Mesocorticolimbic pathway Addiction

understanding pathways in drugs act , how drugs can alter pathways key when examining biological basis of drug addiction. reward pathway, known mesolimbic pathway, or extension, mesocorticolimbic pathway, characterized interaction of several areas of brain.

the projections ventral tegmental area (vta) network of dopaminergic neurons co-localized postsynaptic glutamate receptors (ampar , nmdar). these cells respond when stimuli indicative of reward present. vta supports learning , sensitization development , releases da forebrain. these neurons project , release da nucleus accumbens, through mesolimbic pathway. virtually drugs causing drug addiction increase dopamine release in mesolimbic pathway, in addition specific effects.
the nucleus accumbens (nacc) 1 output of vta projections. nucleus accumbens consists of gabaergic medium spiny neurons (msns). nacc associated acquiring , eliciting conditioned behaviors, , involved in increased sensitivity drugs addiction progresses. overexpression of Δfosb in nucleus accumbens necessary common factor in known forms of addiction; Δfosb strong positive modulator of positively reinforced behaviors.
the prefrontal cortex, including anterior cingulate , orbitofrontal cortices, vta output in mesocorticolimbic pathway; important integration of information helps determine whether behavior elicited. critical forming associations between rewarding experience of drug use , cues in environment. importantly, these cues strong mediators of drug-seeking behavior , can trigger relapse after months or years of abstinence.

other brain structures involved in addiction include:

the basolateral amygdala projects nacc , thought important motivation.
the hippocampus involved in drug addiction, because of role in learning , memory. of evidence stems investigations showing manipulating cells in hippocampus alters dopamine levels in nacc , firing rates of vta dopaminergic cells.




^ cite error: named reference nestler2 invoked never defined (see page).
^ nestler ej, barrot m, self dw (september 2001). deltafosb: sustained molecular switch addiction . proc. natl. acad. sci. u.s.a. 98 (20): 11042–11046. doi:10.1073/pnas.191352698. pmc 58680 . pmid 11572966. although Δfosb signal relatively long-lived, not permanent. Δfosb degrades gradually , can no longer detected in brain after 1–2 months of drug withdrawal ... indeed, Δfosb longest-lived adaptation known occur in adult brain, not in response drugs of abuse, other perturbation (that doesn t involve lesions) well. 
^ jones s, bonci (2005). synaptic plasticity , drug addiction . current opinion in pharmacology. 5 (1): 20–5. doi:10.1016/j.coph.2004.08.011. pmid 15661621. 
^ eisch aj, harburg gc (2006). opiates, psychostimulants, , adult hippocampal neurogenesis: insights addiction , stem cell biology . hippocampus. 16 (3): 271–86. doi:10.1002/hipo.20161. pmid 16411230. 
^ rang, h. p. (2003). pharmacology. edinburgh: churchill livingstone. p. 596. isbn 0-443-07145-4. 
^ kourrich s, rothwell pe, klug jr, thomas mj (2007). cocaine experience controls bidirectional synaptic plasticity in nucleus accumbens . j. neurosci. 27 (30): 7921–8. doi:10.1523/jneurosci.1859-07.2007. pmid 17652583. 
^ cite error: named reference cellular basis invoked never defined (see page).
^ kalivas pw, volkow nd (august 2005). neural basis of addiction: pathology of motivation , choice . american journal of psychiatry. 162 (8): 1403–13. doi:10.1176/appi.ajp.162.8.1403. pmid 16055761. 
^ floresco sb, ghods-sharifi s (february 2007). amygdala-prefrontal cortical circuitry regulates effort-based decision making . cerebral cortex. 17 (2): 251–60. doi:10.1093/cercor/bhj143. pmid 16495432. 
^ perry cj, zbukvic i, kim jh, lawrence aj (october 2014). role of cues , contexts on drug-seeking behaviour . british journal of pharmacology. 171 (20): 4636–72. doi:10.1111/bph.12735. pmc 4209936 . pmid 24749941.