The Medial Prefrontal Cortex Is Involved in Spatial Memory Retrieval under Partial-Cue Conditions

Jo, Yong Sang; Park, Eun Hye; Kim, Il Hwan; Park, Soon Kwon; Kim, Hyun; Kim, Hyun Taek; Choi, June-Seek

doi:10.1523/jneurosci.3589-07.2007

Cited by 113 publications

(75 citation statements)

References 51 publications

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“…In the absence of SAH, rats with selective mPFC lesions were subjected to a MWM test similar to that used in this study and no deficits were observed [38]. Others have reported selective mPFC lesions can alter MWM performance when spatial cues are minimized or task demands are changed, which indicates an interaction between hippocampal and mPFC function in MWM performance [39,40]. Because our lesions were not selective, further speculation regarding the neuroanatomical substrate for the cognitive deficits in each model is necessarily limited, but consistent with histologic damage to these structures.…”

Section: Discussionmentioning

confidence: 76%

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

et al. 2016

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Background Cognitive dysfunction can be a long-term complication following subarachnoid hemorrhage (SAH). Preclinical models have been variously characterized to emulate this disorder. This study was designed to directly compare long-term cognitive deficits in the context of similar levels of insult severity in the cisterna magna double-blood (DB) injection versus prechiasmatic blood (PB) injection SAH models. Methods Pilot work identified blood injectate volumes necessary to provide similar mortality rates (20-25 %). Rats were then randomly assigned to DB or PB insults. Saline injection and naïve rats were used as controls. Functional and cognitive outcome was assessed over 35 days. Results DB and PB caused similar transient rotarod deficits. PB rats exhibited decreased anxiety behavior on the elevated plus maze, while anxiety was increased in DB. DB and PB caused differential deficits in the novel object recognition and novel object location tasks. Morris water maze performance was similarly altered in both models (decreased escape latency and increased swimming speed). SAH caused histologic damage in the medial prefrontal cortex, perirhinal cortex, and hippocampal CA1, although severity of injury in the respective regions differed between DB and PB. Conclusion Both SAH models caused long-term cognitive deficits in the context of similar insult severity. Cognitive deficits differed between the two models, as did distribution of histologic injury. Each model offers unique properties and both models may be useful for study of SAH-induced cognitive deficits.

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Section: Discussionmentioning

confidence: 76%

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

et al. 2016

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“…This view expands the role of the mPFC to context-sensitive learning and memory systems in general rather than fear inhibition in particular. Such a role is supported by various behavioral paradigms testing other forms of context-sensitive learning and memory (36)(37)(38)(39). This more general role for the mPFC in contextual processing is also parsimonious with its role in remote long-term contextual fear memories (10,11) and the idea that the mPFC and hippocampus are continuously in communication to allow for the systems consolidation of contextual memories as they move from a recent to remote state (15,40).…”

Section: Discussionmentioning

confidence: 94%

Prefrontal microcircuit underlies contextual learning after hippocampal loss

Zelikowsky

Bissière

Hast³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

155

147

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Specific brain circuits have been classically linked to dedicated functions. However, compensation following brain damage suggests that these circuits are capable of dynamic adaptation. Such compensation is exemplified by Pavlovian fear conditioning following damage to the dorsal hippocampus (DH). Although the DH normally underlies contextual fear and fear renewal after extinction, both can be learned in the absence of the DH, although the mechanisms and nature of this compensation are currently unknown. Here, we report that recruitment of alternate structures, specifically the infralimbic and prelimbic prefrontal cortices, is required for compensation following damage to the hippocampus. Disconnection of these cortices in DH-compromised animals and immediate early gene induction profiles for amygdala-projecting prefrontal cells revealed that communication and dynamic rebalancing within this prefrontal microcircuit is critical. Additionally, the infralimbic cortex normally plays a role in limiting generalization of contextual fear. These discoveries reveal that plasticity through recruitment of alternate circuits allows the brain to compensate following damage, offering promise for targeted treatment of memory disorders.anxiety | recovery of function | amnesia | medial prefrontal cortex A widely accepted view is that the brain is comprised of multiple independent circuits dedicated to performing specific functions and encoding specific information. This view is exemplified in the field of learning and memory, where it is held that different circuits specialize in integrating and storing different classes of memories (1). However, studies looking at learning following brain damage clearly demonstrate that the brain can also behave dynamically. For example, in Pavlovian fear conditioning, contextual memories can be formed in the absence of circuits classically thought to underpin integration and storage of information about an animal's environment or context (2).In fear conditioning, contexts play two key roles in controlling fear learning and expression. First, a context can act as a conditional stimulus (CS), to which fear can be directly conditioned when an aversive experience, such as a foot shock [unconditional stimulus (US)] is signaled by the context. Second, contexts can modulate responding to a discrete cue, such as a tone-CS, which has acquired multiple meanings. For example, in extinction, a tone previously conditioned to elicit fear is presented in the absence of the aversive foot shock US, such that the conditional fear response begins to extinguish. However, because extinction is not an erasure of the original fear but rather new learning that interferes with retrieval of the original fear memory, an extinguished cue has multiple meanings (shock/no shock), which compete for behavioral expression (3). This competition is mediated by context, as fear renewal occurs when an extinguished stimulus is presented outside of the extinction context (4).These context-sensitive effects provide excellent models t...

