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Cocaine is a non-selective, competitive inhibitor of monoamine transporters, sharing a similar mechanism with that of methylphenidate. Cocaine interacts with DAT, SERT, and NET, although the behavioral and reinforcing effects of cocaine depend on its inhibition of DAT and the increase in extracellular dopamine. [1]
Synaptogyrin-3, a synaptic vesicle protein, binds to dopamine transporters and regulates the effects of cocaine on dopamine neurotransmission and rodent self-administration behavior. [39] Elevating levels of synaptogyrin-3 made animals resilient to cocaine, and a possible future treatment for cocaine addiction might be based on targeting this ...
Cocaine (from French cocaïne, from Spanish coca, ultimately from Quechua kúka) [13] is a tropane alkaloid that acts as a central nervous system stimulant.As an extract, it is mainly used recreationally and often illegally for its euphoric and rewarding effects.
Cocaine- and amphetamine-regulated transcript, also known as CART, is a neuropeptide protein that in humans is encoded by the CARTPT gene. [ 1 ] [ 2 ] CART appears to have roles in reward, feeding, and stress, [ 3 ] and it has the functional properties of an endogenous psychostimulant .
Each neurotransmitter has very specific degradation pathways at regulatory points, which may be targeted by the body's regulatory system or medication. Cocaine blocks a dopamine transporter responsible for the reuptake of dopamine. Without the transporter, dopamine diffuses much more slowly from the synaptic cleft and continues to activate the ...
This receptor had been seen to modulate the rewarding effects of cocaine, and receptor antagonists had blocked the acute locomotor stimulating effect and lowered behavioral sensitization. Changes in the sigma 1 receptor have been shown to modulate dopamine release, so shifts in its expression can change the behavioral responses to cocaine with ...
Cocaine is a nonselective, reuptake inhibitor of the norepinephrine, serotonin, and dopamine transporters. This thwarts the absorption of these chemicals into the presynaptic terminal [ 27 ] and allows a large concentration of dopamine, serotonin and norepinephrine to build up in the synaptic cleft.
The neurotransmitter dopamine is a key candidate for explanation of reinforcing actions drugs. [6] [7] It's unclear to which extent NET is involved in the reinforcing actions of cocaine (an SNDRI). [8] Animal studies show evidence that inhibiting the SERT might reduce cocaine intake. [9]