I am curious if there is a drug out there that can induce REM sleep? Mabey Ill go as far as to ask if there are any that can force REM sleep? I have a few questions..... Next is there any drugs that can induce a coma at any certain dose. Finally can cardiac arrest wake u from a coma or rem sleep?
This may not be the right forum but I hope it is. If it is not, I apologize ahead of time for my ignorance.
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- Join Date
- May 2010
- Morristown, TN
Don't think anything can force REM sleep except lack of REM sleep. If you do one of those special sleeping schedules where you only sleep four hours a day, every time you sleep (nap, really) you are almost instantly thrown into REM sleep. The concept behind it is that you sleep a total of four hours a day, but all of it is REM sleep. It's weird, but people do it. My room mate tried to get the schedule down but he fucked up. They say if you do it correctly for 2 weeks your body becomes adjusted.
- Join Date
- Dec 2009
This is probably not what you are looking for, but it's a proof of concept: http://www.springerlink.com/content/u108p01773l88135/
"The effect of -Br on the sleep-wakefulness cycle was to increase REM sleep and to slightly decrease wakefulness or NREM sleep."
I don't think this is the same as forcing REM sleep, but it shows that there are drugs that can induce REM. Maybe someone who knows a bit more than I about this subject can continue?
supposedly some constituents of Nymphaea caerulea (blue lotus) cause much more vivid dreams, though I don't think this is currently supported empirically. There are plenty of relatively cheap extracts available though, so if you wanted to test it out it wouldn't be difficult.
Maybe not exactly what you were looking for, but somewhat related.
Mirtazapine is great for inducing REM activity. It's probably called REMeron for a reason
- Join Date
- Jan 2009
I don't know if I would say it forces REM sleep, but Cyproheptadine increases the amount of REM sleep.
J Pharmacol Sci. 2007 Feb;103(2):201-6. Epub 2007 Feb 8.
Effects of some H1-antagonists on the sleep-wake cycle in sleep-disturbed rats.
Tokunaga S, Takeda Y, Shinomiya K, Hirase M, Kamei C.
Department of Medicinal Pharmacology, Okayama University Graduate School of
Medicine, Dentistry and Pharmaceutical Sciences, Tsushima-naka 1-1-1, Okayama
The present study was undertaken to investigate the effects of some
H(1)-antagonists on the sleep-wake cycle in sleep-disturbed rats in comparison
with those of nitrazepam. Electrodes were chronically implanted into the frontal
cortex and the dorsal neck muscle of rats for the electroencephalogram (EEG) and
electromyogram (EMG), respectively. EEG and EMG were recorded with an
electroencephalograph. SleepSign ver. 2.0 was used for EEG and EMG analysis. The
total times of waking, non-rapid eye movement (non-REM), and rapid eye movement
(REM) sleep were measured from 10:00 to 16:00. Nitrazepam showed a significant
decrease in sleep latency, total waking time, and delta activity and an increase
in the total non-REM sleep time. A significant decrease in the sleep latency was
observed with diphenhydramine, chlorpheniramine, and cyproheptadine.
Cyproheptadine also caused a significant decrease in the total waking time and
increases in total non-REM sleep time, REM sleep time, slow wave sleep, and delta
activity, although no remarkable effects were observed with diphenhydramine and
chlorpheniramine. In conclusion, cyproheptadine can be useful as a hypnotic,
having not only sleep inducing-effects, but also sleep quantity- and
PMID: 17287588 [PubMed - indexed for MEDLINE]
Xyrem (Prescription GHB) is used for narcolepsy with cataplexy. It helps by giving the patient fuller sleep. Not sure if this is actually increasing REM sleep. Anyone know a bit more about this?
Yeah GHB (and GBL in my case) can produce vivid dreams and sometimes even lucid dreams if used correctly.
It can also cause a reversible "coma" at a slightly higher dose than your "sweet spot", ie it's very difficult to wake you up as long as the drug takes effect (usually a short period, 3 to 4 hours), but when it's over you just wake up normally, provided you didn't take really too much. I wanted to post this but wasn't sure it corresponds to the OP question, sort of.
Melatonine ? Google give some trials result showing recovery of REM sleep using melatonine.
