Following transfer, the membrane was briefly washed in transfer buffer, and incubated in blocking solution 0. The membrane was incubated with anti-Fos antibodies Genosys Ltd. The staining of the specifically labeled 55 KDa c-Fos band was scanned on a flat bed scanner and quantified with the NIH software program.
Male Sprague Dawley rats weighing — g were killed by decapitation and brains were rapidly removed and cooled on ice. The synaptosomes were prepared as previously described [ 16 ] with some modifications.
The striatum and nucleus accumbens were dissected, weighed and homogenized using a glass teflon homogenizer in 20 volumes of 0. Measurement of [ 3 H]dopamine uptake into synaptosomes was carried out according to previously published methods [ 17 , 18 ]. Post-hoc tests were performed using the Tukey test to compare significance between the individual groups.
The significance was taken when p -values were less than 0. The relative c-Fos response in nucleus accumbens and striatum was measured by densitometry of immunostained bands in a Western blot assay. The peak c-Fos response was reached at 1.
It was maintained for up to 30 further minutes and was just above control at 3 hours after treatment results not shown. The bands represent the 55 KDa c-Fos peptide. Pseudoephedrine induced c-Fos expression. To determine effect of pseudoephedrine chronic treatment, rats were chronically injected with either saline or pseudoephedrine twice a day for 8 days and sacrificed 1. Effect of chronic drug treatment on acute c-Fos response.
The data quantification of bands from western blots is expressed as percentage of c-Fos value of control animals injected with saline. The following experiments were designed to test whether chronic treatment with pseudoephedrine also affected the acute response to other psychostimulants. Rats were chronically injected with either saline, amphetamine or psuedoephedrine for 8 days as described, and on day 9 they received a final injection of either pseudoephedrine or amphetamine respectively i.
Cross tolerance between amphetamine and pseudoephedrine. A: acute response to amphetamine in rats chronically treated with saline, amphetamine and pseudoephedrine 8 day treatment of drug twice a day with an increasing dose schedule; rats were killed 1.
There was no significant difference in the acute response to amphetamine between rats chronically treated with amphetamine or pseudoephedrine. B: acute response to pseudoephedrine in rats chronically treated with saline, pseudoephedrine and amphetamine 8 day treatment of drug twice a day with an increasing dose schedule, rats were killed 1.
There was no significant difference in the acute response to pseudoephedrine between rats treated with amphetamine or pseudoephedrine. The data are expressed as percentage of c-Fos value of control animals injected with saline. In order to investigate the mechanism of action of pseudoephedrine and to compare it to that of amphetamine, the effect of pseudoephedrine and amphetamine on [ 3 H]dopamine uptake was assayed in synaptosomal preparations from rat brain areas.
Both amphetamine and pseudoephedrine inhibited the uptake of [ 3 H]dopamine into nucleus accumbens and striatal synaptosomes, with amphetamine being more potent than pseudoephedrine Fig.
The amphetamine and pseudoephedrine curves were parallel to each other with the curve for pseudoephedrine inhibition of [ 3 H]dopamine uptake shifted to the right. The IC 50 values for amphetamine and pseudoephedrine inhibition reported here see legend Fig.
IC 50 is defined as the concentration of drug producing a 50 percent inhibition in 1 nM [ 3 H]dopamine uptake. Values represent uptake as percentage of control.
The IC 50 values of amphetamine in inhibiting [ 3 H]dopamine uptake in striatum and nucleus accumbens are 4. Chronic injection of pseudoephedrine resulted in desensitisation of the acute pseudoephedrine induced c-Fos induction in the striatum and nucleus accumbens. It has previously been shown that chronic treatment with cocaine and amphetamine reduces the immediate-early-gene expression response to these drugs in specific brain areas [ 19 — 21 ].
Pseudoephedrine effects on c- Fos expression is thus similar to that of other psychostimulants both at the acute and chronic level.
The c-Fos response to psychomotor stimulant drugs appears to be a direct response to the drug rather than to a general drug-related altered state. For example other studies have shown that there are no significant changes in c-Fos expression following withdrawal from chronic treatment of psychostimulants To further test the hypothesis that amphetamine and pseudoephedrine work through similar mechanisms, cross tolerance tests were carried out. This result is consistent with our previous findings that pseudoephedrine has similar effects and mechanisms of action as amphetamine in terms of c-Fos expression [ 13 ] and internal behavioral cues [ 12 ].
