Nicotine vs Glutamate/GABA/Dopamin

[[Kr...]]

 

Hi guys!

@[Co...] @[Th...] @[Ch...]

You seem to be knowledgeable on this topic, so I would like to ask for your insights if possible.

As I was not sure why my symptoms are so severe after a short period & low dose Xanax use (2,5 months 3 x 0,25 mg, now down to 2 x 0,1875 mg + 40 mg cinolazepam (equivalent to around 0,5 mg Xanax) so I can sleep more than 1 hour).

My symptoms:

I have apathy, anhedonia, no appetite (loosing weight rapidly), insomnia, can't really leave my flat, occasional strong stomach pain, restlessness,  walking up & down in my room (anxiety akathisia?), can't really sit down during the day, erectile dysfunction, can't watch videos or listen to music, depression, loss of interest in everything I used to enjoy, etc. Basically barely functioning. I mostly have been in this stage weeks before even cutting on my benzo dose. Then when I started to cut, all symptoms got stronger.

I was thinking that maybe now I have a paradoxical reaction to Xanax, as it doesn't calm me down at all and causing all these symptoms, and maybe it would be best to just cold turkey the whole thing. My best part of the day when I go back to my sleeping room, there I can lay down (no akathisia there) and read peacefully. I usually do this from 7 PM, although I used to be an owl type. I was put on 50mg of Zoloft by my psychiatrist 5 days ago.

So back until October-November I was a chain vaper, for 10+ years. I smoked the lowest nicotine eliquid (3mg) but almost constantly. I thought it's okay. Then I asked my eliquid provider that based on the amount of eliquid I consume, how much normal packs that would be equivalent wth. He said, that it's around 5 packs of Marlboro Gold/Light daily. I was shocked. So I was vaping 5 packs worth of nicotine for few multiple years. At around that time I started smoking regular cigarettes again, not because of this information, but somehow I got back to it, around a pack a day + also vaping next to it. Then when some of my above symptoms started, I switched to almost exclusively to cigarettes, around 2 packs a day. I did not smoke a regular cigarette before October for about 7 years.

 

So I did some research on the topic. I put the research link front and then some quotations that might be relevant. Have to mention, in all studies they used really high nicotine level of eliquids.

https://www.news-medical.net/news/2007/12/10/33328.aspx

 

Researchers wanted to explore how a specific type of neuron that releases dopamine, a chemical that has been associated with pleasure, can prolong and intensify the pleasurable effects of nicotine. Although GABA inhibits those neurons, nicotine works against the ability of GABA to inhibit dopamine neurons after about 20 minutes, so the gratifying effects of nicotine are prolonged.

Researchers gave people who smoked regularly nicotine inhalers that deliver the same amount of the drug as in one cigarette. The amount of GABA in the subjects' brains rose about 10%, but the brain was found to make GABA four times faster after using the inhalers, and the rate of new GABA generation remained high for at least 45 minutes. In other words, keeping the supply of GABA levels high has the potential to reduce the pleasurable effects of smoking, in terms of duration and intensity.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3662348/

The actions of nicotine in the brain are mediated by excitatory nACh receptors. These excitatory nACh receptors are present on several different types of neurons and regulate the release of a number of neurotransmitters, including the major excitatory and inhibitory neurotransmitters in the brain, namely glutamate and γ-aminobutyric acid (GABA) (Wonnacott 1997). The present review focuses on the role of glutamate and GABA in nicotine dependence. More specifically, this review covers the following: (1) the effects of acute nicotine administration on glutamatergic and GABAergic neurotransmission; (2) alterations in glutamatergic and GABAergic neurotransmission after chronic nicotine exposure;

Chronic nicotine use leads to neuroadaptations in the function of brain reward systems, leading to the development of nicotine dependence and resulting in aversive withdrawal effects upon abstinence from smoking (i.e., the withdrawal phase). In humans, withdrawal from nicotine produces both affective and somatic adverse effects. Adverse affective symptoms in humans are more pronounced than adverse somatic symptoms and include depressed mood, dysphoria, anxiety, irritability, difficulty concentrating, and craving.

