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Cocaine exposure in utero may affect the structure and function of the brain, predisposing children to developmental problems later, or these effects may be explained by children of crack-using mothers being at higher risk for domestic violence, deadbeat parenting, and maternal depression. [2]
They also established patterns of changes in brain regions (e.g., dorsal vs. ventral striatum, prefrontal cortical subregions, other areas of the neocortex), their similarity after experimenter- or self-administered drugs (2002), [43] and the impact of past experience (2003), [44] and context (2004), [45] along with other features.
These chemicals inhibit the action of DAT and, to a lesser extent, the other monoamine transporters, but their effects are mediated by separate mechanisms. Monoamine transporters are established targets for many pharmacological agents that affect brain function, including the psychostimulants cocaine and amphetamine. Cocaine and amphetamine ...
Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40–60 minutes after the peak effects are attained. [104] Cocaine crosses the blood–brain barrier via both a proton-coupled organic cation antiporter [18] [19] and (to a lesser extent) via passive diffusion across cell membranes. [20]
Cocaine's mechanism of action in the human brain includes the inhibition of dopamine reuptake, [49] which accounts for cocaine's addictive properties, as dopamine is the critical neurotransmitter for reward. However, cocaine is more active in the dopaminergic neurons of the ventral tegmental area than the substantia nigra.
One form of behavioral neuropharmacology focuses on the study of drug dependence and how drug addiction affects the human mind. Most research has shown that the major part of the brain that reinforces addiction through neurochemical reward is the nucleus accumbens. The image to the right shows how dopamine is projected into this area.
Through lines of D1 receptor mutant mice, it had also been implicated in mediating both the locomotor sensation and rewarding effects of cocaine. Acute cocaine injections induced c-fos and CREB expression via D1 receptors and repeat cocaine administration, which is associated with long lasting AP-1 transcription complexes containing ΔFosB ...
Cocaine is a powerful stimulant known to make users feel energetic, cheerful, talkative, etc. In time, negative side effects include increased body temperature, irregular or rapid heart rate, high blood pressure, increased risk of heart attacks, strokes and even sudden death from cardiac arrest.