In this work we have also analysed another reported effect of psychostimulants namely inhibition of [ 3 H]dopamine uptake and report that both amphetamine and pseudoephedrine inhibit [ 3 H]dopamine uptake.
The role of dopamine in pseudoephedrine induced c-Fos response is further corroborated by the effect of the D1 receptor antagonist SCH which as previously described [ 13 ] inhibited acute response to pseudoephedrine results not shown. Our studies thus indicate that pseudoephedrine, notwithstanding the higher doses required, acts in manner indistinguishable from amphetamine. This may have sociological and medical implications as pseudoephedrine is a legal over-the-counter drug.
However, it is unknown whether the efficacy of the pseudoephedrine in humans is different from rats. An additional potential risk of pseudoephedrine is reinstatement of drug seeking behaviour in individuals that have overcome previous addiction to psychostimulants. It would be useful to determine whether pseudoephedrine could induce a reinstatement of drug seeking behaviour in rats that had first been chronically treated with amphetamine and that had then been allowed to extinguish their amphetamine seeking behaviour.
Particular attention would need to be paid to the genetic background of the animals as it has been shown to affect relapse behaviour [ 23 ]. The data here reported and the additional approach described above would inform further studies in human subjects aimed at determining the potency of pseudoephedrine in humans to identify what doses may constitute a health, addiction or relapse risk.
When phenylephrine is injected, it reduces the blood flow and relieves priapism. It is also used as a vasopressor i. At the same time, this causes increase in blood pressure, hence limiting the use in people suffering from high blood pressure.
This drug is also used as an eye drop to dilate pupils i. It is generally used by ophthalmologists for visualization of the retina.
Despite pseudoephedrine being a more effective decongestant, it is being replaced by phenylephrine. This is because of it being used in illegal manufacturing of methamphetamine as it belongs to the amphetamine class of drugs. In low doses methamphetamine causes mood elevation, increases alertness, concentration and energy in fatigued people and can lead to addiction too. Often, pseudoephedrine is used for its stimulant properties by various athletes to enhance their performance.
In order to curb this rampant usage of this drug, various laws have been passed in different countries for procuring this drug from the pharmacies. Difference between phenylephrine and pseudoephedrine. Difference Between Similar Terms and Objects. MLA 8 P, Rachita. How phenylephrine nasal spray could affect your coronary arteries?
Name required. MLA 8 J, John. In the past I have used a stack of ephedrine caffeine and aspirin to raise my core temperature to burn body fat getting ready to compete in bodybuilding competition.
I have been using bronkaid to get ephedrine because pure ephedrine is no longer available. A friend told me otc sudafed has ephedrine in it. The bronkaid has ephedrine sulfate and the sudafed is pseudoephedrine. Is there a difference? Will either work to raise the core temperature in the body to accelerate fat loss in moderation of course?
Thank you. I am stunned no one has answered you! Or should I say lectured you! What you are doing is so beyond dangerous, I am still unable to lift my lower jaw from the floor! Forget that garbage about core heat, what you are really doing is jacking up your blood pressure while inhibiting blood clotting.
In theory, you are trying to negate the chance of stroke due to clotting, but you are now increasing your odds of stroke due to bleeding. My God, man, this is insane! If you are still doing this, stop.
Stop completely, stop immediately, STOP!!!! You notice how he did not reply? When I read his request for information, I had the exact same reaction that you did, and I believe his ultimate disposition has been garnered. The gene pool, and therefore the future of humanity, are both enhanced by their absence of contribution. I cannot afford to add up what they are made of as their societal value is problematic, at best. Spending any time around them at all will reduce your will to live.
Ephedrine, caffeine, and aspirin is a pretty common fat burning stack. Particularly if you have a heart issue you are unaware of or exercise while under the effects of this combination.
Many know the risks and choose to do it anyway. Best advice you can offer these people, since they are likely to be stubborn is at least keep it to your non exercise days, and do not accidently increase the caffeine consumption via your diet.
And I do in fact know someone who dropped dead on a treadmill on an eca stack. So yes it happens. Additionally no, psuedo ephedrine is not going to work like ephedrine does.
The article above actually explains why, it has less effect on the whole cv system and is more localized. To a degree. Ephedrine is legal in Canada. You are an idiot!!!! Do you think? Obviously not from your post.
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