Microdialysis studies suggest that nicotine increases glutamate release in both the ventral tegmental area (VTA) and nucleus accumbens (NAcc) (Schilstrom et al. 1998; Fu et al. 2000; Reid et al. 2000). Nicotine increases glutamate release by activating excitatory α₇ nACh receptors located on presynaptic glutamatergic terminals (Mansvelder and McGehee 2002). α₇ nACh receptors are highly permeable to calcium, and the binding of nicotine to these receptors leads to calcium-mediated glutamate release from presynaptic glutamatergic terminals

In summary, acute nicotine administration increases the release of glutamate via excitatory nACh receptors located on presynaptic glutamatergic terminals. Additionally, nicotine exposure facilitates nicotine-induced presynaptic glutamate release, increases postsynaptic glutamate receptor-mediated neurotransmission, and alters the expression of ionotropic glutamate receptor expression.

Nicotine induces GABA release by binding to excitatory nACh receptors located on presynaptic GABA neurons. The cellular mechanism by which the activation of nACh receptors results in GABA release is not clearly understood. Recent work showed that activation of nACh receptors on GABAergic terminals depolarized cells, resulting in the opening of T-type Ca²⁺ channels and leading to GABA release

Knowledge of the composition of nACh receptors on GABA neurons is essential because nAChR composition determines the rate at which nACh receptors undergo desensitization or functional inactivation on exposure to nicotine (Fenster et al. 1999; Quick and Lester 2002). The desensitization of nACh receptors can result in decreased GABA release and consequently decreased inhibition of mesolimbic dopaminergic neurons, thus facilitating the nicotine-induced excitation of mesolimbic dopaminergic neurons. The desensitization of β₂-containing nACh receptors on GABAergic interneurons may be involved in the decreased GABA-mediated inhibition of dopaminergic neurons (Mansvelder et al. 2002). A recent study reported that decreased GABA release on repeated nicotine exposure was mediated by α₆β₂-containing nACh receptors located on presynaptic GABA neurons in the VTA

https://www.pnas.org/doi/10.1073/pnas.1413947111

https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2020.604583/full

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9229830/

E-cigarette vapor containing nicotine may increase glutamate transmission and modulate postsynaptic glutamate receptors [27,28]. Specifically, nicotine activation of nAChRs influences glutamate production, which leads to increased glutamate neurotransmission [29,30], which in turn contribute to behavioral changes such as drug-seeking behavior. Another important factor is the vesicular glutamate transporter (VGLUT1), which is essential for the transport and release of glutamate from presynaptic glutamatergic neurons into the synaptic cleft; its expression has been linked to extracellular glutamate concentrations in the mesocorticolimbic pathways.

A second key neurotransmitter is GABA, which attenuates the behavioral changes produced by neuron overexcitation. Short-term exposure to nicotine has been found to elevate GABA neurotransmission, while prolonged exposure is associated with desensitization to the GABAergic system [31]. This biphasic effect is also mediated by nicotine activation of nAChRs, with an initial response and subsequent desensitization after prolonged exposure [31,32]. The decline in GABA concentrations in the frontal cortex and increase in glutamate concentrations in the striatum were observed in mice exposed to e-cigarette vapors containing nicotine for six months [27]. The transport and release of GABA from presynaptic GABAergic neurons into the synaptic cleft depends on the vesicular GABA transporter (VGAT), the expression of which has been linked to extracellular GABA concentrations in the mesocorticolimbic pathways.

At the molecular level, we found that mice exposed to nicotine-containing aerosols exhibited increased hippocampal expression of VGLUT1, an essential transporter of glutamate into the synaptic cleft in the mesocorticolimbic system. In addition, this elevated expression may result in increased glutamate release. These results align with those of a previous study that revealed a significant increase in glutamate concentration in the striatum of C57BL/6J mice exposed to nicotine-containing vapors for six months [27]. It is important to note that glutamatergic projections from the hippocampus to the nucleus accumbens (a ventral striatum major component) was documented previously [45].

Previous studies have reported that exposure to e-cigarette vapors containing nicotine chronically reduces the expression of astroglial glutamate transporters, including glutamate transporter-1 (GLT-1) in the striatum and hippocampus, and cystine/glutamate antiporter (xCT) in the hippocampus [23,37]. They documented lower expression of GLT-1 and xCT in animals exposed for three and six months. Another study revealed that three-month exposure to vapors containing 50 mg/mL nicotine modulated levels of metabotropic glutamate receptors-1 (mGluR1) and mGluR5 expression in the nucleus accumbens shell [28]. In conjunction with this prior data, our findings suggest that as a consequence of reduced glutamate uptake, nicotine could increase the release of glutamate into the synapses in the mesocorticolimbic system.

