![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 5 to 29 of 29. Go back in thread:
Posted by Phillipa on January 25, 2009, at 12:30:38
In reply to * Seroquel - Why does it help so many conditions?, posted by SLS on January 25, 2009, at 11:03:14
Scott as you know I don't have the knowledge you do so if it stops it it then starts it? I don't think I understand trying to. That receptor comes up a lot is there a simple definition of it? I'm serious? I'm not a good or quick researcher. Thanks Phillipa
Posted by SLS on January 25, 2009, at 13:58:35
In reply to Re: * Seroquel - Why does it help so many conditions?, posted by desolationrower on January 25, 2009, at 12:04:44
> quetiapine is also a pretty strong alpha2 antagonist. it might interact with the sigma receptor as well. and 5ht6 and some other receptors not well understood.
I know nothing about sigma receptors.
- Scott
Posted by Incubusfan on January 25, 2009, at 20:14:49
In reply to Seroquel - Why does it help so many conditions?, posted by SLS on January 25, 2009, at 10:54:32
Can the effects of Seroquel be matched by combinations of other drugs?
Posted by desolationrower on January 25, 2009, at 21:51:54
In reply to Re: * Seroquel - Why does it help so many conditions? » desolationrower, posted by SLS on January 25, 2009, at 13:58:35
> > quetiapine is also a pretty strong alpha2 antagonist. it might interact with the sigma receptor as well. and 5ht6 and some other receptors not well understood.
>
>
> I know nothing about sigma receptors.
>
>
> - Scottits probably worth looking into...
Sigma-1 receptor ligands: potential in the treatment of neuropsychiatric disorders.
The sigma receptor was originally proposed to be a subtype of the opioid receptor. However, it is now clear that sigma receptors are unique non-opioid, non-phencyclidine brain proteins. Two types of sigma receptor exist, the sigma-1 receptor and the sigma-2 receptor. sigma-1 receptors have been cloned and their distribution, physiological functions and roles in signal transduction were recently characterised. Certain sex hormones in the brain (neurosteroids) are known to interact with sigma-1 receptors. sigma-1 receptors regulate glutamate NMDA receptor function and the release of neurotransmitters such as dopamine. They are thus proposed to be involved in learning and memory as well as in certain neuropsychiatric disorders. Selective sigma-1 receptor ligands have been suggested to represent a new class of therapeutic agents for neuropsychiatric disorders, although none have yet been introduced into therapeutic use. Early studies showed that psychotomimetic benzomorphans, as well as several antipsychotics, can bind to sigma-1 receptors. As a result of these findings, sigma-1 receptor ligands have been proposed as being of potential use in the treatment of schizophrenia. Nevertheless, the relationship of sigma-1 receptors to the underlying pathogenesis of schizophrenia is still unclear. sigma-1 receptor ligands have failed to improve acute psychotic symptoms of schizophrenia in clinical trials, but, interestingly, a few studies have shown an improvement in negative symptoms in schizophrenic patients. A number of preclinical studies have shown that selective agonists of sigma-1 receptors affect higher-ordered brain functions such as learning and memory, cognition and mood. These studies indicate that sigma-1 receptor agonists may exert therapeutic effects in depression and senile dementia. Indeed, the sigma-1 receptor agonist igmesine, has been shown to improve depression in a clinical trial. The most distinctive feature of the action of sigma-1 receptor ligands is their "modulatory" role. In behavioural studies of depression and memory, they exert beneficial effects only when brain functions are perturbed.Given the recently accumulated preclinical and clinical data, it is time to reconstruct the concept of sigma-1 receptors and the associated pathophysiological conditions that ligands of these receptors target. This would allow clinical trials to be performed more efficiently, and the results may confirm a long-speculated possibility that sigma-1 receptor ligands represent a new class of therapeutic agents for neuropsychiatric disorders.
PMID: 15089113
Phencyclidine-induced cognitive deficits in mice are improved by subsequent subchronic administration of fluvoxamine: role of sigma-1 receptors.
