Þetta er helbert reginbull.
Metamfetamín er mjög ólíkt dextroamfetamíni eða levoamfetamíni sem hafa verið mest notuð; það getur valdið óafturkræfum heilaskemmdum við fyrstu notkun.
Það er fræg rannsókn sem var gerð fyrir uþb 15 árum síðan og átti að sanna að Ecstasy (MDMA) ylli óafturkræfum heilaskemmdum. Þessar niðurstöður fóru eins og eldur í sinu um alla heimspressuna, en hins vegar fór ekki jafn mikið fyrir því nokkrum mánuðum síðan þegar það uppgötvaðist að könnunin var gölluð; efnið sem var rannsakað var í raun metamfetamín.
Sjá hvað methylation er:
http://en.wikipedia.org/wiki/MethylateSjá hér um meth:
http://en.wikipedia.org/wiki/MethamphetamineSjá t.d. þetta hér:
The methyl group is responsible for the potentiation of effects as compared to the related compound amphetamine, rendering the substance on the one hand more lipid-soluble, enhancing transport across the blood-brain barrier, and on the other hand more stable against enzymatic degradation by monoamine oxidase (MAO). Methamphetamine causes the norepinephrine, dopamine, and serotonin (5HT) transporters to reverse their direction of flow. This inversion leads to a release of these transmitters from the vesicles to the cytoplasm and from the cytoplasm to the synapse (releasing monoamines in rats with ratios of about NE:DA = 1:2, NE:5HT= 1:60), causing increased stimulation of post-synaptic receptors. Methamphetamine also indirectly prevents the reuptake of these neurotransmitters, causing them to remain in the synaptic cleft for a prolonged period (inhibiting monoamine reuptake in rats with ratios of about: NE:DA = 1:2.35, NE:5HT = 1:44.5).[15]
Methamphetamine is a potent neurotoxin, shown to cause dopaminergic degeneration.[16][17] High doses of methamphetamine produce losses in several markers of brain dopamine and serotonin neurons. Dopamine and serotonin concentrations, dopamine and 5HT uptake sites, and tyrosine and tryptophan hydroxylase activities are reduced after the administration of methamphetamine. It has been proposed that dopamine plays a role in methamphetamine-induced neurotoxicity because experiments that reduce dopamine production or block the release of dopamine decrease the toxic effects of methamphetamine administration. When dopamine breaks down it produces reactive oxygen species such as hydrogen peroxide.
It is likely that the approximate 1200% increase in dopamine levels and subsequent oxidative stress that occurs after taking methamphetamine mediates its neurotoxicity.[18]