We also found that chronic exposure to nicotine-containing aerosols decreases hippocampal expression of VGAT, an essential protein for GABA transport into the synapses. Furthermore, our results indicate that this decreased VGAT expression might reduce GABA concentrations. This is consistent with a previous study that revealed significantly decreased concentrations of GABA in the frontal cortex of C57BL/6J mice exposed to nicotine-containing vapors for six months [27]. Importantly, GABAergic projections are reported to be projected from the hippocampus and these projections innervate the frontal cortex [46]. Multiple studies similarly indicated that exposure to nicotine could lead to desensitization of the GABA system [31,32], possibly the presynaptic nicotinic receptors. More importantly, the rate of desensitization of nAChRs in glutamatergic neurons is slower than that of nAChRs in GABAergic neurons [31]. This reduces in the GABA-mediated inhibition of dopamine release, leading to greater excitability of the dopamine reward system, which in turn enhances reinforcement of nicotine self-administration [31]. Based on these findings, we suggest that chronic nicotine inhalation might exert a desensitizing effect on the GABAergic system. A short-term increase in the frequency of GABA postsynaptic currents is associated with continuous exposure to low nicotine concentrations, and may result from desensitization of presynaptic nAChRs [47]. In addition, chronic exposure to nicotine increases transcription of corticotropin-releasing hormone (Crh) mRNA, which simulates the corticotropin-releasing factor in dopaminergic neurons of the ventral tegmental area and consequently inhibits GABAergic transmission to dopaminergic neurons [48]. Conversely, use of a viral vector to decrease Crh mRNA expression in dopaminergic neurons has been found to prevent nicotine-induced GABA neurotransmitter dysregulation [48]. Thus, the evidence indicates that stimulating GABA release reduces dopamine-mediated nicotine dependence.

It has been reported that exposure to 500 nM nicotine for 25 min elevates GABA release with subsequent long-term inhibition of GABAergic neurons, as evidenced by the frequency of spontaneous inhibitory postsynaptic currents. At the same time, the same exposure increases glutamatergic activity without any long-term inhibitory effect on glutamatergic neurons, as determined by spontaneous excitatory postsynaptic currents. These findings indicate that nicotine plays a role in GABAergic system desensitization [32].

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712012/

Previous studies from our laboratory showed that chronic exposure to e-cigs, containing 24 mg/mL nicotine, was associated with dysregulation of glutamate transporters and neurotransmitter levels in the brain of a mouse model.

These findings demonstrated that three-month exposure to e-cig vapor containing high nicotine concentrations induced differential effects on the glutamatergic system in the NAc and HIP, suggesting dysregulation of glutamatergic system activity in mesolimbic brain regions

Recent studies from our laboratory showed that chronic exposure to e-cigs was associated with dysregulation of glutamate transporters and neurotransmitters levels in the brain [17,18]. Exposure to e-cigs for six months induced downregulation of glutamate transporter 1 (GLT-1) in the striatum, and downregulation of cystine/glutamate antiporter (xCT) in the striatum and hippocampus (HIP) of female CD-1 mice [17]. It is important to note that GLT-1 is responsible for the clearance of the majority of extracellular synaptic glutamate [19,20]. Alternatively, chronic e-cig exposure in male C57BL/6 mice was associated with a reduction in dopamine concentration and increase in glutamate concentration in the striatum, while GABA concentration was decreased in the frontal cortex [18].

Exposure to e-cigs containing nicotine induced comparable plasma nicotine levels as compared to conventional tobacco smoking

We demonstrated in this study that three-month exposure to mint- or mango-flavored JUUL pods (containing 59 mg /mL nicotine) altered the protein expression of mGluR1, mGluR5 and GLT-1 in the NAc-shell and HIP.

Nicotine self-administration enhanced glutamate transmission in the NAc-shell, and this effect was attenuated by systemic treatment with mGluR2/3 agonist LY379268 [61].