This study was undertaken to examine the effects of the selective serotonin reuptake inhibitors fluvoxamine and paroxetine on cognitive deficits in mice after repeated administration of the N-methyl-D-aspartate receptor antagonist phencyclidine (PCP). In the novel object recognition test, repeated administration of PCP (10 mg/kg/day, 10 days) significantly decreased the exploratory preference in the retention test session, but not in the training test session. PCP-induced cognitive deficits were significantly improved by subsequent subchronic (2-week) administration of fluvoxamine (20 mg/kg/day), but not paroxetine (10 mg/kg/day). Furthermore, the effect of fluvoxamine on PCP-induced cognitive deficits was antagonized by co-administration of the selective sigma-1 receptor antagonist NE-100 (1 mg/kg/day). Moreover, PCP-induced cognitive deficits were also significantly improved by subsequent subchronic (2-week) administration of the selective sigma-1 receptor agonist SA4503 (1 mg/kg/day) or neurosteroid dehydroepiandrosterone 3-sulfate (DHEA-S; 25 mg/kg/day). The effects of SA4503 or DHEA-S were also antagonized by co-administration of NE-100 (1 mg/kg/day), suggesting the role of sigma-1 receptors in the active mechanisms of these drugs. In contrast, acute single administration of these drugs (fluvoxamine, paroxetine, SA4503) alone or combination with NE-100 did not alter PCP-induced cognitive deficits. The present study suggests that agonistic activity of fluvoxamine at sigma-1 receptors plays a role in the active mechanisms of fluvoxamine on PCP-induced cognitive deficits in mice. Therefore, sigma-1 receptor agonists such as fluvoxamine would be potential therapeutic drugs for the treatment of the cognitive deficits of schizophrenia.
PMID: 16495935
[Sigma-receptor ligands and anti-stress actions]
[Article in Japanese]Noda Y, Kamei H, Nabeshima T.
Department of Neuropsychopharmacology, Nagoya University Graduate School of Medicine, Japan.
The functional role of sigma receptors in the central nervous system has been investigated extensively. Sigma1-receptors have been shown to play an important role in antidepressive effects since selective sigma1-receptor agonists, as well as typical antidepressants, reduced the immobility time in the forced swimming and tail suspension tests. The reduction of immobility by sigma1-receptor agonists is antagonized by NE-100, a sigma1-receptor antagonist. It has been suggested that sigma receptors are involved in anxiety since Lu 28-179, a sigma2-receptor agonist, has anxiolytic properties in rodents. In addition to the depressive animal model, phenytoin-sensitive sigma1-receptor agonists such as (+)-SKF-10,047 and dextromethorphan attenuate the conditioned fear stress (CFS) response (which is not influenced by typical anxiolytics and antidepressants) in rodents, the attenuating effects being mediated through phenytoin-sensitive sigma1 receptors, which are closely connected to the mesolimbic dopaminergic systems. Furthermore, neurosteroids such as dehydroepiandrosterone sulfate also attenuate the CFS response, the effect being mediated via sigma1 receptors. These findings suggest that sigma receptors are involved in stress-induced pathophysiological changes such as depression and anxiety and that phenytoin-sensitive sigma1-receptor ligands are useful for the treatment of affective disorders, particularly those considered to be treatment-resistant.
PMID: 10562964
(+)-SKF-10,047 and dextromethorphan ameliorate conditioned fear stress through the activation of phenytoin-regulated sigma 1 sites.
Kamei H, Kameyama T, Nabeshima T.Department of Chemical Pharmacology, Meijo University, Nagoya, Japan.
Mice exhibited a marked suppression of motility when they were replaced in the same environment in which they had previously received an electric footshock. This psychological stress-induced motor suppression, known as conditioned fear stress, was dose dependently attenuated by (+)-N-allylnormetazocine ((+)-SKF-10,047) and by dextromethorphan, putative sigma receptor agonists, but not by other sigma receptor ligands, (+)-pentazocine and 1,3-di-(2-tolyl)guanidine (DTG). Unlike (+)-SKF-10,047 and dextromethorphan, the non-competitive NMDA receptor antagonists, phencyclidine and dizocilpine, attenuated the conditioned fear stress only at high doses that induced marked hypermotility in non-stressed mice. The effects of (+)-SKF-10,047 and dextromethorphan, but not phencyclidine and dizocilpine, on the conditioned fear stress were antagonized by the sigma receptor antagonists, NE-100 (N,N-dipropyl-2-[4-methoxy-3-(2- phenylethoxy)phenyl]-ethylamine monohydrochloride) and BMY-14802 (alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazine- butanol hydrochloride). Interestingly, the effects of (+)-SKF-10,047 and dextromethorphan on the stress response were enhanced by combination with phenytoin, an anticonvulsant drug, whereas those of (+)- pentazocine, DTG, phencyclidine, and dizocilpine were not. These results suggest that activation of phenytoin-regulated type sigma 1 receptors, but not of phencyclidine receptors, is involved in the ameliorating effects of (+)-SKF-10,047 and dextromethorphan on stress-induced motor suppression.
