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Top Initial amphetamine CPP in rats to be subsequently exposed to extinction training. All groups showed a significant CPP. Oxotremorine at doses of 0. Oxotremorine injections 0.
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Figure 1 bottom shows the mean time spent in the amphetamine-paired and saline-paired compartments after extinction training for each of the groups. This finding in the control rats is consistent with our previous report that using the present training parameters, administration of two extinction trials is not sufficient to produce extinction of CPP behavior Schroeder and Packard Similarly, rats receiving the lowest dose of oxotremorine 0.
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In contrast, rats that received postextinction training injections of 0. Rats administered oxotremorine 0. Importantly, this finding also indicates that the immediate postextinction trial injections of oxotremorine did not facilitate CPP extinction via a proactive effect on nonmnemonic factors i. Figure 2 top shows the mean time spent in the amphetamine-paired and saline-paired compartments on the initial test session prior to group assignment.
Effects of intra-amygdala oxotremorine on amphetamine CPP extinction. Figure 2 bottom shows the mean time spent in the amphetamine- and saline-paired compartments after extinction training for each of the groups. Again, this finding in the control rats is consistent with our previous report that using the present training parameters, administration of two extinction trials is not sufficient to produce extinction of CPP behavior Schroeder and Packard This finding also indicates that the immediate postextinction trial injections of oxotremorine did not facilitate CPP extinction via a proactive effect on nonmnemonic factors i.
Postextinction training peripheral or intra-amygdala administration of the cholinergic muscarinic receptor agonist oxotremorine facilitated the extinction of an amphetamine CPP. To our knowledge, the findings are the first to demonstrate enhanced memory consolidation for CPP extinction training by a specific neurotransmitter agonist.
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Other recent findings using memory impairing treatments also suggest that the new learning underlying extinction for inhibitory avoidance training Santini et al. The present findings are consistent with those of previous studies that used pretraining peripheral injections of cholinergic agents to examine the role of acetylcholine in extinction for review, see Mason For example, pre-extinction injections of the muscarinic receptor antagonist atropine attenuate extinction of passive avoidance behavior Buresova et al.
Although cholinergic agents were administered prior to extinction in these earlier studies, the present findings raise the possibility that the enhancement of extinction rate that was observed may have been mediated by a facilitation of cholinergic function during the postextinction training time period.
We have previously observed that posttraining blockade of acetylcholine receptors within the basolateral amygdala by the cholinergic muscarinic receptor antagonist scopolamine impairs the acquisition of food and amphetamine CPPs Schroeder and Packard Taken together with the present findings, this suggests a neurochemical similarity between processes mediating memory consolidation for CPP acquisition and extinction.
This conclusion is consistent with recent evidence indicating that the neurochemical processes that mediate memory formation and extinction are often similar in other types of behavioral tasks see Falls et al. Specifically, the ability of posttrial intra-amygdala infusions of oxotremorine to facilitate extinction of CPP behavior are consistent with evidence that intra-amygdala infusion of this cholinergic agonist also enhances the initial acquisition of contextual fear conditioning Vazdarjanova and McGaugh , inhibitory avoidance Intrioni-Collison et al.
However, this explanation seems unlikely given that at the doses used in the present study, posttraining oxotremorine enhances initial memory consolidation in many tasks see Intrioni-Collison et al. In the present study, peripheral and intra-amygdala postextinction trial injection of oxotremorine enhanced memory consolidation for CPP extinction in a fashion similar to that previously observed with glucose Schroeder and Packard Other evidence indicates that glucose and acetylcholine can interact during memory formation, raising the possibility that the memory-enhancing effects of postextinction trial glucose may ultimately involve a cholinergic mechanism.
