![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 31 to 55 of 56. Go back in thread:
Posted by AndrewB on April 13, 2000, at 10:57:45
In reply to Re: Uprima - libido vs erection, posted by Scott L. Schofield on April 13, 2000, at 10:08:18
Thanks Scott,
Sounds like apomorphine makes one more functional but we're still looking for the love potion that makes the one beside us the object of our desire.
Posted by Sherry on April 13, 2000, at 18:15:22
In reply to Re: Uprima - libido vs erection, posted by Scott L. Schofield on April 13, 2000, at 10:08:18
Scott,
I'm glad you're back!
Sherry> Although of Uprima (apomorphine) can be made to induce copulatory behavior when injected into specific areas of the brain in rats, I have not encountered anything to suggest that oral or parenteral administration results in increased libido in humans. It may prove itself to do so, but I don't find enough medical literature on Medline to indicate this with any confidence. The CNN report seems accurate.
>
> Apomorphine has long been recognized as being capable of producing erections. There seem to be two mechanisms involved.
>
> 1. Stimulation of the medial preoptic area and/or paraventricular nucleus of the hypothalamus.
> - I believe these are the same mechanisms involved in the induction of the nocturnal erections that occur during rapid eye movement sleep (REM).
> * The preoptic area may also be involved with libido.
>
> 2. Increasing the pressure of the "balloon" (corpus cavernosum) located within the penis, causing it to grow in size and stiffness.
>
> Among the more important observations regarding this issue is the lack of the ability of apomorphine to reverse the decrease of libido in mice caused by the loss of testosterone brought about through castration.
>
>
> ------------------------------------------
>
>
> For Andrew:
>
> Apomorphine is one of those drugs that produce opposite effects at low dosages versus high dosages. Apomorphine represents the antithesis of sulpiride and amisulpride. Low dosages produce sedation, while high dosages produce activation and stereotypic behavior. Presynaptic versus postsynaptic regulation.
>
>
> - Scott
Posted by FP on April 13, 2000, at 21:12:39
In reply to Re: Uprima, apomorphine, posted by AndrewB on April 12, 2000, at 9:45:11
I'm dating myself, but William S Burroughs, the junky and "Beat" writer claimed that Apomorphine permanantly cured his craving for heroin. Has anyone ever examined his claim and debunked it, or could there be something to it?
Thanks,
FP
Posted by Fred Potter on April 13, 2000, at 22:35:16
In reply to Re: Uprima, apomorphine - Cam W?, posted by FP on April 13, 2000, at 21:12:39
> I'm dating myself,
I hope you'll both be very happy
>but William S Burroughs, the junky and "Beat" writer claimed that Apomorphine permanantly cured his craving for heroin
But seriously, I wouldn't trust William Burroughs to keep a budgie's pot filled with water
Posted by Cam W. on April 13, 2000, at 23:18:46
In reply to Re: Uprima, apomorphine - Cam W?, posted by FP on April 13, 2000, at 21:12:39
> I'm dating myself, but William S Burroughs, the junky and "Beat" writer claimed that Apomorphine permanantly cured his craving for heroin. Has anyone ever examined his claim and debunked it, or could there be something to it?
>
> Thanks,
> FPFP - I dunno about the apomorphine curing his craving for morphine. For the amount of crap he put into his body, I'm amazed he lived as long as he did. Apomorphine is a dopamine agonist, which perhaps raises dopamine signals (or levels) in the nucleus accumbens (pleasure center thought to be involved in the reinforcement of addictions). Most (if not all) drugs to make you "high" or feel good increase dopamine levels in the nucleus accumbens. When the dopamine levels fall after the drug wears off you crave the increase of dopamine in the nucleus accumbens again, so you take another dose. I think this is how reinforcement works. - Cam W.
P.S. - Burroughs, Kerouac, Cassidy, Ginsberg, et al, were a wacky bunch, weren't they?