PMID: 8901003
[Anti-amnesic effects of sigma (sigma)-receptor agonists]
[Article in Japanese]Matsuno K.
Discovery Research Division, Santen Pharmaceutical Co., Ltd., Osaka, Japan.
Both traditional and novel sigma (sigma)-receptor agonists have been reported to possess anti-amnesic effects in rodents. In particular, the anti-amnesic effects induced by the novel sigma1-receptor agonists, such as (+)-pentazocine, SA4503 and PRE-084, were shown in beta amyloid-peptide-induced, basal forebrain (BF)-lesioned and carbon monoxide (CO)-induced amnesia models and senescence-accelerated mouse (SAM). In addition, these sigma1-receptor agonists have good profiles for the central acetylcholine and dopamine systems. Moreover, they also have neuroprotective and anti-depressive effects. These evidence suggested that the sigma1-receptor agonists may be promising compounds for the treatment of dementing disorders such as Alzheimer's disease, senile dementia and vascular dementia. However, the sigma-receptor family is still considered to be enigmatic molecular targets. More molecular cloning and biochemical studies on the sigma-receptor family are needed.
PMID: 10562962
Dehydroepiandrosterone alleviates copulatory disorder induced by social stress in male rats.
INTRODUCTION: Social stress induces sexual dysfunction and reduces serum testosterone (T) level in rats. Stressful events exert an influence on a variety of behaviors and physiology through hormonal changes. The mechanism of stress-induced sexual dysfunction is unknown. AIM: To investigate the role of dehydroepiandrosterone (DHEA) in copulatory behavior induced by social stress in rats. METHODS: Stress-induced male rats were subjected to social stress in which the males lived in a wire-mesh siege located in a colony of male and female rats and were exposed daily to a brief defeat by the colony of males for five consecutive days. After the stress period, copulatory behavior and serum concentrations of DHEA and T were measured. MAIN OUTCOME MEASURES: The effects of DHEA, T, and NE-100, a selective sigma 1 receptor antagonist, on copulatory behavior following social stress were examined. RESULTS: The males exhibited a marked suppression of copulatory behavior (elongation of intromission and ejaculation latencies). Serum concentrations of DHEA and T were significantly lower than those in nonstressed control males. Another three groups of social stressed males were injected daily with DHEA, T, or DHEA + NE-100 during the stress period. Injections of DHEA attenuated the stress-induced suppression of copulatory behavior, whereas T had no effect. The combined treatment of NE-100 made DHEA ineffective at restoring copulatory behavior. CONCLUSIONS: These results indicate that DHEA, but not its conversion to T, alleviates the suppressive effect of social stress on copulatory behavior via sigma 1 receptors. We suggest that the decreased endogenous DHEA is involved in copulatory disorders induced by social stress in rats.
PMID: 16839317
i think it is also anticarcinogenic in some way...
cocaine, memantine, and dextromethorphan also are ligands for it...haldol is a strong antagonist.
-d/r
Posted by linkadge on January 26, 2009, at 8:23:24
In reply to Re: * Seroquel - Why does it help so many conditions? » SLS, posted by desolationrower on January 25, 2009, at 21:51:54
At some point in time most other AP's were lauded for their broad spectrum efficacy.
Take Zyprexa. It has been used as a mood stabilizer, an antipsychotic, unipolar depressive adjunctive, GAD (although not approvied), insomnia, etc. etc.
Although I think doctors lean more towards seroquel now because of less precived metabolic risks.
I think seroquel is just the new zyprexa.
Linkadge
Posted by desolationrower on January 26, 2009, at 11:14:17
In reply to Re: Its just like every other AP, posted by linkadge on January 26, 2009, at 8:23:24
iirc seroquel was less effective for schiz than the others.
