Spatial Memory and Learning in Transgenic Mice: Fact or Artifact?

Wolfer, David P; Stagljar-Bozicevic, Marijana; Errington, Mick L.; Lipp, Hans‐Peter

doi:10.1152/physiologyonline.1998.13.3.118

Cited by 117 publications

(127 citation statements)

References 12 publications

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“…An assessment of behavioral changes at multiple time points over a longer period will provide more detailed information about the progression of the DFP-induced deficits. Finally, limitations of the water maze as an assay for psychological function in rodents have been noted across a variety of research disciplines [33][34][35]. Rodents use a variety of search strategies to navigate towards a goal (i.e., escape from water) and may explain differences in swim latencies, even slower latencies in control animals (i.e., the Naltrexoneonly rats in this study).…”

Section: Discussionmentioning

confidence: 87%

“…Rodents use a variety of search strategies to navigate towards a goal (i.e., escape from water) and may explain differences in swim latencies, even slower latencies in control animals (i.e., the Naltrexoneonly rats in this study). About two-thirds of the variability in Morris maze results are accounted for by non-cognitive factors such as thigmotaxis and passivity [33]. Furthermore, variations in system setup and protocol (i.e., pool size, extramaze cues, experimenter movement), species and strain differences and even stress in the animal may contribute largely to inconsistent acquisition (latency, distance traveled) results across labs, thereby adversely influencing the allocentric aspects of rodent spatial learning [34,36].…”

Section: Discussionmentioning

confidence: 99%

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Chronic Treatment with Naltrexone Prevents Memory Retention Deficits in Rats Poisoned with the Sarin Analog Diisopropylfluorophosphate (DFP) and Treated with Atropine and Pralidoxime

2015

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Humans and rats poisoned with sarin develop chronic neurological disabilities that are not prevented with standardized antidotal therapy. We hypothesized that rats poisoned with the sarin analogue diisopropylfluorophosphate (DFP) and resuscitated with atropine and pralidoxime would have long-term memory deficits that were preventable with naltrexone treatment. Long Evans rats (250-275 g) were randomized to: DFP (N=8): single subcutaneous (SC) injection of DFP (5 mg/kg). Treatment (N=9): DFP (5 mg/kg) followed by chronic naltrexone (5 mg/kg/day × 12 weeks). Control (N= 12): single SC injection of isopropyl alcohol, (DFP vehicle) followed by chronic naltrexone (5 mg/kg/day). If toxicity developed after injection, antidotal therapy was initiated with atropine (2 mg/kg) and pralidoxime (25 mg/kg) and repeated as needed. After 12 weeks, rats underwent testing for place learning (acquisition) across 5 days of training using the Morris Water Maze. On day 6 a memory retention test was performed. Statistical analysis was performed using IBM SPSS Statistics. Rats receiving DFP rapidly developed toxicity requiring antidotal rescue. No differences in acquisition were seen between the DFP vs. DFP+naltrexone rats. During memory testing, DFP-poisoned rats spent significantly less time (29.4±2.11 versus 38.5±2.5 s, p<0.05) and traveled less distance (267±24.6 versus 370±27.5 cm, p<0.05) in the target quadrant compared to the treatment group. Treatment rats performed as well as control rats (p>0.05) on the test for memory retention. Poisoning with DFP induced impaired memory retention. Deficits were not prevented by acute rescue with atropine and pralidoxime. Chronic naltrexone treatment led to preserved memory after DFP poisoning.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Chronic Treatment with Naltrexone Prevents Memory Retention Deficits in Rats Poisoned with the Sarin Analog Diisopropylfluorophosphate (DFP) and Treated with Atropine and Pralidoxime

2015

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“…In initial training trials, naive mice tend to spend the majority of their time searching the periphery of the pool (Wolfer et al, 1998). This thigmotaxic behavior tends to decline rapidly over training (Fig.…”

Section: Inactivating the Acc Disrupts Expression Of Remote Spatial Mmentioning

confidence: 98%

Involvement of the Anterior Cingulate Cortex in the Expression of Remote Spatial Memory

et al. 2006

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Although the hippocampus plays a crucial role in the formation of spatial memories, as these memories mature they may become additionally (or even exclusively) dependent on extrahippocampal structures. However, the identity of these extrahippocampal structures that support remote spatial memory is currently not known. Using a Morris water-maze task, we show that the anterior cingulate cortex (ACC) plays a key role in the expression of remote spatial memories in mice. To first evaluate whether the ACC is activated after the recall of spatial memory, we examined the expression of the immediate early gene, c-fos, in the ACC. Fos expression was elevated after expression of a remote (1 month old), but not recent (1 d old), water-maze memory, suggesting that ACC plays an increasingly important role as a function of time. Consistent with the gene expression data, targeted pharmacological inactivation of the ACC with the sodium channel blocker lidocaine blocked expression of remote, but spared recent, spatial memory. In contrast, inactivation of the dorsal hippocampus disrupted expression of spatial memory, regardless of its age. We further showed that inactivation of the ACC blocked expression of remote spatial memory in two different mouse strains, after training with either a hidden or visible platform in a constant location, and using the AMPA receptor antagonist CNQX. Together, our data provide evidence that circuits supporting spatial memory are reorganized in a time-dependent manner, and establish that activity in neurons intrinsic to the ACC is critical for processing remote spatial memories.

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“…However, it is important to remember that the escape latency data by itself are not compelling and do not indicate the type of search strategy being used; data from some type of test trial is necessary to determine whether a group of mice is using a spatially biased search strategy. Recent reports have found that mouse performance during training often does not predict what type of search performance will be elicited during a probe trial (Owen et al 1997;Wolfer et al 1998). In addition, other researchers have observed mutant mice that do not have an impairment during training, and do not show a selective The average time to locate the platform during the random platform test trials.…”

Section: Impaired Spatial Learning In Lis1hetmentioning

confidence: 99%

Impaired Learning and Motor Behavior in Heterozygous Pafah1b1 (Lis1) Mutant Mice

Paylor¹,

Hirotsune²,

Gambello³

et al. 1999

Learn. Mem.

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Spatial Memory and Learning in Transgenic Mice: Fact or Artifact?

Cited by 117 publications

References 12 publications

Chronic Treatment with Naltrexone Prevents Memory Retention Deficits in Rats Poisoned with the Sarin Analog Diisopropylfluorophosphate (DFP) and Treated with Atropine and Pralidoxime

Chronic Treatment with Naltrexone Prevents Memory Retention Deficits in Rats Poisoned with the Sarin Analog Diisopropylfluorophosphate (DFP) and Treated with Atropine and Pralidoxime

Involvement of the Anterior Cingulate Cortex in the Expression of Remote Spatial Memory

Impaired Learning and Motor Behavior in Heterozygous Pafah1b1 (Lis1) Mutant Mice

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