Posted by Liz on April 15, 2000, at 12:49:52
In reply to Re: sign me up! (to liz) any opinion Cam?, posted by CarolAnn on April 11, 2000, at 18:05:27
I was cruising through some pharmacy sites this morning and got interested in some of the new drug trials, etc. There is a drug in trials right now from Zonagen, Inc. called Vasofem. (They already market a drug called Vasomax for men which is used treat erectile dysfunction in men.) The oral tablet for women had positive results in pilot studies and is proceeding to phase I trials. The drug is described as "an alpha adrenegic receptor blocker" designed to increase blood flow to the genitals. (generic name: phentolamine mesylate) The initial tests used only post-menopausal women that had complained of vaginal dryness, decreased sexual response, pain w/intercourse and/or anorgasmia. Apparently all the women reported an improved sexual response, enough to encourage further study at least! Also of interest was a summary of the use of Viagra for women. (Pasted quote below) The main point is that research has shown that women who suffer sexual dysfunction due to SSRIs seem to have the best response to Viagra!
"Studies of Viagra in women whose sexual dysfunction may stem from antidepressant use report a more significant effect, however. One study assessed 50 mg Viagra in 9 women who reported sexual dysfunction induced by antidepressant medication, primarily selective serotonin reuptake inhibitors. Patients were instructed to take Viagra approximately 1 hour before sexual activity and were told to increase the dose to 100 mg on the next occasion if they experienced a partial response or a lack of response. The nine patients, all of whom had experienced either anorgasmia or delayed orgasm with or without associated disturbances, reported significant reversal of sexual dysfunction, usually with the first 50 mg dose of Viagra."
Now for the guys: Another drug just got FDA approval and should be available by prescription by mid-summer; its called Androgel and is for a topical application of testosterone to be applied at 24 hour dosing intervals to the upper torso area. Its a colorless get that dries quickly, then is absorbed into the blood stream. I understand that prior to this, men who benefitted from increasing their level of testosterone had previously a choice between deep muscle injections or transdermal patches only. The condition for which it is to be prescribed is called hypogonadism, which I think is another name with perhaps additional symptoms that all result from low levels of testosterone. Anyway, the last sentence of the summary states that virtually all men (w/ lowered testosterone levels) in the study reported an increase in libido, pleasure, ability to maintain erections longer, etc; they also reported significant anti-depressive results from the gel. Are men screened for lower than average testosterone levels as a routine part of their healthcare?? Seems like that would be a place to start for many men w/ a sexual dysfunction. I thought this might have bearing on the libido vs. erection discussion we've been having here....maybe depressed mean with lower libido complaints would benefit even if their testosterone levels are within "normal" ranges.
Just a thought...
PS I'm supposed to be packing our family to catch a plane to Florida tomorrow and here I am, spending hours surfing the web instead...where has all my usual anxiety and panic gone??!! Today I might benefit from no meds! For anyone who might miss me, I'll be severed from my computer for more than a week; I'll look forward to catching up with babblelanders on my return. Liz
*************************************************Your reasoning sounds right to me, liz. Also, the dopamine factor intrigues me. If the drug signals the hypothalmous to release dopamine, I wonder if it could be researched as a possible antidepressant? At any rate, if dopamine affects the genitals the way it affects the brain, well, that's got to be a good thing! CarolAnn
Posted by Scott L. Schofield on April 16, 2000, at 13:59:08
In reply to CarolAnn, et al: an update/Vasomax Vasofem, etc , posted by Liz on April 15, 2000, at 12:49:52
> I was cruising through some pharmacy sites this morning and got interested in some of the new drug trials, etc. There is a drug in trials right now from Zonagen, Inc. called Vasofem. (They already market a drug called Vasomax for men which is used treat erectile dysfunction in men.) The oral tablet for women had positive results in pilot studies and is proceeding to phase I trials. The drug is described as "an alpha adrenegic receptor blocker" designed to increase blood flow to the genitals. (generic name: phentolamine mesylate) The initial tests used only post-menopausal women that had complained of vaginal dryness, decreased sexual response, pain w/intercourse and/or anorgasmia. Apparently all the women reported an improved sexual response, enough to encourage further study at least! Also of interest was a summary of the use of Viagra for women. (Pasted quote below) The main point is that research has shown that women who suffer sexual dysfunction due to SSRIs seem to have the best response to Viagra!