-d/r
Posted by ricker on January 26, 2009, at 13:26:01
In reply to Re: Its just like every other AP, posted by linkadge on January 26, 2009, at 8:23:24
> At some point in time most other AP's were lauded for their broad spectrum efficacy.
>
> Take Zyprexa. It has been used as a mood stabilizer, an antipsychotic, unipolar depressive adjunctive, GAD (although not approvied), insomnia, etc. etc.
>
> Although I think doctors lean more towards seroquel now because of less precived metabolic risks.
>
> I think seroquel is just the new zyprexa.
>
>
> Linkadge
Agree, although I had to dump seroquel and go back on Zyprexa...too many side effects. I find zypreza much smoother.
Posted by SLS on January 26, 2009, at 16:27:46
In reply to Re: Its just like every other AP, posted by linkadge on January 26, 2009, at 8:23:24
> I think seroquel is just the new zyprexa.
Some percentage of people are going to glean a POTENT antidepressant response from Seroquel whom won't respond to Zyprexa.
- Scott
Posted by linkadge on January 26, 2009, at 18:09:26
In reply to Re: Its just like every other AP, posted by SLS on January 26, 2009, at 16:27:46
>Some percentage of people are going to glean a >POTENT antidepressant response from Seroquel >whom won't respond to Zyprexa.
I am sure the converse statemet is also true.
I personally found zyprexa to be a bit smoother than seroquel too. I think I would probably still be on zyprexa if it didn't mess with my blood sugar.
Linkadge
Posted by Nadezda on January 26, 2009, at 19:16:33
In reply to Re: Its just like every other AP, posted by SLS on January 26, 2009, at 16:27:46
I was wondering what would be your guess as to a minimum dose where the non-sedating effect you describe would take place.
I've been taking seroquel 25 mg every other night or so as a soporific, and when I took a brief vacation to renew that effect, my level of depression increased noticeably. It seems clearly related to the seroquel, and remits when I start seroquel again. This has happened on several other occasions with seroquel holidays.
I was wondering if I should (possibly at least) discuss a somewhat higher dose with my pdoc. He had given me the seroquel for sleep, but mentioned previously that he thought it might also be affecting my depression. (I tend to respond to small doses of meds.) There are obviously other considerations and I wouldn't want to take too large a dose.
Nadezda
Posted by SLS on January 26, 2009, at 20:07:39
In reply to Re: Its just like every other AP » SLS, posted by Nadezda on January 26, 2009, at 19:16:33
I think you can start to see an energizing effect begin between 100-200mg. I witnessed an incredible turn around in a woman who added Seroquel to Wellbutrin. Initially, her doctor had tried a low dosage of Risperdal. To that, he added 50mg or Seroquel. Upon the addition, it was if she awoke out of a coma. Her depression remitted withing 12 hours. At that point, they decided to discontinue the Risperdal, but found that they needed to use at least 400mg of Seroquel to maintain the antidepressant response.
Everyone is so different. It is hard to try to recommend a course of action for someone when there is so much uncertainty. You could probably go right up to 100mg and go from there.
- Scott
Posted by sam K on January 26, 2009, at 21:53:25
In reply to Re: Its just like every other AP » Nadezda, posted by SLS on January 26, 2009, at 20:07:39
I'm just curious, what do you take zyprexa for? When I took zyprexa I felt incredibly strage. But I also felt very relaxed for the first time. Do you guys feel more normal on AP's? I just get a wierd feeling on all of them. The only thing that seems to make me feel more normal is antidepressants and maybe mood stabilzers
Posted by JadeKelly on January 27, 2009, at 8:35:38
In reply to Re: * Seroquel - Why does it help so many conditions? » SLS, posted by desolationrower on January 25, 2009, at 21:51:54
> > > quetiapine is also a pretty strong alpha2 antagonist. it might interact with the sigma receptor as well. and 5ht6 and some other receptors not well understood.
> >
> >
> > I know nothing about sigma receptors.
> >
> >
> > - Scott
>
> its probably worth looking into...
>
> Sigma-1 receptor ligands: potential in the treatment of neuropsychiatric disorders.
