2010
DOI: 10.1111/j.1369-1600.2010.00262.x View full text |Buy / Rent full text
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Abstract: Relapse is one of the most problematic aspects in the treatment of alcoholism and is often triggered by alcohol-associated environmental cues. Evidence indicates that glutamate neurotransmission plays a critical role in cue-induced relapse-like behavior, as inhibition of glutamate neurotransmission can prevent reinstatement of alcohol-seeking behavior. However, few studies have examined specific changes in extracellular glutamate levels in discrete brain regions produced by exposure to alcohol-associated cues.… Show more

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“…Consistent with the fact that nicotine has been classified as a psychostimulant (30), this long term potentiation (LTP)-like state after self-administered nicotine is similar to what is produced by cocaine self-administration (17, 24) but opposite to that elicited by heroin self-administration (11). Although differential effects on resting synaptic strength in the NAcore between psychostimulants and heroin would seem to support different underlying mechanisms of relapse vulnerability (31), we also found that reinstating nicotine seeking with conditioned cues elicits glutamate overflow in the NAcore akin to what is seen during heroin, alcohol, and cocaine reinstatement (13,15,32). Furthermore, the glutamate overflow was associated with rapid, transient synaptic plasticity as illustrated by cue-induced increases in d h and A/N, and this rapid synaptic plasticity is also produced during cocaine or heroin reinstatement (11,33).…”
Section: Discussionsupporting
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“…Consistent with the fact that nicotine has been classified as a psychostimulant (30), this long term potentiation (LTP)-like state after self-administered nicotine is similar to what is produced by cocaine self-administration (17, 24) but opposite to that elicited by heroin self-administration (11). Although differential effects on resting synaptic strength in the NAcore between psychostimulants and heroin would seem to support different underlying mechanisms of relapse vulnerability (31), we also found that reinstating nicotine seeking with conditioned cues elicits glutamate overflow in the NAcore akin to what is seen during heroin, alcohol, and cocaine reinstatement (13,15,32). Furthermore, the glutamate overflow was associated with rapid, transient synaptic plasticity as illustrated by cue-induced increases in d h and A/N, and this rapid synaptic plasticity is also produced during cocaine or heroin reinstatement (11,33).…”
Section: Discussionsupporting
“…Notably, the phenomenon of alcohol-induced glutamate sensitization is not only observed upon noncontingent (i.e., experimenter-administered; vapor-exposed) alcohol administration, but also occurs in animals exhibiting voluntary alcohol intake under limited-access procedures when assayed either by in vivo microdialysis within the NAC (Szumlinski et al, 2007) or electrophysiological approaches within the VTA (Stuber et al, 2008). Interestingly, glutamate sensitization is also observed within the basolateral amygdala and the NAC in response to cues associated previously with ethanol reinforcement (Gass, Sinclair, Cleva, Widholm, & Olive, 2011). This suggests that glutamate sensitization is a pharmacodynamic response to repeated alcohol exposure that does not depend upon the route of alcohol administration and can be triggered by re-exposure to alcohol-associated cues.…”
Section: Glutamate Release / Uptakementioning
“…Reinstatement to cocaine, heroin, alcohol, and nicotine is associated with potentiated release of glutamate within the NAc (Gass et al, 2011;Gipson et al, 2013;LaLumiere and Kalivas, 2008;Lutgen et al, 2012;McFarland et al, 2003). Given that all of these drugs reduce GLT-1 in the NAc, the reduced uptake of synaptically released glutamate is a likely mediator of the increase in extracellular glutamate associated with reinstatement.…”
Section: Restoration Of Glt-1 Is a Critical Mechanism For Control Ofmentioning