Thanks mucho for this post.
All of this time while watching the Johnny-On-The-Spot commercials, I had no idea that Vasomax was actually phentolamine. This drug is also used as an antihypertensive and is called Regitine. It was at one time available as an oral preparation, but was discontinued in favor of the injectable. It is always available in hospital emergency rooms, and has been considered the treatment of choice for MAO-inhibitor related hypertensive reactions, such as the tyramine "cheese-effect". I've been hoping that an oral form would again appear so as to carry it around with me as a safety precaution. Previously, I had been using nifedipine (Procardia), to be administered sub-lingually (under the tongue, similar to nitroglycerine). I am hoping that Vasomax would be more effective than Procardia.
When I looked into the Vasomax / Vasofem situation, I discovered why there would be "one for him" and "one for her". Vasofem and Vasomax are both preparations of phentolamine. However, Vasofem is a vaginal suppository that is thought may be more effective than the oral preparation for treating the more severe cases of sexual impairment.
Have you seen anything regarding the use of Vasomax in females?
> Your reasoning sounds right to me, liz. Also, the dopamine factor intrigues me. If the drug signals the hypothalmous to release dopamine, I wonder if it could be researched as a possible antidepressant? At any rate, if dopamine affects the genitals the way it affects the brain, well, that's got to be a good thing!
With regard to Uprima (apomorphine), I think somebody at CNN really screwed-up. Uprima does not induce the release of dopamine from the hypothalamus, it induces the release of oxytocin. This oxytocin then travels through the blood-stream to reach its target tissues. The little red line on the CNN graphic should have been labelled "oxytocin", not "dopamine". I believe oxytocin is also responsible for the ejection of milk through the nipple in lactating women (as opposed to lactating men).
Apomorphine is actually fake dopamine. It is similar in this regard to such drugs as bromocryptine (Parlodel), pergolide (Permax), and pramipexole (Mirapex), all of which have been used with reported success for treating depression, along with their primary indications for the treatment of Parkinson's Disease.
- Scott
Posted by boB on April 16, 2000, at 21:14:38
In reply to Re:to liz - serotonin and dopamine - musings, posted by Cam W. on April 11, 2000, at 23:19:39
this is a new one on me. ... serotinin and dopamine interact in opposition?
i have heard about norepinephrine interacting more or less in opposition to serotonin, and acetecholine acting in opposition to aminergins...
I'm not very well grounded in neurochemistry, but i can struggle through an article on the subject if you know where to send me. How do serotonin and dopamine interact in opposition
Posted by Cam W. on April 16, 2000, at 22:52:07
In reply to Cam - serotonin and dopamine opposition, posted by boB on April 16, 2000, at 21:14:38
boB - I do believe that dopamine and serotonin antagonize each others actions. I can see in my mind's eye the notes that I took at a schizophrenia conference a few years ago. The notes are in my files at work. I will pull them out for a clearer definition than in the example I am going to give you below.An example of this in action is with the atypical antipsychotics (eg Clozaril, Zyprexa, Risperdal, etc.). All of these have a greater affinity for blocking serotonin-2A (5HT-2A) receptors than dopamine-D2 (D2) receptors, but still have action at the dopamine receptors. The mechanism of action of the traditional neuroleptics (eg Haldol, Largacil, Mellaril, etc.) is thought to be dopamine-D2 blockade.