>
> The sigma receptor was originally proposed to be a subtype of the opioid receptor. However, it is now clear that sigma receptors are unique non-opioid, non-phencyclidine brain proteins. Two types of sigma receptor exist, the sigma-1 receptor and the sigma-2 receptor. sigma-1 receptors have been cloned and their distribution, physiological functions and roles in signal transduction were recently characterised. Certain sex hormones in the brain (neurosteroids) are known to interact with sigma-1 receptors. sigma-1 receptors regulate glutamate NMDA receptor function and the release of neurotransmitters such as dopamine. They are thus proposed to be involved in learning and memory as well as in certain neuropsychiatric disorders. Selective sigma-1 receptor ligands have been suggested to represent a new class of therapeutic agents for neuropsychiatric disorders, although none have yet been introduced into therapeutic use. Early studies showed that psychotomimetic benzomorphans, as well as several antipsychotics, can bind to sigma-1 receptors. As a result of these findings, sigma-1 receptor ligands have been proposed as being of potential use in the treatment of schizophrenia. Nevertheless, the relationship of sigma-1 receptors to the underlying pathogenesis of schizophrenia is still unclear. sigma-1 receptor ligands have failed to improve acute psychotic symptoms of schizophrenia in clinical trials, but, interestingly, a few studies have shown an improvement in negative symptoms in schizophrenic patients. A number of preclinical studies have shown that selective agonists of sigma-1 receptors affect higher-ordered brain functions such as learning and memory, cognition and mood. These studies indicate that sigma-1 receptor agonists may exert therapeutic effects in depression and senile dementia. Indeed, the sigma-1 receptor agonist igmesine, has been shown to improve depression in a clinical trial. The most distinctive feature of the action of sigma-1 receptor ligands is their "modulatory" role. In behavioural studies of depression and memory, they exert beneficial effects only when brain functions are perturbed.Given the recently accumulated preclinical and clinical data, it is time to reconstruct the concept of sigma-1 receptors and the associated pathophysiological conditions that ligands of these receptors target. This would allow clinical trials to be performed more efficiently, and the results may confirm a long-speculated possibility that sigma-1 receptor ligands represent a new class of therapeutic agents for neuropsychiatric disorders.
>
> PMID: 15089113
>
> Phencyclidine-induced cognitive deficits in mice are improved by subsequent subchronic administration of fluvoxamine: role of sigma-1 receptors.
>
> This study was undertaken to examine the effects of the selective serotonin reuptake inhibitors fluvoxamine and paroxetine on cognitive deficits in mice after repeated administration of the N-methyl-D-aspartate receptor antagonist phencyclidine (PCP). In the novel object recognition test, repeated administration of PCP (10 mg/kg/day, 10 days) significantly decreased the exploratory preference in the retention test session, but not in the training test session. PCP-induced cognitive deficits were significantly improved by subsequent subchronic (2-week) administration of fluvoxamine (20 mg/kg/day), but not paroxetine (10 mg/kg/day). Furthermore, the effect of fluvoxamine on PCP-induced cognitive deficits was antagonized by co-administration of the selective sigma-1 receptor antagonist NE-100 (1 mg/kg/day). Moreover, PCP-induced cognitive deficits were also significantly improved by subsequent subchronic (2-week) administration of the selective sigma-1 receptor agonist SA4503 (1 mg/kg/day) or neurosteroid dehydroepiandrosterone 3-sulfate (DHEA-S; 25 mg/kg/day). The effects of SA4503 or DHEA-S were also antagonized by co-administration of NE-100 (1 mg/kg/day), suggesting the role of sigma-1 receptors in the active mechanisms of these drugs. In contrast, acute single administration of these drugs (fluvoxamine, paroxetine, SA4503) alone or combination with NE-100 did not alter PCP-induced cognitive deficits. The present study suggests that agonistic activity of fluvoxamine at sigma-1 receptors plays a role in the active mechanisms of fluvoxamine on PCP-induced cognitive deficits in mice. Therefore, sigma-1 receptor agonists such as fluvoxamine would be potential therapeutic drugs for the treatment of the cognitive deficits of schizophrenia.
>
> PMID: 16495935
>
>
> [Sigma-receptor ligands and anti-stress actions]
> [Article in Japanese]
>
> Noda Y, Kamei H, Nabeshima T.