Given that REM sleep and the atonia that accompanies it involves near-total monoaminergic shutdown in key regions as a requisite for initiating the dream state, the rest of the experimental data follow intuitively, and the information therein could be easily acquired inductively. Following initiation of REM, the neuromodulatory roles of most amines take a back seat to cholinergic transmission, the blockade of which at the M2 muscarinic receptors (Benadryl, scopolamine) tends to increase REM latency and disturb normal sleep architecture. The corollary here is also true - as a rule, any drug tending to increase cholinergic neurotransmission within the brainstem, particularly the pontine reticular formation and the mesopontine tegmentum (independent of an upstream serotonergic or noradrenergic mechanism) will greatly decrease REM latency and subjectively increase both the frequency and intensity of the dream state. As for 'forcing' REM, you'd be hard-pressed to find a drug used for clinical or recreational purposes that doesn't do the exact opposite, minus (maybe) the benzodiazepines, which certainly aren't powerful enough in that regard to meet your demand. You'd be left with the limited territory of indirect cholinergics, which for these purposes fall into the broad pigeonholes of the nootropics and nerve agents, the pharmacolgic line sometimes tending to blur between the two. Anecdotal reports of the allosteric NMDA-Glycine agonist 'racetams' increasing dream vividness and frequency, coupled with some sparse literature to back it up lend support here, as does the well-documented capacity of the acetylcholinesterase inhibitors to amplify REM. Mustard agents, some pesticides, tacrine, stigmines, and their more agreeable cousins galantamine and donepezil (the latter of which I'm on at the moment) all take care of much of the same business. But outside of direct, high-ish affinity full M2 agonists, you'll be consistently underwhelmed by the comparatively 'amplifying' effects of the indirect cholinergics, something to which I can anecdotally attest on only 5mg of Aricept. The reason for this is simple - drugs that act as indirect agonists typically can only augment already-extant paracrine signaling, while full agonists are capable of stimulating a postsynaptic receptor independent of a presynaptic action potential. In other words, you're piss-out of luck with the readily available cholineric drugs, though I think there might be a way...
Going back the "monoamine-choline" hypothesis, it also follows that antagonists/inverse agonists at serotonin receptors implicated in maintaining consciousness and arousal (read: 5-HT2A) or known for depressing cholinergic activity (5-HT6) would similarly decrease latency to REM, if not 'forcing' it in higher doses - and if I remember right, they do. Mirtazapine is a well-studied culprit, as mentioned by mecaib. Melatonin is well known for boosting REM time, and from what I can pull out of my ass at the moment:
Melatonin agonists modulate 5-HT2A receptor-mediated neurotransmission: behavioral and biochemical studies in the rat.
EISON AS, FREEMAN RP, GUSS VB, MULLINS UL, WRIGHT RN.
J Pharmacol Exp Ther 1995;273(1):304-8.
CNS Developmental Pharmacology, Pharmaceutical Research Institute, Bristol-Myers Squibb Company, Wallingford, Connecticut, USA.
Interactions between melatonin and serotonin type 2A (5-HT2A) receptors in the regulation of the sleep-wakefulness cycle in the rat have been reported. We studied the acute effects of melatonin and related agonists on 5-HT2A neurotransmission as reflected in behavioral (head shake) and biochemical [phosphoinositide (PI) hydrolysis] responses to 5-HT2A receptor stimulation. Like 5-HT1A agonists and antidepressants, acute administration of melatonin and related agonists inhibited the 5-HT2A-mediated (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane-induced head shake in a dose-dependent manner. Consistent with these behavioral findings, in vitro incubation of cortical slices with melatonin agonists robustly inhibited 5-HT2A receptor-mediated PI hydrolysis in a noncompetitive manner. 2-Iodomelatonin-induced reductions in 5-HT2A-stimulated PI hydrolysis were blocked by preincubation with the melatonin antagonist N-acetyltryptamine. Further, pretreatment of rats in vivo with melatonin and related agonists reduced the cortical PI hydrolysis response to the 5-HT2A agonist alpha methyl-5-HT but did not alter cortical 5-HT2A receptor density. The present data support an interaction between melatonin and 5-HT2A receptors in the central nervous system.
