Systemic administration of ghrelin increases extracellular dopamine in the shell but not the core subdivision of the nucleus accumbens

The alcohol-induced locomotor stimulation and accumbal dopamine release is suppressed in ghrelin knockout mice

“…Even though the ability of ghrelin to pass the BBB is somewhat limited (Banks et al, 2002), peripheral ghrelin has been shown to target the CNS including dopaminergic cell group in the ventral tegmental area (Abizaid et al, 2006;Jerlhag et al, 2006;Jerlhag, 2008;Kawahara et al, 2009;Quarta et al, 2009;Jerlhag et al, 2010a). However, a role for centrally produced ghrelin should not be excluded since ghrelin containing cells have been identified in the hypothalamus (Lu et al, 2001) and ghrelin mRNA has been found in the hypothalamus, specifically adjacent to the third ventricle in the brain and in the arcuate nucleus (Cowley et al, 2003;Mondal et al, 2005).…”

Ghrelin directly targets the ventral tegmental area to increase food motivation

“…To target the VTA, the following coordinates were chosen modified from : ±0.75 from the midline, 5.7 mm posterior to bregma, and 6.5 mm ventral from the surface of the skull, with injector aimed 8.0 mm ventral to skull. For the NAcc shell, the following coordinates were used (modified from (Quarta et al, 2009): ±0.75 from the midline, 1.7 mm anterior to bregma, and 6.0 mm ventral to skull, with injector aimed 7.5 mm ventral). Cannulae were attached to the skull with dental acrylic cement and jeweler's screws and closed with an obturator, as described previously (Skibicka et al, 2009).…”

The role of the central ghrelin system in reward from food and chemical drugs

“…Both central and intra-VTA administration of ghrelin induces an increase in accumbal dopamine release and also induces a locomotor stimulation (Jerlhag et al 2006a;Jerlhag et al 2007) as well as an increase in dopamine turnover in N.Acc (Abizaid et al 2006). Peripherally injected ghrelin also stimulates the mesolimbic dopamine system (Jerlhag 2008;Quarta et al 2009) suggesting that peripherally produced ghrelin is able to access (or indirectly activate) the mesolimbic reward circuits. Interestingly, administration of a GHS-R1A antagonist into the VTA blocks the ability of ghrelin to increase food intake (Abizaid et al 2006) and to release dopamine in the N.Acc suggesting that ghrelin activates GHS-R1A expressed on dopaminergic cell bodies in the VTA.…”