>
> Department of Neuropsychopharmacology, Nagoya University Graduate School of Medicine, Japan.
>
> The functional role of sigma receptors in the central nervous system has been investigated extensively. Sigma1-receptors have been shown to play an important role in antidepressive effects since selective sigma1-receptor agonists, as well as typical antidepressants, reduced the immobility time in the forced swimming and tail suspension tests. The reduction of immobility by sigma1-receptor agonists is antagonized by NE-100, a sigma1-receptor antagonist. It has been suggested that sigma receptors are involved in anxiety since Lu 28-179, a sigma2-receptor agonist, has anxiolytic properties in rodents. In addition to the depressive animal model, phenytoin-sensitive sigma1-receptor agonists such as (+)-SKF-10,047 and dextromethorphan attenuate the conditioned fear stress (CFS) response (which is not influenced by typical anxiolytics and antidepressants) in rodents, the attenuating effects being mediated through phenytoin-sensitive sigma1 receptors, which are closely connected to the mesolimbic dopaminergic systems. Furthermore, neurosteroids such as dehydroepiandrosterone sulfate also attenuate the CFS response, the effect being mediated via sigma1 receptors. These findings suggest that sigma receptors are involved in stress-induced pathophysiological changes such as depression and anxiety and that phenytoin-sensitive sigma1-receptor ligands are useful for the treatment of affective disorders, particularly those considered to be treatment-resistant.
>
> PMID: 10562964
>
> (+)-SKF-10,047 and dextromethorphan ameliorate conditioned fear stress through the activation of phenytoin-regulated sigma 1 sites.
> Kamei H, Kameyama T, Nabeshima T.
>
> Department of Chemical Pharmacology, Meijo University, Nagoya, Japan.
>
> Mice exhibited a marked suppression of motility when they were replaced in the same environment in which they had previously received an electric footshock. This psychological stress-induced motor suppression, known as conditioned fear stress, was dose dependently attenuated by (+)-N-allylnormetazocine ((+)-SKF-10,047) and by dextromethorphan, putative sigma receptor agonists, but not by other sigma receptor ligands, (+)-pentazocine and 1,3-di-(2-tolyl)guanidine (DTG). Unlike (+)-SKF-10,047 and dextromethorphan, the non-competitive NMDA receptor antagonists, phencyclidine and dizocilpine, attenuated the conditioned fear stress only at high doses that induced marked hypermotility in non-stressed mice. The effects of (+)-SKF-10,047 and dextromethorphan, but not phencyclidine and dizocilpine, on the conditioned fear stress were antagonized by the sigma receptor antagonists, NE-100 (N,N-dipropyl-2-[4-methoxy-3-(2- phenylethoxy)phenyl]-ethylamine monohydrochloride) and BMY-14802 (alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazine- butanol hydrochloride). Interestingly, the effects of (+)-SKF-10,047 and dextromethorphan on the stress response were enhanced by combination with phenytoin, an anticonvulsant drug, whereas those of (+)- pentazocine, DTG, phencyclidine, and dizocilpine were not. These results suggest that activation of phenytoin-regulated type sigma 1 receptors, but not of phencyclidine receptors, is involved in the ameliorating effects of (+)-SKF-10,047 and dextromethorphan on stress-induced motor suppression.
>
> PMID: 8901003
>
> [Anti-amnesic effects of sigma (sigma)-receptor agonists]
> [Article in Japanese]
>
> Matsuno K.
>
> Discovery Research Division, Santen Pharmaceutical Co., Ltd., Osaka, Japan.
>
> Both traditional and novel sigma (sigma)-receptor agonists have been reported to possess anti-amnesic effects in rodents. In particular, the anti-amnesic effects induced by the novel sigma1-receptor agonists, such as (+)-pentazocine, SA4503 and PRE-084, were shown in beta amyloid-peptide-induced, basal forebrain (BF)-lesioned and carbon monoxide (CO)-induced amnesia models and senescence-accelerated mouse (SAM). In addition, these sigma1-receptor agonists have good profiles for the central acetylcholine and dopamine systems. Moreover, they also have neuroprotective and anti-depressive effects. These evidence suggested that the sigma1-receptor agonists may be promising compounds for the treatment of dementing disorders such as Alzheimer's disease, senile dementia and vascular dementia. However, the sigma-receptor family is still considered to be enigmatic molecular targets. More molecular cloning and biochemical studies on the sigma-receptor family are needed.