For example, the cholinergic muscarinic receptor antagonist atropine blocks the memory-enhancing effects of posttraining glucose Kopf and Baratti In addition, coadministration of subeffective doses of glucose and the acetylcholine precursor choline act synergistically to enhance consolidation of inhibitory avoidance memory, and this effect is attenuated by administration of atropine Kopf et al. One mechanism by which glucose may enhance acetylcholine function is by serving as a precursor to this neurotransmitter in conditions of high acetylcholine demand. Acetylcholine is synthesized by the reaction of choline and acetyl-Co-A, and glucose serves as the main source of acetyl-Co-A Quastel Although high-affinity choline uptake is generally the rate-limiting step for acetylcholine synthesis Simon et al.
In addition to acetylcholine, the neurotransmitter glutamate has also been implicated in the acquisition of CPP behavior and in extinction processes underlying other forms of emotional memory Bespalov et al.
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For example, peripheral Baker and Azorlosa and intra-amygdala Falls et al. Moreover, recent evidence indicates that pre-extinction administration of the NMDA receptor agonist D-cycloserine either through the system or into the amygdala facilitates the extinction of fear conditioning Walker et al.
Therefore, future research examining the role of intra-amygdala NMDA receptors in the extinction of stimulus-reward associations mediating CPP behavior is warranted. The present experiments do not reveal the cellular mechanism s by which posttraining peripheral and intra-amygdala infusions of the acetylcholine agonist oxotremorine facilitate memory for CPP extinction. Muscarinic receptor activation increases the excitability of basolateral amygdala neurons Washburn and Moises ; Womble and Moises , , which could conceivably enhance consolidation of memory traces directly within the amygdala.
Consistent with this possibility, acetylcholine can modulate the induction of long-term potentiation LTP , a putative cellular model of learning and memory that has been demonstrated in the amygdala Chapman et al. Although to our knowledge the role of acetylcholine in amygdala LTP has not been investigated, this transmitter has been shown to play a role in LTP in other brain regions. For example, application of oxotremorine Iga et al.
Acetylcholine also influences neocortical LTP in freely moving rats, as the cholinergic agonist pilocarpine enhances, whereas scopolamine attenuates LTP induction Boyd et al. Alternatively, the activity of amygdala output neurons may ultimately modulate memory consolidation processes underlying extinction of CPP behavior occurring in other brain regions. Extensive evidence indicates that the basolateral amygdala modulates memory consolidation occurring in other brain regions during initial acquisition of some types of learning tasks e. One brain area that receives a prominent glutamatergic input from the basolateral amygdala is the nucleus accumbens see Wright et al.
Extinction exposure to a cocaine self-administration environment results in decreases in c-fos expression in the nucleus accumbens, and this reduction correlates with the strength of subsequent drug-seeking behavior Neisewander et al. Other findings indicate interactions between the basolateral amygdala and nucleus accumbens in mediating the memory-enhancing effects of posttraining glucocorticoid administration Roozendaal et al. The medial prefrontal cortex is an additional brain region that shares functional connectivity with the basolateral amygdala see McDonald et al. Further research is necessary to examine whether extinction of CPP behavior ultimately involves the formation of memory traces directly within the amygdala or modulation of memory processes occurring in other brain areas.
Finally, the present findings may have implications for the treatment of human drug addiction. Exposure of addicts to formerly drug-related cues induces drug craving Childress et al. The ability of drug-paired cues to induce craving is presumably one of the mechanisms by which addiction endures. Our findings present study; Schroeder and Packard indicating that posttraining administration of memory-enhancing agents can facilitate extinction of approach behavior to environmental stimuli associated with drug reward may therefore aid in the development of pharmacological therapies aimed at reducing drug-seeking behaviors in humans.
The subjects were 65 adult male Long-Evans rats to g. Bilateral guide cannulae 23 gauge, 15 mm in length were implanted overlying the basolateral amygdala by 1 mm, using standard stereotaxic techniques. Jeweler's screws were anchored to the skull and attached to the cannula with dental acrylic. These coordinates were selected based on our previous research indicating that infusion of local anesthetics into this area blocks memory consolidation for food and amphetamine CPPs Schroeder and Packard ; Hsu et al.
The locations of injection sites in the basolateral amygdala are shown in Figure 3.