5HT-2A receptors are concentrated in the reticular activating system (raphe nuclei) and in limbic regions. D2 receptors are concentrated in the limbic system and in the prefrontal cortex. So by blocking D2 receptors in the prefrontal cortex you are relieving the postive symptoms of schizophrenia. But (here is where the opposition occurs) by blocking 5HT-2A receptors in the limbic system and sparing dopamine transmission (due to receptor affinity differences) you do not get the movement disorders from the atypical antipsychotics, as you would with the traditional antipsychotics. The 5-HT-2A blockade in the limbic system increase the flow of dopamine, but in the prefrontal cortex (where there is a lack of 5HT-2A receptors) the D2 blockade acts upon the positive symptoms of schizophrenia.
If I remember (and can find my notes) I will post a more insightful answer tomarrow. I will also give you the reference so you can look up the article from where I got this as well. - Cam W.
Posted by Cam W. on April 16, 2000, at 23:28:50
In reply to Re: Cam - serotonin and dopamine opposition, posted by Cam W. on April 16, 2000, at 22:52:07
boB - Well, I'll be horse-whipped! Never underestimate the power of the Google Search Engine. I found the article right away in The American Journal of Psychiatry. If you have access to a university library, look up the following article. It is very interesting (they want you to pay for an on-line subscription). The abstract does mention the serotonin/dopamine interaction though (see FINDINGS).
http://ajp.psychiatryonline.org/cgi/content/abstract/153/4/466
S.Kapur and G.Remington -
"Serotonin-dopamine interaction and its relevance to schizophrenia."Happy reading - Cam W.
Posted by boB on April 17, 2000, at 17:42:32
In reply to Re: Cam - serotonin and dopamine opposition, posted by Cam W. on April 16, 2000, at 23:28:50
> Cam - it might be a few weeks until I can get hold of that entire article. I think I get a sense of what you are saying about working in opposition, but I don't get the sense you are saying high serotinin activity neccesarily means low dopamine activity and vice versa. Am I on the right track?
Posted by Cam W. on April 17, 2000, at 18:44:16
In reply to Re: Cam - serotonin and dopamine opposition, posted by boB on April 17, 2000, at 17:42:32
boB - Yes I blieve that you are on the right track. I don't think that a high serotonin level means that there is a low dopamine levels or vice versa. I think it is more of a situation where one neurotransmitter 'influences' the other. I believe that there could be situations where both are high and both are low. These two neurotransmitter do not work in a vacuum and several of the other neurotransmitters (eg glutamate, GABA, norepinephrine, peptides, endorphins, etc.) also play a role in serotonin and dopamine levels. Also genetics would have a role, as would the endocrine system. I do not have a total grasp on this concept, so I cannot be sure of exactly how it works. Sincerely - Cam W.
Posted by boB on April 17, 2000, at 20:48:41
In reply to Re: Cam - serotonin and dopamine opposition, posted by Cam W. on April 17, 2000, at 18:44:16
thanks, Cam,
Maybe you can help me with this one though - doesn't a lot of sensory processing and learning have to do with an inititial jolt of norepenephrine, which is somehow ...what is the word?. it - the norepenephrine networks - continue to increase in amplitude or something until a familiar network - like a familiar concept or experience - allows a reinforcing neurotransmitter to establish a stable .. uh a stable uh .. thought?
i cant remember where I got that idea but I know I'm not smart enough to make it up. I don't have ready access to the libraries where I was boning up on neurochemistry, so I can't recall if I synthesized the idea from several sources or if that is the way a very well informed brain scientist explained it in a very expensive book.
i am much more confident of my understanding of acetecholine dominating sleep and aminergins (?) such as nore., dopa., and serotonin dominating waking states. I could find at least two reliable books about that, real easy.
Any clues?
- boB
Posted by Scott L. Schofield on April 17, 2000, at 20:54:18
In reply to Re: Cam - serotonin and dopamine opposition, posted by Cam W. on April 17, 2000, at 18:44:16
I think it is time to think of the brain as a network of different railroads, each of which using a different fuel to power their trains as they deliver the mail.
