Response by the neurotensin systems of the basal ganglia to cocaine treatment
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Cited by (46)
Intra-accumbens shell injections of SR48692 enhanced cocaine self-administration intake in rats exposed to an environmentally-elicited reinstatement paradigm
2009, Brain ResearchCitation Excerpt :Similar results have been found in the mPFC where cocaine pretreatment induces an increase in NT immunoreactivity in rats, and where activation of NT receptors stimulates firing of DA neurons (Rompré et al., 1998; Alburges and Hanson, 1999). Additional evidence of a link between NT and cocaine is provided by studies showing an increase in NT in the striatum, substantia nigra, NAc, and frontal cortex after cocaine exposure, apparently due to the failure of the DA reuptake mechanism (Cain et al., 1993; Hanson et al., 1989), while at the same time cocaine causes a decrease in NT binding in the VTA and PFC (Pilotte et al., 1991). Taken together, these findings suggest that NT is involved in mediating the rewarding properties of psychostimulants such as cocaine.
Striatal and ventral pallidum dynorphin concentrations are markedly increased in human chronic cocaine users
2008, NeuropharmacologyCitation Excerpt :The likely explanation for these changes is that COC, via dopamine transporter inhibition, stimulates the DA D-1 and/or D-2 receptors and increases synthesis of NT, DYN (Adams et al., 2003) and SP (Adams et al., 2001). This is supported by findings that D-1 antagonists block, and a selective D-1 agonist mimics, these COC effects (Hanson et al., 1989) while either D-1 or D-2 selective antagonists block increased levels of DYN (Smiley et al., 1990) or SP (Alburges et al., 2000). Our finding of increased caudate DYN in human COC users (who all had used the drug chronically and recently) is somewhat supported by the early report of modestly increased expression of preprodynorphin mRNA in the putamen (with a trend in caudate) in human COC users (Hurd and Herkenham, 1993) and suggests that COC is able to stimulate production of striatal DYN even after long-term repeated exposure.
Nicotinic and dopamine D<inf>2</inf> receptors mediate nicotine-induced changes in ventral tegmental area neurotensin system
2007, European Journal of PharmacologyCo-localization of GABA with other neuroactive substances in the basal ganglia
2007, Progress in Brain ResearchBioactive analogs of neurotensin: Focus on CNS effects
2006, Peptides