In summary, this study demonstrated that three-month exposure to e-cig vapor, containing a high nicotine concentration, induced differential effects on several targets of the glutamatergic system in the NAc subregions and HIP, and probably similar to the effects induced by chronic nicotine exposure. Three-month JUUL exposure induced an increase in mGluR1 expression and reduction in mGluR5 and GLT-1 expression in the NAc-shell. However, the expression of mGluR5 and GLT-1 were increased in the HIP, with no change in their expression in the NAc-core. These findings suggest dysregulation of glutamatergic system activity in the NAc-shell subregions and HIP in response to chronic e-cig exposure.

https://royalsocietypublishing.org/doi/10.1098/rstb.2008.0095

Exogenously administered nicotine increases dopamine transmission by direct stimulation of nAChRs, primarily α4β2-containing and α7 homomeric nAChRs within the VTA. Nicotine stimulates nAChRs on glutamatergic terminals that release glutamate, an excitatory neurotransmitter, which results in increased dopamine release in the nucleus accumbens and the frontal cortex. Nicotine also excites nAChRs on GABA-releasing terminals. Thus, the levels of GABA, an inhibitory neurotransmitter, are increased by nicotine as well. However, the interplay between the quick desensitization of nAChRs on the GABA neuron and the higher doses of nicotine required to desensitize the α7 homomeric nAChRs on the glutamate neuron results in a greater overall increase in dopamine levels (figure 2).

As discussed above, nicotine increases glutamate release by agonist actions at excitatory presynaptic nAChRs on glutamatergic terminals in various brain sites, including the VTA, nucleus accumbens, prefrontal cortex and hippocampus (for reviews, see Mansvelder & McGehee 2002; Kenny & Markou 2004). Furthermore, glutamatergic afferents project from areas such as the frontal cortex, amygdala and hippocampus to brain site that contain dopaminergic cell bodies or terminals, such as the VTA and the nucleus accumbens (for a review, see Kenny & Markou 2004). Indeed, experimenter-administered nicotine has been shown to increase glutamate levels in the VTA (Fu et al. 2000), which presumably acts at metabotropic and ionotropic glutamate receptors on postsynaptic dopamine neurons and increases their bursting activity and neurotransmitter release. Considerable evidence suggests that these actions partly mediate the reinforcing effects of acute nicotine.

With chronic exposure to nicotine and the development of nicotine dependence, adaptations in glutamate neurotransmission occur, which are likely to mediate the behavioural signs of nicotine withdrawal. In a series of studies, we investigated adaptations in glutamate receptors that may mediate the deficits in brain reward function measured by elevations in ICSS thresholds associated with nicotine withdrawal in rats.

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830589/

Nicotine binds to nicotinic acetylcholine receptors (nAChRs) in the brain, resulting in the release of a wide range of neurotransmitters, including glutamate and γ-aminobutyric acid (GABA). This review article focuses on the role of the excitatory glutamate system and inhibitory GABA system in nicotine dependence.

Nicotine activates α4β2-containing nAChRs located on VTA dopamine neurons and increases dopamine release in the NAc (Picciotto et al., 1998). Importantly, nAChRs exist as heteroreceptors on glutamatergic and GABAergic neurons and modulate the release of glutamate and GABA. For example, the nicotine-induced activation of α7 nAChRs located on glutamatergic terminals increases the release of glutamate in the VTA (McGehee et al., 1995; Schilstrom et al., 2000). Furthermore, nicotine activates α4β2-containing nAChRs located on GABAergic terminals and leads to GABA release in the VTA (Corrigall et al., 2000).

Finally, nicotine increases glutamatergic transmission by acting on excitatory α7 nAChRs located on glutamatergic afferents in the VTA and the NAc (McGehee et al., 1995).

Chronic exposure to nicotine modulates dopamine transmission by directly activating dopamine neurons in the VTA or indirectly by modulating excitatory glutamate or inhibitory GABA transmission as described above. Studies have shown a significant decrease in dopamine during nicotine withdrawal in the striatum (Fung et al., 1996; Varani et al., 2011), cortex (Hildebrand et al., 1998; Varani et al., 2011); but see (Carboni et al., 2000), and NAc (Zhang et al., 2012) and decreased 5-hydroxytryptamine (5-HT) transmission in the striatum (Slotkin and Seidler, 2007; Varani et al., 2011) but not cortex or hippocampus (Varani et al., 2011).

The majority of the aforementioned studies investigated the neurochemical changes that occur during precipitated nicotine withdrawal Chronic nicotine exposure induces adaptive changes in the glutamate system and is hypothesized to lead to decreased glutamatergic transmission. Thus, compounds that decrease glutamatergic transmission may be expected to worsen nicotine withdrawal, and compounds that increase glutamate release may be expected to improve nicotine withdrawal.