Things make a lot more sense this way.
- Scott
Posted by Cam W. on April 17, 2000, at 21:49:55
In reply to Re: Cam - serotonin and dopamine opposition, posted by boB on April 17, 2000, at 20:48:41
boB - I am woefully deficient in my understanding of the mechanisms behind how working memory becomes long term memory. I think it has more to do with the NMDA (N-methyl-D-aspartate?) receptor complex. These receptor complexes have a near saturation of glycine attached to them (a basal glycine level) and are stimulated by the neurotransmitter glutamate. I am not sure whether norepinephrine triggers (or amplifies) the process in which the NMDA complex 'lays down' the neural circuitry for long term memory, but I'll bet it involves a number of neurotransmitters. (Actually I am not positive NMDA is involved, but I have a nagging feeling it is - I need my file cabinet at home rather than at work).Like yourself, I am piecing together this information from a number of different articles and I am still missing several of the puzzle pieces. Sorry that I cannot help more than this. If I remember which file I put these articles (either in neuroanatomy or antipsychotics or schizophrenia or consciousness) and can find them, I will try to get back to you on this tomarrow. - Cam W.
Posted by Zeke on April 18, 2000, at 15:13:52
In reply to Re: Cam - serotonin and dopamine opposition, posted by Cam W. on April 17, 2000, at 21:49:55
Serotonin and dopamine opposition -- well yes and no...
The actions of neurotransmitters are complex. Saying DA and 5HT antagonize one another (or one another's actions) is best viewed as a generalization. Many subcortical circuits use serotonin at one junction and dopamine at another.
Consider also that dopamine and serotonin also act to oppose (inhibit) themselves, eg, through autoreceptors. (Or through action: ACh 'opposes' its actions in the PNS.)
Other considerations:
Be careful generalizing from results of studies in persons with abnormal brain chemistry like schizophrenia. (Does a non-schizophrenic brain act like a schizophrenic brain? In schizophrenia, some dopamine circuits are hyperactive, some hypoactive.)
Be careful generalizing transmitter function with higher level functions such as mood; Different dopamine agonists have different effects for example on mood: amphetamine tends to improve mood while levodopa tends to lower mood.
IMHO, much is to be learned from the happenings inside neurons. Along with genetics this will involve neurosteroids etc. This seems to me why antidepressants have an effective (affective) time lag whis their synaptic action is immediate.
Another complicating issue is the recent finding that transmission can occur electrically without any neurotransmitter (in certain processes).
Lastly, if one transmitter inhibits the other, we can say 'oppose' or we can say 'modulate'. I tend to see DA/5HT more in the 'modulate' sense.
Posted by Cam W. on April 18, 2000, at 23:46:58
In reply to Re: Cam - serotonin and dopamine opposition, posted by boB on April 17, 2000, at 20:48:41
Zeke and boB - I have tried twice to post a very long answer as a follow-up to Zeke's thread. I have some very complicated info on neurotransmitter interactions, but after 1.5h of trying to post a synopsis of the studies, I will just give you the bibliography. The answers I was going to give were too involved for this site and taken out of context of the original articles may have made things more confusing.Zeke is correct about using modulating, rather than opposition when taking of the interactions between dopamine and serotonin. Stimulation of different serotonin receptor subtypes will either increase or decrease dopamine synthesis and release in different parts of the brain.
The good articles I have found on the interactions between neurotransmitters are:
Murphy D et al. Brain serotonin neurotransmission: an overview and update with an emphasis on serotonin subsystem heterogeneity, multiple receptors, interactions with other neurotransmitter systems, and consequent implications for understanding the actions of serotonergic drugs, J Clin Psychiatry, 1998; 59[suppl 15]: 4- 12.
(yes, that is the title)Kapur S & Remington G. Serotonin-dopamine interaction and its relevance to schizophrenia, Am J Psychiatry, April, 1996; 153(4): 466-476.