Looks like a common mechanism. I'm guessing direct 5-HT2A drugs would be more powerful, either alone or in combination with negative modulators like melatonin, tianeptine, and such. Think ultra-low-dose risperidone, ziprasidone, asenapine, nefazodone, mianserin, trimipramine, methysergide, and friends. Mixing these and a reasonable cholinergic (huperzine, arecoline, galantamine, donepezil) would probably reduce your slow-wave sleep to a wee choad, kicking REM into something akin to an overnight dream anthology. Sorry for the lack of citations. Sleep deprived/don't have time to go science this shit. Alot of what I said is probably mostly bullshit anyway. Correct me.
I would call any sleep in which I dream abundantly "good sleep," and mirtazapine helps with that. Other people I've talked to also experience better sleep with increased dream recall while on that drug, so it isn't just me.
It it possible that even though I feel like I'm getting good sleep, and am experiencing multiple dreams per night, that I'm not in fact getting good sleep?
31-05-2010 00:04It it possible that even though I feel like I'm getting good sleep, and am experiencing multiple dreams per night, that I'm not in fact getting good sleep?
Selective 5HT2A and 5HT6 receptor antagonists promote sleep in rats.
MORAIRTY SR, HEDLEY L, FLORES J, MARTIN R, KILDUFF TS.
Biosciences Division, SRI International, Menlo Park, CA 94025, USA. email@example.com
STUDY OBJECTIVES: Serotonin (5-HT) has long been implicated in the control of sleep and wakefulness. This study evaluated the hypnotic efficacy of the 5-HT6 antagonist RO4368554 (RO) and the 5-HT2A receptor antagonist MDL100907 (MDL) relative to zolpidem. DESIGN: A randomized, repeated-measures design was utilized in which Wistar rats received intraperitoneal injections of RO (1.0, 3.0, and 10 mg/kg), MDL (0.1, 1.0 and 3.0 mg/kg), zolpidem (10 mg/kg), or vehicle in the middle of the dark (active) period. Electroencephalogram, electromyogram, body temperature (Tb) and locomotor activity were analyzed for 6 hours after injection. MEASUREMENTS AND RESULTS: RO, MDL, and zolpidem all produced significant increases in sleep and decreases in waking, compared with vehicle control. All 3 doses of MDL produced more consolidated sleep, increased non-rapid eye movement sleep (NREM) sleep, and increased electroencephalographic delta power during NREM sleep. The highest dose of RO (10.0 mg/kg) produced significant increases in sleep and decreases in waking during hour 2 following dosing. These increases in sleep duration were associated with greater delta power during NREM sleep. ZO Zolpidem induced sleep with the shortest latency and significantly increased NREM sleep and delta power but also suppressed rapid eye movement sleep sleep; in contrast, neither RO nor MDL affected rapid eye movement sleep. Whereas RO did not affect Tb, both zolpidem and MDL reduced Tb relative to vehicle-injected controls. CONCLUSIONS: These results support a role for 5-HT2A receptor modulation in NREM sleep and suggest a previously unrecognized role for 5-HT6 receptors in sleep-wake regulation.
At least you're not taking something obnoxious/contentious, like an SRI or MAO inhibitor. Or are you?
31-05-2010 03:23It's getting harder and harder to get motivated and/or interested enough to accomplish much. I chalked it up to not being able to get out of the house for exercise.
I've been around SSRI Street, and it's an ugly neighborhood. I couldn't handle the brain zaps, or the fact that they did *nothing* for my depression. I've never been on an MAO(I).
Actually, come to think of it, I'm surprised you're on mirtazapine given the mushroom in your pic (or am I inferring too much here?).
maybe dmt? isnt that secreted from the pineal when you hit rem? an oral dose at bed time that kicks in when you hit stage 2 or 3 of your rhythm
He mentioned Nefazodone and the likes, I would point you towards Trazodone as its one of the few a.d.'s improving sleep architecture (Shrink also mentioned Surmontil, but its again a trycyclic with H1 antagonsim which I refused).
I tried Remeron only once and I was so fucked up the other day that I quit it and took Trazodone. It has a much reduced hangover the next day, 1 Red Bull will make you going. I've become a friend of Trazodone, unlike all other general Monoamine reuptake inhibitors, it doesen't pave you all over with effects, and down there, no losses, quite the opposite! After 4 days it had a wonderful a.d. effect (I suffered from a bad burn-out depression). And you can play with dose and altough its overall antidepressive yield is quite low, in doses north of 200-300, it shifts in a second gear with an added SSRI property.
