I have a new idea about why krill oil + PS isn't working anymore.
When neurons are stimulated, they release dopamine from the vesicles. The krill oil + PS made extra dopamine release from the vesicles, but in time the vesicles are depleted.
Genistein and amphetamines work different; they inhibit the reuptake or destruction of dopamine (not working on release), so they work independent of the dopamine storage. This is why I never had tolerance on these 2 compounds.
Vitamin B complex and precursors such as l-tyrosine work yet different, they stimulate the production of dopamine. If the production of dopamine is increased, more can be released too. This is why I will try using vitamin b complex together with krill oil and also add l-tyrosine.
In other words; I have to find something that increases dopamine production so that more can be released as well (more in = more out).
A part of this scientific article shows what I am thinking about:
http://www.tbiomed.com/content/6/1/21G. The effect of single action potentials and bursts
It is known [3,4] that there are two typical firing patterns seen in the dopaminergic neurons of the SNc, tonic firing at about 5 Hz and
bursts of action potentials with an intraburst frequency of about 15-30 Hz.
Dopaminergic neurons respond to reward-related stimuli with increased burst firing [8,79] and
burst firing is more effective at raising dopamine levels than tonic firing [80,45]. Recently bursts have been measured in awake, freely-moving animals [81,47,82] in response to rewards and in response to cues for the rewards when the cues have been learned; for a review, see [83].
We see in our model responses that quite similar to those observed experimentally. Panel A of Figure 10 shows the time course of extracellular dopamine in response to steady firing at 5 Hz. All extra dopamine is cleared from the extracellular space before the next action potential arrives as reported in [76]. Note that on this short time scale cytosolic dopamine and vesicular dopamine remain approximately constant. However, Panel B shows that a burst of action potentials at 15 Hz causes a substantial rise in average eda [76]. The model results shown in Figure 10 are similar to the model and experimental results reported in [82], figure 2. Thus, even a very short term shift from tonic firing at 5 Hz to burst firing at 15 Hz produces a
large dopamine signal. This shows how
sensitive the system is to a brief short-term change in frequency of firing.
Figure 10:
http://www.tbiomed.c...1/21/figure/F10Bursts increase extracellular dopamine. Panel A shows the eda concentration as a function of time when the tonic firing rate is 5 Hz. The eda from the previous action potential is cleared from the extracellular space before the next action potential arrives. Notice that vesicular dopamine and cytosolic dopamine are not noticeably affected on this short time scale. Panel B shows that a short burst of action potentials at 15 Hz raises extracellular dopamine dramatically during the burst. Even a very short term change from tonic firing at 5 Hz to burst firing at 15 Hz produces a large dopamine signal.
However, if firing continues for a long time at 15 Hz, the feedback on TH via the autoreceptors will cause eda to decline to an intermediate level, higher than normal but not as high as the short term response.
The inhibition of TH (TH = Tyrosine hydroxylase?) by increased binding to the autoreceptors happens quickly, but the resulting decrease in cda and vda happens slowly over a nine hour period (Figure 11), and this causes a gradual decrease in eda even though the firing rate remains elevated. Thus, over the long term, the eda concentration gradually habituates to the increased firing rate. It would be interesting to test this prediction of the model experimentally.
Figure 11:
http://www.tbiomed.c...1/21/figure/F11Habituation to increased firing. At one hour, the firing rate of the neuron is increased from 5 Hz to 15 Hz and eda immediately triples. Then eda gradually decreases to an intermediate value since the increased binding of eda to the autoreceptors inhibits TH and this causes a gradual decline in vesicular dopamine over a nine hour period. Thus the level of eda habituates to the increased firing rate.
So I have to find something to restore (stimulate/ increase) the "Tyrosine hydroxylase" so that more dopamine will be in the vesicles. Or perhaps take l-dopa because it's one step after the TH in dopamine synthesis?Remember how krill oil+PS was suppost to work:
The brain cells membrane is made of fat. One of these fats is phosphatidyl serine. Krill oil has DHA/EPA connected to phosphatidyl choline. This works as an anchor and enables more phosphatidyl serine to anchor to the cell membrane. More phosphatidyl serine improves the brain electral conduction and makes the electrical signals stronger, causing more neurotransmitters to be released. Something like that...
Edited by steven d, 01 December 2009 - 04:10 PM.
