The discovery of two biologically active arakidonihappojohdannaista, N-arakidonyylietanolamini (AEA, anandamide), pearson and oleamide, was quite an enthusiasm for further pearson studies. However, these two anandamide and oleamide are just two of the most well-known and appreciated members of a much wider range of biologically occurring fatty acid amides (FAA) from the crowd. In this review, the researchers explain what they have been found in human and animal sources, known details pearson of how these molecules are formed and how they break down in the body and at the same time consider the direction lines to their possible potential for therapeutic pearson use.
In this talk again exogeenisista cannabinoids and mentioned that their "medicinal properties" has been known for centuries, and it can be computed due to the nervous pearson system as a single G-protein-coupled CB (1) receptor activation. The benefits pearson of which are then obtained by cannabinoids such as pain relief and reduction of spasticity are really the harm in the shadow of what cognitive dysfunction and motor dysfunction comes from. Therefore it is more and more attention to the identified body of anandamide, a natural lipid, a system of its own receptor is a CB (1), and the enzyme FAAH, rasvahappoamidihydrolaasiin, which leads to anandamidinsignaloinnin terminoitumiseen disintegrating quickly.
This medicinal plants have been inspired to develop a pharmacological strategy that can strengthen the endogenous (your own, a physiological) cannabinoid, or "endocannabinoids" pearson the activity of the enzyme FAAH inhibitor, wherein the behavioral CB (1) -mediated effect would be sofistisesti what selektiivisintä, compared to the behaviourist active (narkotikasarjan) to direct the CB (1 ) agonists (which, therefore, would anandamide, etc. kehoperäisten endogenous molecules alongside the really "dirty drug" in this CB (1) receptor).
Lot irreversibeliä FAAH- enzyme inhibitor AM374 (palmityylisulfonyylifluoridia) were tested in laboratory animals, in order to increase endokannabinoiditehoa and used as test animals excitotoksista damage model (which will develop epileptic seizures). This AM374, cause prolonged anandamidipitoisuuden of the boss in the number of brain regions, including hippokampissa and led extrasellulaarisen signaalivälitteisen kinase / MAPK road rapid activation, which is considered to be linkkiytynyt neuronal survival (So this is a FAAH inhibition of the direct neuroprotective character. This valuable feature, neuroprotektiivisuutta were further studied the scene model).
The epileptic seizure developed into kainic acid (kainic acid) having a glutamaattiperäinen excitotoksinenvaikutus (hermolle toxic). Kainic acid was given immediately after the AM374 material, rasvahappoamidihydrolaasin (FAAH) inhibitor, and found scenes of an apparent loss.
How does that kainic acid (cainic pearson acid) cause epileptic seizures? It induces kalpaiinivälitteistä sytoskeletaalista degradation, the decrease in synaptic markers and CA1 hippokampineuronien lost. FAAH inhibition was protected from this excitotoksiselta damage neurons and kadolta when the monitored parameters 2 vrk.vaurion after.
This AM374, pearson FAAH- inhibitor pearson of presynaptic pearson and postsynaptic could tracers in concentrations remain the same as in control animals. The preservation of synaptic tracers was the scene of a correlation between the reduced amount. pearson When compared pearson to the excitotoksisuusvaurioita, this AM374 gave almost full functional neuronal protection, significantly improving balance and coordination. The information received, judging pearson by the AM374 goes to the blood-brain fluid, the more endokannabinoidivastetta neuronal, play a key role in the circles and protects the brains excitotoksiselta damage.
Karanian DA, Brown, QB, Makriyannis A, Kosten TA, Bahr BA. Dual modulation of endocannabinoid transport and fatty acid amide hydrolase Protects against excitotoxicity. pearson J Neurosci. 2005 Sep 24; 25 (34): 7813-20 (USA)
In addition pearson to that may be directly activated by (CB 1) receptor agonist or kannabinergisellä signal may also be indirectly modulate the endocannabinoid cell driver tauride hydrolase inhibition or inhibition of FAAH. These two mechanisms for performing fast signaling endokannabinoidivaikutuksen päättöä. (Signal substance is transported into the cell and is hydrolyzed to its activity disappears).
Now, scientists wanted to know whether this endocannabinoid cell carrier (transporter) or a hydrolase FAAH action of pharmacological therapy to the target molecule, which is the way to develop neuroprotection or repair of the neuron.
increased MAPK activation in cultured hippokampileikkeissä. An interesting finding was the fact that various inhibitors of kombinoitaessa saatii