- Join Date
- Feb 2007
Gamma Amino Butrate Acid powder is good for sleep IMO
I have a high tolerance for such compounds anyway, and the last time I dropped acid I needed 10 hits to have a decent trip. I was on mirtazapine at the time. OTOH, DXM hits me harder than most people. I'm guessing the mirtazapine is partially to blame there too.
It's only a matter of time before somebody accuses us of going off-topic...
31-05-2010 22:12Um, what's the problem with taking serotonergic psychedelics with mirtazapine? I know mirtazapine can dull the mushroom/acid/etc. experience.I have a high tolerance for such compounds anyway, and the last time I dropped acid I needed 10 hits to have a decent trip. I was on mirtazapine at the time.
On the other hand, chronic treatment with 2A ligands progressively downregulates the receptor (reduces its expression on the surface of the postsynaptic neuron/negatively modifies binding affinity). This could theoretically exacerbate the situation, creating a kind of semi-irreversible tolerance that I couldn't imagine would be particularly pleasing in an average psychedelic user.
Is there something else I should be concerned about?
It's only a matter of time before somebody accuses us of going off-topic...
- Join Date
- Jul 2008
Peptides such as Ipamorelin or the Growth Hormone Releasing Hormone (GHRH) analog made by conjuchem (listed as "mod GRF" on a lot of suppliers) are able to stimulate your body to release growth hormone effectively and this in turn brings more restful sleep (especially when they are taken right before sleep).
I'm not sure if they will enhance the REM sleep phase specifically, but growth hormone enhances slow wave sleep so this is enhanced.
Whether that is what you are looking for I'm not sure. I don't see a clear reason why you want REM sleep over slow wave, just better sleep in general or what the goal really is here?
Growth Horm IGF Res. 2004 Jun;14 Suppl A:S10-7.
Reciprocal interactions between the GH axis and sleep.
Van Cauter E, Latta F, Nedeltcheva A, Spiegel K, Leproult R, Vandenbril C, Weiss R, Mockel J, Legros JJ, Copinschi G.
Department of Medicine, MC 1027, University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637, USA.
For more than 30 years, growth hormone (GH) has been observed to be preferentially secreted during deep, slow-wave sleep (SWS). However, the mechanisms that underlie this robust relationship that links anabolic processes in the body with behavioral rest and decreased cerebral metabolism remain to be elucidated. Current evidence indicates that GH secretion during the beginning of sleep appears to be primarily regulated by GH-releasing hormone (GHRH) stimulation occurring during a period of relative somatostatin withdrawal, which also is associated with elevated levels of circulating ghrelin. Apparently, two populations of GHRH neurons need to be simultaneously active to stimulate, in a coordinated fashion, SWS and pituitary GH release. Pharmacological interventions that are capable of increasing the duration and/or the intensity of SWS such as oral administration of gamma-hydroxybutyrate (GHB), also increase the rate of GH release. Because the normal negative feedback exerted by GH on central GHRH is inoperative in patients with GH deficiency, it is possible that the decreased energy levels and fatigue often reported by GH-deficient adults partly reflect an alteration in sleep-wake regulation. Preliminary data from a sleep study of adults with GH deficiency using wrist actigraphy for 6 nights at home and polysomnography in the laboratory indeed show decreased total sleep time and increased sleep fragmentation in GH-deficient patients as compared with normal controls.
I know its already been said but GHB (or GBL) forcefully induces REM sleep.. ime..
Alot of phenibut does it too
Yeah, ghb I thought of. even tho its been said. Even if it doesn't really help induce REM, it gets you into a deeper sleep.
Neuroscience and Pharmacology Discussion
Philosophy and Spirituality
- Join Date
- Sep 2001
- Norfair, Zebes
k...GABAnergics tend to interfere with REM sleep (and many with stage 4). The best case with those appears leaving basal REM intact or inducing REM-rebound upon cessation. 5ht action of some sort appears to be the ticket...
but what level of REM induction counts as "forcing" REM sleep?
In my experience melatonin is excellent for sleep. Especially when combined with alcohol, cannabis, kava, or just about any sedative...