• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • The underlying assumption of consolidation re consolidation


    The underlying assumption of consolidation/re-consolidation is that the α-Conotoxin PIA activity initiated during the acquisition trial/re-consolidation trial continues to persist briefly after completion of the trial and it is during this post-trial period that immediate post-trial treatments can influence consolidation/re-consolidation [[18], [19], [20], [21], [22], [23]]. The post-trial apomorphine modulatory behavioral effects were effective following brief exposure to a novel environment [24] or brief exposure to a dopaminergic drug conditioned environment [14,15]. To account for these post-trial inhibitory/excitatory effects of apomorphine, it has been proposed that the post-trial apomorphine drug treatments attenuate/enhance the dopamine trace that persists post-trial [24]. In the case of exposure to a novel environment there is evidence that a dopamine activation state persists briefly post-trial [25] but with regard to post-trial apomorphine effects following brief exposure to drug conditioned contextual cues there is no direct evidence for a post-trial dopamine trace. In these studies, a conditioned hyper-activity response was induced using a high dose of apomorphine (2.0 mg/kg). Subsequently the animals were given a brief non-drug exposure to the test environment and a conditioned stimulant response was elicited selectively in rats that had previously experienced the high dose apomorphine treatment in the test environment. Immediately following this brief CS exposure, the rats were administered either the same high dose of apomorphine (2.0 mg/kg), a low behavioral inhibitory dose of apomorphine (0.05 mg/kg) or vehicle. In the group given the high apomorphine dose immediately post-trial, the conditioned hyperactivity response was potentiated, whereas in the group given the low apomorphine dose immediately post-trial, the conditioned response was suppressed and the conditioned response in the vehicle treated groups underwent extinction. The same apomorphine treatments given after a 15 min. post-trial delay to similarly conditioned groups resulted in extinction or if the immediate post-trial apomorphine treatments were given to unpaired groups they were without effect during subsequent tests. These findings appear to be in keeping with the proposition that the post-trial apomorphine treatments impacted memory reconsolidation by increasing/decreasing the level of dopamine activity during re-consolidation. In previous reports, we have found that an acute high dose (2.0 mg/kg) apomorphine treatment increases the extracellular signal-regulated kinase protein (ERK) in several brain areas that were measured including the medial prefrontal cortex (mPFC) [[26], [27], [28]]. With repeated high dose apomorphine treatments context specific behavioral sensitization was induced and we found that among the brain areas sampled that ERK was selectively potentiated in the mPFC [27]. In a related study we observed that among several brain areas sampled that an increased ERK response was only observed in the mPFC following a 30 min. conditioning test selectively in the paired group but not in the unpaired group [27]. In order to extend the investigation of this association of increased ERK in the mPFC with a conditioned apomorphine response we used a post-trial apomorphine protocol [24,29]. Initially a conditioned apomorphine response is induced using a conventional drug conditioning protocol. Subsequently, brief non-drug exposures to the test environment cues are followed by apomorphine treatments that are administered either immediately post-test that are designed to maintain the conditioned response or after 15 min. posttest delay designed to extinguish the conditioned response in separate groups matched for the conditioned response. In this way, it is possible to ascertain if mPFC ERK changes parallel changes in the conditioned response. That is, are the mPFC ERK increases present with the occurrence of the conditioned response and absent with the extinction of the conditioned response when conditioning induction and apomorphine drug exposure are the same in both groups? The present report details the results of this investigation.