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“…More generally, treatment of experimental animals with glutamate receptor antagonists impairs performance in a variety of cognitive tasks (Ahlander et al, 1999;Hauber and Schmidt, 1989;Karasawa et al, 2008;Venable and Kelly, 1990), whereas endogenous or exogenous glutamate receptor agonists promote cognitive performance (Clem et al, 2008;Lynch et al, 2008;Singer et al, 2010). Although definitive confirmation will require further experimentation and additional brain areas may well be involved (Jo et al, 2007), the present findings suggest that the cognitive impairment caused by elevated KYNA was likely related to reductions in extracellular glutamate in the hippocampus, and that the cognition-enhancing effects of ESBA were the result of elevated extracellular glutamate.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, no data are currently available on the effects of raised KYNA levels on an animal's performance in the Morris water maze (MWM), a classic spatial learning and memory task involving the hippocampus and associated brain regions (Morris, 1984;Jo et al, 2007). The present study was designed to fill this void using experimental rats.…”

Section: Introductionmentioning

confidence: 99%

Fluctuations in Endogenous Kynurenic Acid Control Hippocampal Glutamate and Memory

Pocivavsek

Potter

et al. 2011

Neuropsychopharmacol

146

158

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Kynurenic acid (KYNA), an astrocyte-derived metabolite, antagonizes the a7 nicotinic acetylcholine receptor (a7nAChR) and, possibly, the glycine co-agonist site of the NMDA receptor at endogenous brain concentrations. As both receptors are involved in cognitive processes, KYNA elevations may aggravate, whereas reductions may improve, cognitive functions. We tested this hypothesis in rats by examining the effects of acute up-or downregulation of endogenous KYNA on extracellular glutamate in the hippocampus and on performance in the Morris water maze (MWM). Applied directly by reverse dialysis, KYNA (30-300 nM) reduced, whereas the specific kynurenine aminotransferase-II inhibitor (S)-4-(ethylsulfonyl)benzoylalanine (ESBA; 0.3-3 mM) raised, extracellular glutamate levels in the hippocampus. Co-application of KYNA (100 nM) with ESBA (1 mM) prevented the ESBA-induced glutamate increase. Comparable effects on hippocampal glutamate levels were seen after intra-cerebroventricular (i.c.v.) application of the KYNA precursor kynurenine (1 mM, 10 ml) or ESBA (10 mM, 10 ml), respectively. In separate animals, i.c.v. treatment with kynurenine impaired, whereas i.c.v. ESBA improved, performance in the MWM. I.c.v. co-application of KYNA (10 mM) eliminated the pro-cognitive effects of ESBA. Collectively, these studies show that KYNA serves as an endogenous modulator of extracellular glutamate in the hippocampus and regulates hippocampus-related cognitive function. Our results suggest that pharmacological interventions leading to acute reductions in hippocampal KYNA constitute an effective strategy for cognitive improvement. This approach might be especially useful in the treatment of cognitive deficits in neurological and psychiatric diseases that are associated with increased brain KYNA levels.

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The Medial Prefrontal Cortex Is Involved in Spatial Memory Retrieval under Partial-Cue Conditions

Cited by 113 publications

References 51 publications

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

Prefrontal microcircuit underlies contextual learning after hippocampal loss

Fluctuations in Endogenous Kynurenic Acid Control Hippocampal Glutamate and Memory

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