werking methylfenidaat en dexamfetamine

Wanneer ik Dex, samen gebruik met Methylfenidaat dan wordt er meet Dopamine afgegeven, wat vervolgens niet meer heropgenomen zal worden door de Methylfenidaat.

both amphetamine and methylphenidate are dopaminergic, it should be noted that their methods of action are distinct. Specifically, methylphenidate is a dopamine reuptake inhibitor while amphetamine is both a releasing agent and reuptake inhibitor of dopamine and norepinephrine.

Dopamine appeared very early in the course of evolution and is involved in many functions that are essential for survival of the organism, such as motricity, attentiveness, motivation, learning, and memorization. But most of all, dopamine is a key element in identifying natural rewards for the organism. These natural stimuli such as food and water cause individuals to engage in approach behaviours. Dopamine is also involved in unconscious memorization of signs associated with these rewards.

It has now been established that all substances that trigger dependencies in human beings increase the release of a neuromediator, dopamine, in a specific area of the brain: the nucleus accumbens.

But not all drugs increase dopamine levels in the brain in the same way.

• Some substances imitate natural neuromediators and take their place on their receptors. Morphine, for example, binds to the receptors for endorphin (a natural "morphine" produced by the brain), while nicotine binds to the receptors for acetylcholine.
• Other substances increase the secretion of natural neuromediators. Cocaine, for example, mainly increases the amount of dopamine in the synapses, while ecstasy mainly increases the amount of serotonin.
• Still other substances block a natural neuromediator. Alcohol, for example, blocks the NMDA receptors.

Amphetamines
Amphetamines are drugs used to combat fatigue. Like cocaine, amphetamines increase the concentration of dopamine in the synaptic gap, but by a different mechanism. Amphetamines are similar in structure to dopamine, and so can enter the terminal button of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly. As the animation to the right shows, once inside the presynaptic neuron, amphetamines force the dopamine molecules out of their storage vesicles and expel them into the synaptic gap by making the dopamine transporters work in reverse.

Amphetamines also seem to act by several other mechanisms. For example, they seem to reduce the reuptake of dopamine and, in high concentrations, to inhibit monoamine oxydase A (MAO-A).

Amphetamines may also excite dopaminergic neurons via glutamate neurons. Amphetamines would thus remove an inhibiting effect due to metabotropic glutamate receptors. By thus releasing this natural brake, amphetamines would make the dopaminergic neurons more readily excitable.

Dextroamphetamine, like other amphetamines, elicits its stimulating effects via three distinct actions: first, it inhibits or reverses the transporter proteins for the monoamine neurotransmitters (namely the serotonin, norepinephrine and dopamine transporters) via trace amine-associated receptor 1 (TAAR1); second, it releases these neurotransmitters from synaptic vesicles via vesicular monoamine transporter 2; and third, it reduces the enzymatic breakdown of cytosolic dopamine, norepinephrine, serotonin and related trace amines via inhibition of monoamine oxidase, particularly at high concentrations of amphetamine and monoamine transmitters.

Methylphenidate acts by blocking the dopamine transporter and norepinephrine transporter, leading to increased concentrations of dopamine and norepinephrine within the synaptic cleft. This effect in turn leads to increased neurotransmission of dopamine and norepinephrine.

Amphetamines are central nervous system stimulants which act on serotonin (5-hydroxytryptamine/5-HT), norepinephrine and dopamine transporters (Fleckenstein et al, 2007) (Rang & Dale, 2007), though the primary mechanism of action is on the dopamine transporter (DAT). Amphetamines’ 3 main effects on dopamine transport are depletion of vesicular dopamine (DA), reversal of DAT (efflux of DA into synaptic cleft), and DA uptake inhibition (Caron et al, 1998).

[...]

Amphetamines compete with DA for Na+/Cl--dependent-DAT, competitively inhibiting DA reuptake, hence increasing DA concentration in the synaptic cleft (Baumann et al, 2006).

[...]

It can be seen that amphetamines work by several distinct mechanisms which all lead to an increase in extracellular dopamine (and to a lesser extent 5-HT and norepinephrine), resulting in increased post-synaptic activation and reduced clearance of neurotransmitters, which underlies the psychoactive effects of this class of drugs. Various amphetamine analogues have different affinities for each of the monoamine pathways (for example MDMA displays greater preference for the 5-HT pathway), so their effects are distinguished by what pathway the analogue preferentially acts upon.

The synaptic cleft is a gap between the pre- and postsynaptic cells that is about 20 nm wide. The small volume of the cleft allows neurotransmitter concentration to be raised and lowered rapidly

Chamey schreef:heb Biologie gehad op school, maar nooit goed opgelet. Lette nooit goed op en leraren dachten dat ik achterlijk was. Niet veel opgestoken daar op school, maar achteraf, jaren later.... bleek ik hoogbegaafd.

Dingen zijn dus niet altijd wat ze lijken dus brandt maar los. Ik snap het echt wel

Exceptional schreef:Ik ben hoogbegaafd, dus ik snap alles.

Doei.

Partypipo schreef:Meestal wordt het aan leken uitgelegd dat bepaalde stoffen opraken en dat je daarom een tijdje met bepaalde medicijnen moet stoppen of met drugs moet stoppen om het weer aan te vullen.

Chamey schreef:wat je zei over " het wel erg bond maken met het gebruik" zodat je dopa voorraad uitput.
Dat is met Dex, toch onmogelijk? dat werd me nog niet helemaal duidelijk, sorry. Er is toch immers geen sprake van blokkering van heropname? Dus alles komt weer terug.

Chamey schreef:waar kwam bij mij die vreselijke depressiviteit, vandaan? de tranen liepen op een gegeven moment langs mn wangen en zag niks meer zitten. Was bijna eng om te ervaren. Zonder verdere aanleiding ofzo, ik was van het ene moment op t andere, BOEM. depresief. Als het gevoel van depressie iets leek weg te zakken en ik nam een pilletje Dex en Methyl, kwam het weer. Pas na 10 dagen eiwitten shakes, Tyrosine, vit B en C en ongelooflijk v eel slaapmomenten op een dag, was het weg. Doodmoe was ik. Kon om het uur wel in slaap vallen

Stressors of many types evoke increases in noradrenergic activity, which mobilizes the brain and body to meet the threat.[44] Chronic stress, if continued for a long time, can damage many parts of the body. A significant part of the damage is due to the effects of sustained norepinephrine release, because of norepinephrine's general function of directing resources away from maintenance, regeneration, and reproduction, and toward systems that are required for active movement. The consequences can include slowing of growth (in children), sleeplessness, loss of libido, gastrointestinal problems, impaired disease resistance, slower rates of injury healing, depression, and increased vulnerability to addiction.

Chamey schreef:maargoed, nevermind

Perry schreef:Je had de kans eens een gesprek op niveau met me te hebben, die mogelijkheid geef ik bijna niemand hier