>
> PMID: 10562962
>
> Dehydroepiandrosterone alleviates copulatory disorder induced by social stress in male rats.
>
> INTRODUCTION: Social stress induces sexual dysfunction and reduces serum testosterone (T) level in rats. Stressful events exert an influence on a variety of behaviors and physiology through hormonal changes. The mechanism of stress-induced sexual dysfunction is unknown. AIM: To investigate the role of dehydroepiandrosterone (DHEA) in copulatory behavior induced by social stress in rats. METHODS: Stress-induced male rats were subjected to social stress in which the males lived in a wire-mesh siege located in a colony of male and female rats and were exposed daily to a brief defeat by the colony of males for five consecutive days. After the stress period, copulatory behavior and serum concentrations of DHEA and T were measured. MAIN OUTCOME MEASURES: The effects of DHEA, T, and NE-100, a selective sigma 1 receptor antagonist, on copulatory behavior following social stress were examined. RESULTS: The males exhibited a marked suppression of copulatory behavior (elongation of intromission and ejaculation latencies). Serum concentrations of DHEA and T were significantly lower than those in nonstressed control males. Another three groups of social stressed males were injected daily with DHEA, T, or DHEA + NE-100 during the stress period. Injections of DHEA attenuated the stress-induced suppression of copulatory behavior, whereas T had no effect. The combined treatment of NE-100 made DHEA ineffective at restoring copulatory behavior. CONCLUSIONS: These results indicate that DHEA, but not its conversion to T, alleviates the suppressive effect of social stress on copulatory behavior via sigma 1 receptors. We suggest that the decreased endogenous DHEA is involved in copulatory disorders induced by social stress in rats.
>
> PMID: 16839317
>
> i think it is also anticarcinogenic in some way...
>
> cocaine, memantine, and dextromethorphan also are ligands for it...haldol is a strong antagonist.
>
> -d/r
--------------------------------------------------Thanks for that d/r,
I won't be needing any sleep meds tonight.
Seroquel to me, acts differently than Abilify and Respirdal. It seems in its own class. From what I've seen, it does wonders for Bi-polarI Mania, AND Bi-polar depression. 100mg in morn and 200mg bedtime. Total 300mg day. There isn't any of that emotional blunting or apathy as I've seen with Abilify and Respirdal. This is one personal experience, YMMV.
Hope this helps someone,
~Jade
Posted by SLS on January 27, 2009, at 8:56:48
In reply to Re: Its just like every other AP, posted by sam K on January 26, 2009, at 21:53:25
> I'm just curious, what do you take zyprexa for? When I took zyprexa I felt incredibly strage. But I also felt very relaxed for the first time. Do you guys feel more normal on AP's? I just get a wierd feeling on all of them. The only thing that seems to make me feel more normal is antidepressants and maybe mood stabilzers
Is there anything lacking in the way you feel right now?
I suffer from bipolar disorder - chronic depressive subtype. For me, Risperdal, Zyprexa, Geodon, and Abilify produce a smoothing out of mood. Zyprexa in particular cleared up my thinking and brought me out of a severe suicidal depression several times. However, I still remained profoundly depressed. Abilify seems to increase motivation and energy for me. When added to the other drugs I am taking, it is critical to produce the improvement that I am enjoying today.
Interestingly, Seroquel produced an agitated dysphoria for me. As disgusting as this drug made me feel, I still recognize the effectiveness it has when used by others.
If you experience recurrent depressions, it might be time to think about taking antidepressants indefinitely. That you are still responsive to antidepressants is a blessing. You might want to take advantage of it.
- Scott
Posted by Phillipa on January 27, 2009, at 19:33:45
In reply to Re: Its just like every other AP, posted by SLS on January 27, 2009, at 8:56:48
Scott so sorry you're still depressed but optimistic as always. Love Phillipa
Posted by SLS on January 27, 2009, at 20:30:18
In reply to Re: Its just like every other AP » SLS, posted by Phillipa on January 27, 2009, at 19:33:45
> Scott so sorry you're still depressed but optimistic as always. Love Phillipa
I'm not sure what gave you that idea.
