A Role for Prefrontal Cortex in Memory Storage for Trace Fear Conditioning

Runyan, Jason D.; Moore, Anthony N.; Dash, Pramod K.

doi:10.1523/jneurosci.4880-03.2004

Cited by 193 publications

(155 citation statements)

References 48 publications

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“…In contrast, paired conditioning only induced a transient early wave of ERK1/2 and CREB activation immediately post-training. Our results are congruent with data showing with different behavioral paradigms a learninginduced activation of ERK1/2 (Atkins et al 1998;Blum et al 1999;Cammarota et al 2000;Sananbenesi et al 2002;Runyan et al 2004;Wang et al 2004) in hippocampus. Considering that these studies revealed different time courses of activation, we cannot ascertain that the early activation we found in both conditioning protocols is driven by common molecular mechanisms.…”

Section: Learning and Memory 353supporting

confidence: 93%

Foreground contextual fear memory consolidation requires two independent phases of hippocampal ERK/CREB activation

Trifilieff¹,

Herry²,

Vanhoutte³

et al. 2006

Learn. Mem.

138

124

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Fear conditioning is a popular model for investigating physiological and cellular mechanisms of memory formation. In this paradigm, a footshock is either systematically associated to a tone (paired conditioning) or is pseudorandomly distributed (unpaired conditioning). In the former procedure, the tone/shock association is acquired, whereas in the latter procedure, the context/shock association will prevail. Animals with chronically implanted recording electrodes show enhanced amplitude of the extracellularly recorded field EPSP in CA1 pyramidal cells for up to 24 h after unpaired, but not paired, fear conditioning. This is paralleled by a differential activation of the ERK/CREB pathway in CA1, which is monophasic in paired conditioning (0-15 min post-conditioning), but biphasic (0-1 h and 9-12 h post-conditioning) in unpaired conditioning as revealed by immunocytochemistry and Western blotting. Intrahippocampal injection of the MEK inhibitor U0126 prior to each phase prevents the activation of both ERK1/2 and CREB after unpaired conditioning. Block of any activation phase leads to memory impairment. We finally reveal that the biphasic activation of ERK/CREB activity is independently regulated, yet both phases are critically required for the consolidation of long-term memories following unpaired fear conditioning. These data provide compelling evidence that CA1 serves different forms of memory by expressing differential cellular mechanisms that are dependent on the training regime.

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Section: Learning and Memory 353supporting

confidence: 93%

Foreground contextual fear memory consolidation requires two independent phases of hippocampal ERK/CREB activation

Trifilieff¹,

Herry²,

Vanhoutte³

et al. 2006

Learn. Mem.

138

124

View full text Add to dashboard Cite

show abstract

“…Trace fear conditioned learning requires an intact medial prefrontal cortex, ACC, and hippocampus (Huerta et al, 2000;Blank et al, 2003;Han et al, 2003;Runyan et al, 2004). Consistent with the defect in trace fear conditioning seen in FMR1 KO mice, patients with fragile X syndrome have abnormal activation patterns in the ventromedial prefrontal cortex, ACC, and hippocampus (Menon et al, 2004).…”

Section: Discussionmentioning

confidence: 66%

Deficits in Trace Fear Memory and Long-Term Potentiation in a Mouse Model for Fragile X Syndrome

Zhao¹,

Toyoda²,

Ko³

et al. 2005

J. Neurosci.

267

272

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Trace fear memory requires the activity of the anterior cingulate cortex (ACC) and is sensitive to attention-distracting stimuli. Fragile X syndrome is the most common form of mental retardation with many patients exhibiting attention deficits. Previous studies in fragile X mental retardation 1 (FMR1) knock-out (KO) mice, a mouse model for fragile X, focused mainly on hippocampal-dependent plasticity and spatial memory. We demonstrate that FMR1 knock-out mice show a defect in trace fear memory without changes in locomotion, anxiety, and pain sensitivity. Whole-cell path-clamp recordings in the ACC show that long-term potentiation (LTP) was completely abolished. A similar decrease in LTP was found in the lateral amygdala, another structure implicated in fear memory. No significant changes were found in basal synaptic transmission. This suggests that synaptic plasticity in the ACC and amygdala of FMR1 KO mice plays an important role in the expression of behavioral phenotypes similar to the symptoms of fragile X syndrome.

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“…Although several previous studies have suggested a role for the mPFC in memory consolidation, including inhibitory avoidance (43,44), it is unclear whether glucocorticoid administration induces a local memory trace in the mPFC or whether manipulation of the mPFC modulates memory consolidation via interactions with other brain regions. As indicated above, findings of several electrophysiological and behavioral studies indicate that there are reciprocal connections between the mPFC and BLA (10,12,16) that regulate affect and memory (3,11,14).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Barsegyan

Mackenzie

Kurose

et al. 2010

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

234

169

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It is well established that acute administration of adrenocortical hormones enhances the consolidation of memories of emotional experiences and, concurrently, impairs working memory. These different glucocorticoid effects on these two memory functions have generally been considered to be independently regulated processes. Here we report that a glucocorticoid receptor agonist administered into the medial prefrontal cortex (mPFC) of male Sprague-Dawley rats both enhances memory consolidation and impairs working memory. Both memory effects are mediated by activation of a membrane-bound steroid receptor and depend on noradrenergic activity within the mPFC to increase levels of cAMPdependent protein kinase. These findings provide direct evidence that glucocorticoid effects on both memory consolidation and working memory share a common neural influence within the mPFC.

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A Role for Prefrontal Cortex in Memory Storage for Trace Fear Conditioning

Cited by 193 publications

References 48 publications

Foreground contextual fear memory consolidation requires two independent phases of hippocampal ERK/CREB activation

Foreground contextual fear memory consolidation requires two independent phases of hippocampal ERK/CREB activation

Deficits in Trace Fear Memory and Long-Term Potentiation in a Mouse Model for Fragile X Syndrome

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

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