do new receptors grow?

[stan]

from "joe sent me" :

Seriously, just a question for everyone. Don't you think that the growth of NEW receptors could mean that they are more vibrant than old receptors? I realize that there will still be old receptors present but the new receptors could be better than the old n'est pas. Is my thinking crazy?

At stopping meds(after cold turkey or slow weaning)
If new nerves paths(serotonin receptors) were growing, for me(i am maybe wrong) we would be always improved, linear better feeling because it will adding serotonin receptors paths;
why have we destroyed (after stopping meds, not much during taking meds) receptors of dopamin which appear (new physical problems are dopamin related and not serotonin)?

i think that the body moves dopamin receptors(and adrenal and ...) to change them in serotonin working(the body is of lack because AD is no more between nerves)

to summarize clearly :

when we stop AD(or benzo...), the body has an amount of dopamin receptors, an amount of adrenal receptors, an amount (more less because AD closed definitely many over the body) of serotonin; all this in a bad homeostasis;
with that the body has to create a new homeostasis with all these receptors;

doctors say new receptors grow, nobody is able to check if about 7 billions of different receptors are today 7,2 billions; we cannot count what happen, because they say they do not know how AD function really;

for me, the body do not create much new receptors, he works with what he has and moves dopamin receptors in serotonin when he need;

this explains why we have suddenly lack dopamin physical problems after taking a serotonin closer receptors since years;
for me this explains why i am physically very bad and why it is cyclical, one step forward and two steps back, up and down

and it explains why after years we are a new, and never as well perfect function than before meds

originally we had maybe 8 billions of receptors, ADs burned closed half billion, 4 years after a new homeostasis, we function with 7,5 billions, therefore there is a new recovery, less perfect than original and never a 100 % recovery

and thinking that after 10 years destroying receptors, all will grow back is a nonsense illogical unchecked
sequaels are normal after 10 years poison, the contrary is unreal

all testimonies i have read show this

stan einstein theory universalys

[Sheila]

Dear Einstein Stan, I am having deja vu. We already had this debate somewhere. I, Bohr Sheila, do believe that we grow new neurons and new receptors. I don't think we go back to being how we were before exactly. But I think we can be fully, fully healed in a new version of ourselves. And, as they used to say on pp, even if you didn't take meds, you would be neurologically changed by experience after 20 years.

Samsara -- I read something somewhere about what new neurons are like. I have to try to remember where that was. What I remember at the moment is that new neurons might be more excitable. So, temporarily less stable. But they mature, get myelinated, tired, calm down, or something! So, this might apply to new receptor sites. I'll try to find where this came up -- it was on pp or SA I think.

But, also, my unsubstantiated intuition is that we *are* being rewired in a way that will make us better than before -- more psychic, more our true selves.

[Samsara]

Sheila.....

I agree with what you have presented. I have many research papers that discuss the subject of neuroplasticity, neurogenesis etc.

What you have presented re: excitability of new neuron cells is what I have come to understand as well. I think the new cells are still fragile (infant stages) Something like a baby who's learning to walk (will take a few steps and then fall, will get back up .........take a few more steps and then fall again) Eventually, the wobble phase (unsteady factor) becomes more stable. Perhaps I'm not using the best analogy but that's the best I can come up with this early in the day. (lol)

I also think new brain cells are not receptive enough to inhibitory actions (calming chemicals) and it takes them some time to learn to receive these calming brain chemicals. It's all a process of reaching maturation (as you mentioned).

I do believe in full recovery and Stan, I wasn't questioning whether we grow new brain cells but rather, IF the NEW cells (once matured) are more resilient than older cells.

There are also some areas of the brain that can more easily regenerate while other areas not so much.

Anyway, time to post this and get off-line since, my mind is now feeling overloaded. (lol)


Samsara

[stan]

I do believe in full recovery and Stan, I wasn't questioning whether we grow new brain cells but rather, IF the NEW cells (once matured) are more resilient than older cells.
Samsara

i know your questioning was different and i have no answer for your young and old cells resilient(Sheila has), but it has made me think about this déjà vu again and i had a big desire to rewrite my ideas, i cannot refuse me a desire, i have not much often desire,
sorry for the embarrassing, now i have written, i am so more well, i have relief, i am as a child, after W/D i have all to learn

[Samsara]

i know your questioning was different and i have no answer for your young and old cells resilient(Sheila has), but it has made me think about this déjà vu again and i had a big desire to rewrite my ideas, i cannot refuse me a desire, i have not much often desire,
sorry for the embarrassing, now i have written, i am so more well, i have relief, i am as a child, after W/D i have all to learn

Oh okay Stan. I thought perhaps my question got muddied due to the translation process. BTW, no need to feel embarrassed about anything.

Re: "desires" ............Life's too short ............so follow your desires.


Samsara

[Sheila]

Bravo, Stan, for having a desire and enjoying it!

Samsara -- yes, that's my understanding, too. I found the stuff I was referring to. I had posted it in June 2010 on pp. I will re-post it here.