Richelson E. Receptor pharmacology of neuroleptics: relation to clinical effects, J Clin Psychiatry, 1999; 60[suppl 10] : 5-14.
Bonhomme N. Involvement of serotonin and dopamine in the mechanism of action of novel antidepressant drugs: a review, J Clin Psychopharmacol; 1998; 18(6): 447-454.
These papers should give you a descent basis for some of the neurotransmitter function. I still haven't totally grasped the concepts, yet. I think I need a few more papers and a lot more time. - Cam W.
Posted by Scott L. Schofield on April 19, 2000, at 11:17:42
In reply to Re: Cam - serotonin and dopamine opposition, posted by Zeke on April 18, 2000, at 15:13:52
Nice post, Zeke. Good perspective.
> Consider also that dopamine and serotonin also act to oppose (inhibit) themselves, eg, through autoreceptors. (Or through action: ACh 'opposes' its actions in the PNS.)
What is the PNS?
> Be careful generalizing from results of studies in persons with abnormal brain chemistry like schizophrenia. (Does a non-schizophrenic brain act like a schizophrenic brain? In schizophrenia, some dopamine circuits are hyperactive, some hypoactive.)
Excellent.
> IMHO, much is to be learned from the happenings inside neurons. Along with genetics this will involve neurosteroids etc. This seems to me why antidepressants have an effective (affective) time lag whis their synaptic action is immediate.
"affective" :-)
Definitely: neurotransmitter-stimulated adenylate cyclase-synthesized cAMP-induced protein kinase C-mediated C-FOS-directed gene transcription of G-proteins and stuff like that.
> Another complicating issue is the recent finding that transmission can occur electrically without any neurotransmitter (in certain processes).
I am curious about this. It sounds exciting.
> Lastly, if one transmitter inhibits the other, we can say 'oppose' or we can say 'modulate'. I tend to see DA/5HT more in the 'modulate' sense.
I will now be a pain in the ass:
"If a neuron using one specific neurotransmitter, or the specific neurotransmitter itself, inhibits or promotes the firing of another neuron using a different specific neurotransmitter, we cannot say 'oppose' (oppose is a two-way street). We can say 'modulate'."
Things are, of course, more complex than this, what with neurons using multiple transmitters or being stimulated by false transmitters and all.
"Railroads" obviously represents a simple analogy, but it may have utility in creating a balance of perspective against the conceptualization that the brain consists of a bunch of pools containing different colored liquids that are connected by omnidirectional aqueducts.
- Scott
Posted by Scott L. Schofield on April 19, 2000, at 12:35:21
In reply to Serotonin and dopamine opposition - Railroaded, posted by Scott L. Schofield on April 19, 2000, at 11:17:42
I guess I better comment further on the words "oppose" and "opposition".
The concept of opposition is appropriate when dealing with interactions between neural pathways and subsystems. I guess the one that would provide the best example of this would be the balance that exists between the sympathetic and parasympathetic components of the autonomic nervous system. These two subsystems exert opposing influences on the same organs.
Cam understands this stuff much better than I, but I will jot down a few things that he may want to comment on, add to, and correct.
1. Sympathetic - "fight or flight" - Norepinephrine
- Increases heart rate
- Increases blood pressure
- Shunts blood from the gut and skin to the skeletal muscles
- Decreases pupil diameter
- Decreases blood flow to the genitals2. Parasympathetic - "Eat and have sex" - Acetylcholine
- Decreases heart rate
- Decreases blood pressure
- Shunts blood from the skeletal muscles to the gut and skin.
- Dilates pupils
- Increases blood flow to the genitals
* Norepinephrine becomes involved later on - orgasm.I think the qualification of this interaction can be served by the word "oppose". However, this opposition is accomplished by complex mechanisms and interactions that include neuronal modulation, negative feedback loops, positive feedback loops, and the competition for the activation or inhibition of target nuclei, pathways and subsystems.