I'm doing quite well, actually.
:-)
- Scott
Posted by Phillipa on January 27, 2009, at 23:54:44
In reply to Re: Its just like every other AP » Phillipa, posted by SLS on January 27, 2009, at 20:30:18
Scott that's great. Was in hurry so must have read wrong. Sorry about that but fantastic you're doing great!!!!! Love Phillipa
Posted by parkscat on January 28, 2009, at 9:14:41
In reply to Re: Its just like every other AP » SLS, posted by Phillipa on January 27, 2009, at 23:54:44
Posted by parkscat on January 28, 2009, at 9:18:15
In reply to Re: Its just like every other AP (nm), posted by parkscat on January 28, 2009, at 9:14:41
I just can not get excited about anything but still anxious. Help!
Posted by SLS on January 28, 2009, at 9:34:44
In reply to Am on this and Lamictal and Zoloft, posted by parkscat on January 28, 2009, at 9:18:15
> I just can not get excited about anything but still anxious. Help!
Can you extend your description of what you are experiencing?
Diagnosis?
Treatment History?
- Scott
Posted by parkscat on January 28, 2009, at 9:39:47
In reply to Re: Am on this and Lamictal and Zoloft » parkscat, posted by SLS on January 28, 2009, at 9:34:44
Have been on Effexor then Cymbalta but now on Seraquel, Lamictal and Zoloft. Doc said instead of treating me for depression he started treating me foe anxiety. Before I had highs and lows. Now I am just here. No highs or lows no motivation. No lust for life. When I go home I feel like doing nothing but sleeping. I get through work but not with the exciment I use to but still have a anxious feeling in my chest. Danny
Posted by SLS on January 28, 2009, at 10:08:14
In reply to Re: Am on this and Lamictal and Zoloft, posted by parkscat on January 28, 2009, at 9:39:47
> Have been on Effexor then Cymbalta but now on Seraquel, Lamictal and Zoloft. Doc said instead of treating me for depression he started treating me foe anxiety. Before I had highs and lows. Now I am just here. No highs or lows no motivation. No lust for life. When I go home I feel like doing nothing but sleeping. I get through work but not with the exciment I use to but still have a anxious feeling in my chest. Danny
It is possible, but not guaranteed, that you might recieve an antidepressant effect from Seroquel at higher dosages. Some people have their head clear at the higher dosages. If not, you might want to try Abilify, which is another antipsychotic used for depression. Sometimes, anxiety gets worse before it gets better. This anxiety usually disappears in a week or so. I am on this drug. It is mentally "clean". I am clear-headed, have more energy, and more motivation.
- Scott
Posted by yxibow on January 30, 2009, at 10:54:18
In reply to Re: Its just like every other AP, posted by linkadge on January 26, 2009, at 8:23:24
> At some point in time most other AP's were lauded for their broad spectrum efficacy.
>
> Take Zyprexa. It has been used as a mood stabilizer, an antipsychotic, unipolar depressive adjunctive, GAD (although not approvied), insomnia, etc. etc.
>
> Although I think doctors lean more towards seroquel now because of less precived metabolic risks.
>
> I think seroquel is just the new zyprexa.
>
>
> Linkadge
Perhaps -- metabolic risks per agent though can vary considerably by person, even Risperdal has a potential.There's nothing "new" about Seroquel and Zyprexa, considering they were on the market around 1996-1997 (Seroquel's patent expires 2011) and Risperdal is already generic.
-- Jay
Posted by Neal on February 7, 2009, at 1:15:59
In reply to Seroquel - Why does it help so many conditions?, posted by SLS on January 25, 2009, at 10:54:32
I thought Seroquel was brand name for doxepin generic.
quetiapine - I haven't heard that name.?..
-Neal
Posted by SLS on February 7, 2009, at 5:29:40
In reply to Re: Seroquel - Why does it help so many conditions?, posted by Neal on February 7, 2009, at 1:15:59
> I thought Seroquel was brand name for doxepin generic.
>
> quetiapine - I haven't heard that name.?..
>
> -NealHi Neal. You are probably thinking of Sinequan (doxepin), the tricylic antidepressant. Seroquel (quetiapine) is an antypical antipsychotic.
- Scott
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