Three rats were discarded due to misplacement of guide cannula. Histological analysis revealed that injection needle tip placements in the basolateral amygdala ranged from Needle injection sites in the basolateral amygdala shown with overlap , and ranging from Illustrations were adapted from the rat brain atlas of Paxinos and Watson The apparatus was identical to that used in our previous studies investigating the role of the basolateral amygdala in food and amphetamine CPP behavior Schroeder and Packard , ; Hsu et al. The other compartment was painted white and had wood chips scattered over the floor.
D-Amphetamine and oxotremorine were obtained from Sigma-Aldrich. All peripheral drugs were injected at a volume of 1. The intracerebral infusions were administered over a sec period, and the injection needles 30 gauge, extending from the guide cannula by 1 mm were left in place an additional 60 sec to allow for solution diffusion. The oxotremorine doses were selected based on their ability to enhance memory consolidation in various tasks Baratti et al. The behavioral procedures were identical to those of our previous research examining the effects of posttrial glucose on extinction of amphetamine CPP behavior Schroeder and Packard , and consisted of four general phases: CPP training, initial CPP testing, extinction training, and an additional CPP test.
Training of the initial amphetamine CPP took place over 6 days. The first day consisted of habituation, during which rats were allowed access to all three compartments of the CPP apparatus for 10 min. The next 4 days consisted of two treatments and two nontreatment pairings, during which rats were confined to one of the two pairing compartments for 30 min immediately following administration of D-amphetamine or saline. In the present CPP apparatus, we have found that rats spend equal amounts of time in both of the large compartments during the habituation session Schroeder and Packard Therefore, the present study used an unbiased CPP design in which half of the rats were injected with amphetamine prior to confinement in the black compartment and saline prior to confinement in the white compartment.
The remaining half of the rats received amphetamine injections prior to exposure to the white compartment and saline injection prior to exposure to the black compartment. Half of the rats received their amphetamine injections on odd-numbered days, and the other half received amphetamine injections on even-numbered days. On day 6, the rats were given a min drug-free test session and were allowed access to all three compartments of the apparatus. No treatments were administered prior to the test session, and the amount of time spent in the previous amphetamine-paired and saline-paired apparatus compartments was recorded as a measure of CPP behavior.
Twenty-four hours after the initial CPP test, rats were assigned to extinction groups that were matched with regard to the magnitude of their initial amphetamine CPP. Rats then received two extinction trials that were similar to original training i. However, no treatments were administered prior to the extinction trials. In our previous research Schroeder and Packard using the same training parameters as those of the present study, we observed that two extinction trials were not sufficient to produce extinction, whereas four or eight trials did produce extinction of CPP behavior.
As the present study was designed to investigate whether a posttrial treatment could facilitate extinction, the two-extinction trial procedure was used. Experiment 1 examined the effects of peripheral postextinction trial administration of oxotremorine on CPP extinction.
Experiment 2 examined the effects of intrabasolateral amygdala postextinction trial administration of oxotremorine on CPP extinction. Other groups of rats received initial amphetamine CPP training and testing, and peripheral or intrabasolateral amygdala oxotremorine injections that were delayed until 2 h after the extinction trials. These groups were tested in order to examine whether postextinction trial oxotremorine exerts a time-dependent effect on memory consolidation processes, and to control for potential proactive effects of oxotremorine on nonmnemonic factors e.
The doses of oxotremorine used for the delayed injections 0. Schroeder 1 , 3 and Mark G. Previous Section Next Section. Figure 1 Effects of peripheral oxotremorine on amphetamine CPP extinction. Figure 2 Effects of intra-amygdala oxotremorine on amphetamine CPP extinction. Figure 3 Needle injection sites in the basolateral amygdala shown with overlap , and ranging from Previous Section.
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Baker, J. Bardo, M. Repeated testing attenuates conditioned place preference with cocaine. Psychopharmacology 89 : CrossRef Medline Google Scholar. Baratti, C. The post-training memory enhancement induced by physostigmine and oxotremorine in mice is not state-dependent.