It is impossible to describe the brain and nervous system in just one post. Sorry. :-)
- Scott
Posted by Liz on April 19, 2000, at 18:48:44
In reply to Re: Cam - serotonin and dopamine opposition, posted by Zeke on April 18, 2000, at 15:13:52
> Be careful generalizing transmitter function with higher level functions such as mood; Different dopamine agonists have different effects for example on mood: amphetamine tends to improve mood while levodopa tends to lower mood.Zeke,
I took levadopa (Sinemet) for several months in an attempt to treat a movement disorder. Sinemet is a combination of levadopa / carbidopa which can cross the blood brain barrier and then is converted to dopamine. It was THE most mood altering drug I have ever taken. An hour or two after the a.m. dose I felt like the king of the world. It was really good. However, due to the short half-life of the drug, this effect would wear off in a few hours and subsequent doses did not have the same effect until the next morning. Just my experience although I have heard from others that levadopa improves mood.
Of course, most taking levadopa have Parkinson's disease which has depression as a co-morbidity related to basal ganglia function, not levadopa.
Liz
Posted by Cam W. on April 19, 2000, at 21:59:13
In reply to Serotonin and dopamine opposition - Railroaded, posted by Scott L. Schofield on April 19, 2000, at 11:17:42
> Nice post, Zeke. Good perspective.
1) Agreed - Cam
>
> > Consider also that dopamine and serotonin also act to oppose (inhibit) themselves, eg, through autoreceptors. (Or through action: ACh 'opposes' its actions in the PNS.)
>
> What is the PNS?
>
2) PNS = parasympathetic nervous system - Cam> > Be careful generalizing from results of studies in persons with abnormal brain chemistry like schizophrenia. (Does a non-schizophrenic brain act like a schizophrenic brain? In schizophrenia, some dopamine circuits are hyperactive, some hypoactive.)
>
> Excellent.3) In someone with schizophrenia there is a aberation in the number of dopamine receptors (too many due to a lack of synaptic pruning) or a problem with too much dopamine (perhaps resulting from the extra synapses). The basic biochemistry at the neuron works the same as in anybody. - Cam
>
> > IMHO, much is to be learned from the happenings inside neurons. Along with genetics this will involve neurosteroids etc. This seems to me why antidepressants have an effective (affective) time lag whis their synaptic action is immediate.
>
4) Much of the lag time for effect of antidepressants may come from several sources (eg. downregulation of beta-adrenergic receptors &/or up regulation of glucocorticoid receptors &/or resensitization of ACTH receptors in the adrenals &/or desensitization of post-synaptic serotonin recpeptors, etc. &/or etc. &/or etc.) - Cam5) &/or what you wrote below, Scott - Cam
> Definitely: neurotransmitter-stimulated adenylate cyclase-synthesized cAMP-induced protein kinase C-mediated C-FOS-directed gene transcription of G-proteins and stuff like that.
>
> > Another complicating issue is the recent finding that transmission can occur electrically without any neurotransmitter (in certain processes).
>
> I am curious about this. It sounds exciting.
>
6) Me, too. - Cam
> > Lastly, if one transmitter inhibits the other, we can say 'oppose' or we can say 'modulate'. I tend to see DA/5HT more in the 'modulate' sense.
>
> I will now be a pain in the ass:7) I doubt that, Scott; you are extremely helpful and I have gained much insight from you - Cam
>
> "If a neuron using one specific neurotransmitter, or the specific neurotransmitter itself, inhibits or promotes the firing of another neuron using a different specific neurotransmitter, we cannot say 'oppose' (oppose is a two-way street). We can say 'modulate'."
>
> Things are, of course, more complex than this, what with neurons using multiple transmitters or being stimulated by false transmitters and all.
>
> "Railroads" obviously represents a simple analogy, but it may have utility in creating a balance of perspective against the conceptualization that the brain consists of a bunch of pools containing different colored liquids that are connected by omnidirectional aqueducts.
