Mesocorticolimbic dopamine system

You have to know that we take out most of the mesocorticolimbic dopamine system with that lesion we are not just taking out the nucleus accumbens dopamine projeetion. I am very eareful to put the region of the nucleus accumbens on my slide. 

Fibiger, HansC., and Anthony G. Phillips. 1988. "Mesocorticolimbic Dopamine Systems and Reward." Annals of the New York Academy of Sciences 537 206-15. 

The acute effects of ethanol and other sedative-hypnotics are mediated by actions at a number of receptor systems. For example, ethanol inhibits several excitatory receptor systems, including N-methyl-D-aspartate (NMDA) receptors, kainate receptors, and Ca channels. In addition, ethanol enhances the action of GABA at GABA receptors and appears to modulate serotonergic neurotransmission. Although a component of ethanol reinforcement is mediated by the activation of mesocorticolimbic dopamine neurons, activation of these neurons may not be necessary for ethanol reinforcement, as ethanol remains reinforcing in the absence of these neurons (Samson and Harris, 1992 Koob, 2000b). 

O Virtually all abused substances appear to activate the same brain reward pathway. Key components of the reward pathway are the dopamine (DA) mesocorticolimbic system that projects from the ventral tegmental area (VTA) and the nucleus accumbens (NA) to the prefrontal cortex, the amygdala, and the olfactory tubercle (Figs. 33-3 and 33-4).5 Animal studies... 

Subchronic oral administration of lithium causes a time-dependent increase in the substance P level in the striatum, which is prevented by coadministration of haloperidol. In PC 12 pheochromocytoma cells, lithium dramatically increases the intracellular levels of the neuropeptide neurotensin and the mRNA encoding it. An extensive overlap between specific and high-affinity neurotensin binding sites and dopamine perikarya and dendrites has been shown to occur in the mesocorticolimbic and nigrostriatal projection systems. Consistent with this observation are the results of observations showing that cocaine, an indirect sympathomimetic agent that enhances the extrapyramidal dopaminergic activity, increases dramatically the striatal content of neurotensin-like immunoreactivity. 

Fig. 2. A. Forebrain dopamine projection system in rodents and primates. The nigrostriatal pathway projects from the A8 and A9 groups of the substantia nigra (SN) via the medial forebrain bundle (mfb) to the neostriatum (NS). The mesocorticolimbic pathway projects from the more medially located A10 cell group of the ventral tegmental area (VTA) to the nucleus accumbens (NAcc) and olfactory tubercle (OT) of the ventral striatum (VS) and limbic forebrain areas including prefrontal cortex (Ctx), septum (Se) and amygdala (A). B. Striatal projection areas in the rodent brain are divided into the more dorsal neostriatum, and ventral striatum. C. In the primate brain, including human and illustrated for the marmoset, the neostriatum is divided by the fibers of the internal capsule into caudate nucleus (CN) and putamen (Pu). Correspondingly, the neostriatum of rats is sometimes designated the caudate-putamen (CPu) complex.

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