Investigations of the role of the GABA system in nicotine withdrawal have not been as extensive as investigations of the glutamate system (Vlachou and Markou, 2010). Recent findings showed that decreased levels of dopamine and 5-HT neurotransmission in the cortex and striatum during mecamylamine-precipitated nicotine withdrawal were prevented by an acute injection of the GABA_B receptor agonist baclofen (Varani et al., 2011). However, chronic nicotine administration did not alter GABA_B receptor function. The GABA_B receptor regulation of brain reward function was unchanged in rats chronically exposed to nicotine compared with saline (Paterson et al., 2005a). Thus, chronic nicotine exposure may not induce neuroadaptations in GABA_B receptor function or GABA neurotransmission, but further studies are needed to investigate this issue.

Direct blockade of postsynaptic iGluRs with the AMPA/kainate receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) precipitated elevations of brain reward thresholds in nicotine-dependent but not control rats, suggesting that decreased glutamate transmission is associated with the anhedonic-like signs of nicotine withdrawal

 

https://www.sciencedirect.com/science/article/abs/pii/S0009279720314307

Nicotine exposure increases the release of glutamate in part through stimulatory effects on pre-synaptic nicotinic acetylcholine receptors (nAChRs).

 

 

[[Kr...]]

Few questions:

1, Although the above articles are quite confusing sometimes, it seems that my long term nicotine addiction is not at my favour. Nicotine intake releases glutamate, GABA, dopamine, but also downregulates all these receptors after long exposure. My depression might be caused because of the radical decrease in my nicotine intake because not enough dopamin? Also my symptoms maybe this strong from even the slightest benzo decrease, because of my GABA receptors are downregulated? I now smoke mostly regular cigarettes, around 2 packs a day. So around 3 packs decrease from vaping.

2, I’m confused and not 100% sure what to do. I don’t know now if nicotine intake is good or bad for me. Of course, I can’t just stop. Maybe it would be better if I try to return to ecigarette only?

3, Did you know nicotine affects GABA & glutamate this much? Maybe you have previous experience with other vapers from before? I just can’t seem to understand how my symptoms are this strong after a short amount of time and low dose. I tried to connect the dots & came up with the nicotine connection.  

4, I know that glutamate is bad during withdrawal, but nicotine seems to do everything at the same time. Increases glutamate, GABA & dopamin as well.

5, Is there a connection at all, or I just googled too much?

6, Did any of you smoke during withdrawal?

I was never depressed or anxious really before. I got Xanax because I had a small breakdown after a breakup. Although I always tried to live a stress free life.

Edited February 6 by [Kr...]

[[dj...]]

Probably best for your personal health to not use nicotine, but I wouldn’t get hung up too much on this article.  There are lots of things that have downstream effects on GABA and glutamate.  Nicotine is just well studied which is why you’re getting a detailed article.  Some researches were specifically looking at GABA/glutamate and understanding how they may be used in smoking cessation. 
 

As it relates to benzo withdrawal/injury, I would put nicotine in the same category as higher doses of sugar honestly.  They can exacerbate symptoms.  Both have some stimulant properties but also some relaxant properties via dopamine pathways.  

Edited February 6 by [dj...]

[[WU...]]

Without reading everything as my poor brain can't handle all that detail, I am quite sure there is a connection. In the Ashton Manual she suggests tapering and stopping benzos before stopping smoking which is interesting. I was smoking a fair bit before I quit CT but over the past few months I seem to know intuitively that I needed to stop or significantly cut down as my body tries to recalibrate itself. I smoke maybe 7 or 8 per day and to a strict timetable , treating them as nicotine doses. I do this as I don't want to shock my system any more than it is already. Over more time I will reduce to 5 a day and then it will be much easier to quit altogether. Oh and I switched to rolling tobacco, the one without additives if that makes any difference.

[[bw...]]

I think you may be overthinking it.

When you say 2packs a day is thay around 40 ciggarettes per day? How long have you been doing this?

I smoke aswell.

25 a day for last 20 years. Has made no differnece in my withdrawal or sufferring. Nicotine is actually neuroprotective. Also found to he anti-inflammatory.  now given to alzeimers patients in hospital to build cognitive function. So go figure.. ??