[Sheila]

Interesting bit from Wikipedia --

http://en.wikipedia.org/wiki/Neurogenesis

Adult-born neurons appear to have a role in the regulation of stress. Studies have linked neurogenesis to the beneficial actions of specific antidepressants, suggesting a connection between decreased hippocampal neurogenesis and depression.[20][21] In a subsequent paper, scientists demonstrated that the behavioral benefits of antidepressant administration in mice is reversed when neurogenesis is prevented with x-irradiation techniques.[22] In fact, new-born neurons are more excitable than older neurons due to a differential expression of GABA receptors.[citation needed] A plausible model, therefore, is that these neurons augment the role of the hippocampus in the negative feedback mechanism of the HPA-axis (physiological stress) and perhaps in inhibiting the amygdala (the region of brain responsible for fearful responses to stimuli).[vague] This is consistent with numerous findings linking stress-relieving activities (learning, exposure to a new yet benign environment, and exercise) to increased levels of neurogenesis, as well as the observation that animals exposed to physiological stress (cortisol) or psychological stress (e.g. isolation) show markedly decreased levels of new-born neurons.

Some studies have hypothesized that learning and memory are linked to depression, and that neurogenesis may promote neuroplasticity. One study proposes that mood may be regulated, at a base level, by plasticity, and thus not chemistry. Accordingly, the effects of antidepressant treatment would only be secondary to change in plasticity.[23]



Also, here's a nice, clear explanation of the antidepressant neurogenesis hypothesis --

http://faculty.washington.edu/chudler/hipnd.html

[Sheila]

Bolding is mine --

http://www.springerlink.com/content/w124n645x54w02n1/

Increased hippocampal nitric oxide synthase activity and stress responsiveness after imipramine discontinuation: Role of 5HT 2A/C -receptors

Brian H. Harvey1 Contact Information, Renché Retief1, Ané Korff1 and Gregers Wegener2
(1) School of Pharmacy (Pharmacology), Faculty of Health Sciences, North-West University, Potchefstroom, South Africa
(2) Center for Basic Psychiatric Research, University of Aarhus, Aarhus, Denmark

Received: 21 June 2005 Accepted: 25 August 2005 Published online: 22 July 2006
Abstract Chronic depressive illness may cause shrinkage of the hippocampus with stress-induced release of glutamate and nitric oxide possibly causally linked to this pathology. Poor antidepressant compliance may contribute to this pathology as well as to long term morbidity. However, antidepressant withdrawal-associated symptoms in depressed patients often reflect hyperserotonergia. The effect of chronic imipramine (IMI; 15 mg/kg/d ip × 3wks) treatment and withdrawal on swim stress responsiveness was studied in Sprague-Dawley rats together with assay of hippocampal NO synthase (NOS) activity. The dependence of any biobehavioral changes following IMI withdrawal on 5HT2A/C receptor-mediated events was studied using the 5HT2A/C receptor antagonist, ritanserin (RIT; 4 mg/kg/day ip × 7 days), administered alone or during IMI withdrawal. IMI significantly inhibited the situational stress response to forced swimming while also significantly decreasing NOS activity. IMI withdrawal was associated with a significant increase in swim immobility together with a significant increase in NOS activity compared to both control and IMI-treated groups. RIT re-established the anti-immobility effects and reversed NOS hyper-function during IMI withdrawal, although alone it increased NOS activity. Antidepressant discontinuation therefore increases stress responsiveness together with disinhibition of hippocampal NOS through a mechanism involving 5HT2A/C receptor activation. The resulting increased nitrergic activity may have significant implications for depressive illness and its treatment.


From Wiki -- Nitric oxide synthase (NOS) is an enzyme in the body that contributes to transmission from one neuron to another.

[Sheila]

So, based on these little snippets --

Things that might be happening neurologically during w/d --

1) Newer neurons that were made via SS/NRI use are more excitable than older neurons, possibly because they have fewer GABA receptors. (GABA is an inhibitory neurotransmitter and generally calming.)
2) Rebound of the hippocampus suppressing the HPA axis and of the amygdala being inhibited. IOW, in w/d the HPA axis and amygdala rebound into overactivity.
3) Increase in stress responsiveness.
4) Disinhibition of inter-neuron transmission in the hippocampus. IOW, the hippocampus is now more hyperactive.
5) Disinhibition of limbic glutamatergic activity. IOW, the limbic system is now more hyperactive. (Glutamate is an excitatory neurotransmitter and generally stimulating.)

Let me know if I got anything backwards!

[Sheila]

New neurons made during antidepressant usage are more excitable. In fact, Harvey even mentions that "discontinuation" "...symptoms suggest increased excitability of serotonergic neurons" (Harvey et al., 2003, p. 8 ). Eventually, those young neurons will age and become more staid and respectable.

Perhaps people who take longer to recover had more neurogenesis during antidepressant usage. So, even though they may have upregulated their serotonin receptors, they may still need to do extra work on seasoning all those new neurons.

Here's where all the things that promote neuroplasticity come into play -- exercise, meditation, therapy, fish oil, placebo, epigenesis, prayer....

So, my amateur hypothesis is that people who take longer to recover may have had more neurogenesis. Now, maybe they (we?) not only have to upregulate serotonin receptors on our old neurons, but we have to do so on the new neurons. More work. I realize this is highly speculative -- we aren't even talking about blood flow and how it might be increased/decreased to certain areas while on meds, and then reversed when off meds. We're not even talking about parts of the brain that may have, shall we say, less support for the old neurons in that location while on the meds.....It's just fun and creative to speculate, and we *might* just come up with something useful.