>
8) Also, with serotonin receptors on dopaminergic neurons; GABA receptors basically on all neurons; alpha-adrenergic receptors on serotonin receptors; ad nauseum; plus the fact that there are several subtypes of receptors, some that can bind more than one neurotransmitter, makes understanding this system pure hell. I pity the poor grad student who wants to tackle this, but would definitely like to read his/her thesis. - CamCool thread, but too much thinking. You guys are fun. - Cam W.
Posted by Fred Potter on April 19, 2000, at 22:06:25
In reply to Re: Serotonin and dopamine opposition - Railroaded, posted by Cam W. on April 19, 2000, at 21:59:13
Sometimes I think you guys know more about neurophysiology than my family doctor
Posted by Scott L. Schofield on April 19, 2000, at 22:42:03
In reply to Re: Serotonin and dopamine opposition - Railroaded, posted by Cam W. on April 19, 2000, at 21:59:13
Wow!
This was great!
Now I have to read it a few more times just to understand what it is I don't understand.
Thanks Cam!
More homework.
:-)
One thing, though.> > Be careful generalizing from results of studies in persons with abnormal brain chemistry like schizophrenia. (Does a non-schizophrenic brain act like a schizophrenic brain? In schizophrenia, some dopamine circuits are hyperactive, some hypoactive.)
>
> Excellent.> In someone with schizophrenia there is a aberation in the number of dopamine receptors (too many due to a lack of synaptic pruning) or a problem with too much dopamine (perhaps resulting from the extra synapses). The basic biochemistry at the neuron works the same as in anybody. - Cam
Perhaps the point that Zeke was trying to make (not sure) is that the net response of a less-than-perfect brain to chemical challenges is different from that of a closer-to-perfect brain. One example might be that the behavioral effects of stimulants given to children with ADD or AD/HD differ from those seen in healthy children. If one were to experiment with stimulants only with AD/HD children, one might conclude that noradrenergic and dopaminergic neurons are responsible for sedation.
> Also, with serotonin receptors on dopaminergic neurons; GABA receptors basically on all neurons; alpha-adrenergic receptors on serotonin receptors; ad nauseum; plus the fact that there are several subtypes of receptors, some that can bind more than one neurotransmitter, makes understanding this system pure hell. I pity the poor grad student who wants to tackle this, but would definitely like to read his/her thesis.
Yeah. It's a hell of a mess. A wonderful mess. I just wish that I could read well enough to enjoy it. (I complain too much)
- Scott
Posted by Cam W. on April 20, 2000, at 0:08:26
In reply to Re: Serotonin and dopamine opposition - Railroaded, posted by Fred Potter on April 19, 2000, at 22:06:25
> Sometimes I think you guys know more about neurophysiology than my family doctor
Fred - Yeah, we may know more neurophysiology than your family doc, but we can't properly diagnose worth sh**. We all have our strengths and weaknesses. - Cam W.
Posted by bob on April 20, 2000, at 1:49:13
In reply to Re: Us versus Your Doc - To Fred, posted by Cam W. on April 20, 2000, at 0:08:26
> > Sometimes I think you guys know more about neurophysiology than my family doctor
>
> Fred - Yeah, we may know more neurophysiology than your family doc, but we can't properly diagnose worth sh**. We all have our strengths and weaknesses. - Cam W.... add to that there there are, geez -- I dunno, 20 or so of us who respond frequently and many, many more who chime in when they can. We can gang up on most doctors real good!
... add as well that maybe -- you gotta judge this for yourself -- you interact with us in a different way than you do with your doctor.
If you find out something here you haven't heard from your doc, print it out and bring it in. Maybe your doc will appreciate the info, maybe not. I know that my pdoc appreciates the wisdom I can share from this board if only that it broadens his own perspective beyond what he sees with his own patients, and often for something more substantial.
cheers
bob
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