I dont react to ciggarettes at all.

But i react to many foods and medications that cam cause long setbacks. I am way too scared to try E ciggarettes made in some chinese lab with somr mystery vape juice and synthetic chemicals and flavanoids. No thanks.

Im australian so we dont have a good range of ciggarettes like americans do. If i was in the USA i would try camel unfiltered. Or even better would be natural american spirit without the additive shit inside of it. Just el natural tobacco!!.

Best of luck.

Edited February 28 by [bw...]

[[PE...]]

Omg that's a long post @[Kr...]. As a smoker and vaper I feel that it's not interfering with healing. I also use Swedish chewing tobacco. I will stop smoking after this is done.

That you feel worse and get lots of symptoms when you go down in dose is normal. Also the SSRI you been subscribed might not have started working yet as it's only five days.

 

[[PE...]]

When I was in acute wd from CT I was smoking every 15 minutes. As soon the commercial came on. Me like you couldn't sit. I was walking, or mor like aggressive marching, around and around the apartment. It was a torture for sure! 

It will pass!

Edited February 28 by Guest

[[Kr...]]

Hi @[ne...]!

Thanks for your input! I read that your were on 20 mg of V for five years and jumped in last July. Are you healed now? How are things going?

 I stopped Xanax CT like 2 weeks ago, but at that time I only took it in the morning and afternoon, around 0,45 mg. At the same time I added Mirtazapine, 7,5 mg first, then after a few days 15 mg. So right now I take 15 mg Mirt, 50 mg Zoloft, and a quarter of the Gerodorm pill, usually at around 3 AM.

Most of my symptoms went away, I feel much better. I almost completely switched back to vaping. Appetite kinda back, going up&down much less, I more or less function now. Not everyday though unfortunately. Like every second day. I tried to cut the last benzo pill as well (Gero), but could not sleep after 3 am like that. So mainly insomnia is my only symptom, but that makes everything worse.

[[PE...]]

1 minute ago, [[K...] said:

Hi @[ne...]!

Thanks for your input! I read that your were on 20 mg of V for five years and jumped in last July. Are you healed now? How are things going?

 I stopped Xanax CT like 2 weeks ago, but at that time I only took it in the morning and afternoon, around 0,45 mg. At the same time I added Mirtazapine, 7,5 mg first, then after a few days 15 mg. So right now I take 15 mg Mirt, 50 mg Zoloft, and a quarter of the Gerodorm pill, usually at around 3 AM.

Most of my symptoms went away, I feel much better. I almost completely switched back to vaping. Appetite kinda back, going up&down much less, I more or less function now. Not everyday though unfortunately. Like every second day. I tried to cut the last benzo pill as well (Gero), but could not sleep after 3 am like that. So mainly insomnia is my only symptom, but that makes everything worse.

Hi! I tried to taper the whole last year. I was in a really bad state dosing between 0.5 to 150mg diazepam and sometimes other benzos. I CT 5 months ago. But before that I was prescribed 20mg that is right.

I get quentapine for insomnia and it really helps me sleep. And is also good for Nassau. I know mirt can work for insomnia if taken at night.

I'm not healed all together but it's like night and day compared to 5 months ago. CT as you might know is a badass experience! In my case tolerance wd was taken to it extremes and no dose was enough so I had to just quit.

 

[[Kr...]]

1 hour ago, [[n...] said:

Hi! I tried to taper the whole last year. I was in a really bad state dosing between 0.5 to 150mg diazepam and sometimes other benzos. I CT 5 months ago. But before that I was prescribed 20mg that is right.

I get quentapine for insomnia and it really helps me sleep. And is also good for Nassau. I know mirt can work for insomnia if taken at night.

I'm not healed all together but it's like night and day compared to 5 months ago. CT as you might know is a badass experience! In my case tolerance wd was taken to it extremes and no dose was enough so I had to just quit.

I see! Happy for you that you are feeling better. Do you take any other meds if I may ask other than quentapine? Like an SSRI or something?

[[PE...]]

4 minutes ago, [[K...] said:

I see! Happy for you that you are feeling better. Do you take any other meds if I may ask other than quentapine? Like an SSRI or something?

No thats about it

I haven't yet experienced any depression or anxiety so i stick with quetiapine. I done SSRI in the past but had no problem stopping. Brainzaps i had those.