Following presynaptic dopamine and glutamate co-release by such psychostimulants, ΔFos B functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.ΔFos B is the most significant biomolecular mechanism in addiction because the overexpression of ΔFos B in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and behavioral effects (e.g., expression-dependent increases in drug self-administration and reward sensitization) seen in drug addiction.Founded in 2002 by Nobel Laureate Carl Wieman, the Ph ET Interactive Simulations project at the University of Colorado Boulder creates free interactive math and science simulations.
ΔFos B overexpression (i.e., an abnormally and excessively high level of ΔFos B expression which produces a pronounced gene-related phenotype) triggers the development of addiction-related neuroplasticity throughout the reward system.
ΔFos B differs from the full length Fos B and further truncated Δ2ΔFos B in its capacity to produce these effects, as only accumbal ΔFos B overexpression is associated with pathological responses to drugs.
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This increase has been found to be part of pathways for the negative side effects that such drugs produce.