Facilitation of memory for extinction of drug-induced conditioned reward: role of amygdala and acetylcholine - PubMed (original) (raw)

Comparative Study

. 2004 Sep-Oct;11(5):641-7.

doi: 10.1101/lm.78504.

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Comparative Study

Facilitation of memory for extinction of drug-induced conditioned reward: role of amygdala and acetylcholine

Jason P Schroeder et al. Learn Mem. 2004 Sep-Oct.

Abstract

These experiments examined the effects of posttrial peripheral and intra-amygdala injections of the cholinergic muscarinic receptor agonist oxotremorine on memory consolidation underlying extinction of amphetamine conditioned place preference (CPP) behavior. Male Long-Evans rats were initially trained and tested for an amphetamine (2 mg/kg) CPP. Rats were subsequently given limited extinction training, followed by immediate posttrial peripheral or intrabasolateral amygdala injections of oxotremorine. A second CPP test was then administered, and the amount of time spent in the previously amphetamine-paired and saline-paired apparatus compartments was recorded. Peripheral (0.07 or 0.01 mg/kg) or intra-amygdala (10 etag/0.5 microL) postextinction trial injections of oxotremorine facilitated CPP extinction. Oxotremorine injections that were delayed 2 h posttrial training did not enhance CPP extinction, indicating a time-dependent effect of the drug on memory consolidation processes. The findings indicate that memory consolidation for extinction of approach behavior to environmental stimuli previously paired with drug reward can be facilitated by posttrial peripheral or intrabasolateral amygdala administration of a cholinergic agonist.

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Figures

Figure 1

Figure 1

Effects of peripheral oxotremorine on amphetamine CPP extinction. (Top) Initial amphetamine CPP in rats to be subsequently exposed to extinction training. Mean time spent (±SEM) in the previously paired (amphetamine) and unpaired (saline) compartments. All groups showed a significant CPP. (Bottom) Mean time spent (±SEM) in the previously paired (amphetamine) and unpaired (saline) compartments following extinction training. Oxotremorine at doses of 0.07 and 0.10 mg/kg significantly facilitated CPP extinction. Oxotremorine injections (0.07 mg/kg) delayed 2 h postextinction training were ineffective.

Figure 2

Figure 2

Effects of intra-amygdala oxotremorine on amphetamine CPP extinction. (Top) Initial amphetamine CPP in rats to be subsequently exposed to extinction training. Mean time spent (±SEM) in the previously paired (amphetamine) and unpaired (saline) compartments. All groups showed a significant CPP. (Bottom) Mean time spent (±SEM) in the previously paired (amphetamine) and unpaired (saline) compartments following extinction training. Oxotremorine at 10 ηg/0.5μL significantly facilitated CPP extinction. Oxotremorine injections (10 ηg/0.5μL) delayed 2 h postextinction training were ineffective.

Figure 3

Figure 3

Needle injection sites in the basolateral amygdala (shown with overlap), and ranging from -2.30 to -3.30 mm from Bregma. Illustrations were adapted from the rat brain atlas of Paxinos and Watson (1997).

References

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