risperidone or aripiprazole with gabapentin in combination with alcohol

i know they're particularly nonlethal but I don't know what type of reaction they'd have to alcohol

Okay, thanks for the details!

So Gabapentin acts indirectly on calcium channels, which makes it a great anticonvulsant. The side effects (or effects of taking too much) would be drowsiness and respiratory depression. Aripiprazole is a dopamine receptor agonist, and side effects include drowsiness and vomiting/nausea. Risperidone acts on serotonin and dopamine receptors and has side effects such as muscle coordination issues and drowsiness.

So the main issue with drinking alcohol with these is that alcohol is a depressant, and can cause drowsiness and muscle coordination issues. Respiratory depression is what I am worried about. I've seen a case of someone who took a bunch of gabapentin, oxy, and drank half a bottle of vodka. They passed out, vomited (as the body does when you ingest toxins), and aspirated on their vomit. Horrible way to go, in my opinion.

Let me know in the comments if you have more questions, hope I covered some of what you wanted!

[questionsquartzquiet]

Medical School Journey

Big focus on pharm

Little focus on bugs 🦠

Studied at cafe then at home for a bit

Feeling a little under the weather so let myself nap as long as I needed to

Lots of flashcards on MSK and neuro

Got Thai with my husband

Reviewed

Antiepileptics, local anesthetics, general anesthetics, muscarinic antagonists, cholimimetics, neuromuscular blocking agents, dopamine agonists, comt inhibitors, mao-b inhibitors

Listeria, neisserias, haeomphilus

While it’s hard to catch a break the week before an exam, I always find 4-5 days before taking time to rest and sleep in always helps me pull off my final stretch of studying

[t4t4t]

https://en.m.wikipedia.org/wiki/Abulia

Most current treatments for abulia are pharmacological, including the use of antidepressants. However, antidepressant treatment is not always successful and this has opened the door to alternative methods of treatment. The first step to successful treatment of abulia, or any other DDM, is a preliminary evaluation of the patient's general medical condition and fixing the problems that can be fixed easily. This may mean controlling seizures or headaches, arranging physical or cognitive rehabilitation for cognitive and sensorimotor loss, or ensuring optimal hearing, vision, and speech. These elementary steps also increase motivation because improved physical status may enhance functional capacity, drive, and energy and thereby increase the patient's expectation that initiative and effort will be successful.[2]

There are 5 steps to pharmacological treatment:[2]

Optimize medical status.

Diagnose and treat other conditions more specifically associated with diminished motivation (e.g., apathetic hyperthyroidism, Parkinson's disease).

Eliminate or reduce doses of psychotropics and other agents that aggravate motivational loss (e.g., SSRIs, dopamine antagonists).

Treat depression efficaciously when both DDM and depression are present.

Increase motivation through use of stimulants, dopamine agonists, or other agents such as cholinesterase inhibitors.