Sevoflurane anesthesia induces neither contextual fear memory impairment nor alterations in local population connectivity of medial prefrontal cortex local field potentials networks in aged rats

2016 ◽  
Vol 30 (4) ◽  
pp. 338-346 ◽  
Author(s):  
Xinyu Xu ◽  
Qian Zhang ◽  
Xin Tian ◽  
Guolin Wang
Keyword(s):  
Prefrontal Cortex ◽  
Memory Impairment ◽  
Local Population ◽  
Fear Memory ◽  
Population Connectivity ◽  
Aged Rats ◽  
Sevoflurane Anesthesia ◽  
Field Potentials ◽  
Contextual Fear ◽  
Contextual Fear Memory

Hippocampus and Prefrontal Cortex Modulation of Contextual Fear Memory Is Dissociated by Inhibiting De Novo Transcription During Late Consolidation

2019 ◽  
Vol 56 (8) ◽  
pp. 5507-5519 ◽  
Author(s):  
Luciana M. Pereira ◽  
Caio M. de Castro ◽  
Lorena T. L. Guerra ◽  
Thaís M. Queiroz ◽  
João T. Marques ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
De Novo ◽  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory

scholarly journals Parvalbumin-positive interneurons mediate neocortical-hippocampal interactions that are necessary for memory consolidation

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Frances Xia ◽  
Blake A Richards ◽  
Matthew M Tran ◽  
Sheena A Josselyn ◽  
Kaori Takehara-Nishiuchi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Fear Conditioning ◽  
Medial Prefrontal Cortex ◽  
Memory Consolidation ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Spiking Activity

Following learning, increased coupling between spindle oscillations in the medial prefrontal cortex (mPFC) and ripple oscillations in the hippocampus is thought to underlie memory consolidation. However, whether learning-induced increases in ripple-spindle coupling are necessary for successful memory consolidation has not been tested directly. In order to decouple ripple-spindle oscillations, here we chemogenetically inhibited parvalbumin-positive (PV+) interneurons, since their activity is important for regulating the timing of spiking activity during oscillations. We found that contextual fear conditioning increased ripple-spindle coupling in mice. However, inhibition of PV+ cells in either CA1 or mPFC eliminated this learning-induced increase in ripple-spindle coupling without affecting ripple or spindle incidence. Consistent with the hypothesized importance of ripple-spindle coupling in memory consolidation, post-training inhibition of PV+ cells disrupted contextual fear memory consolidation. These results indicate that successful memory consolidation requires coherent hippocampal-neocortical communication mediated by PV+ cells.

scholarly journals Peroxiredoxin 6 Knockout Mice Demonstrate Anxiety Behavior and Attenuated Contextual Fear Memory after Receiving Acute Immobilization Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1416
Author(s):  
Sarayut Phasuk ◽  
Peeraporn Varinthra ◽  
Andaman Nitjapol ◽  
Korakod Bandasak ◽  
Ingrid Y. Liu
Keyword(s):  
Prefrontal Cortex ◽  
Knockout Mice ◽  
Immobilization Stress ◽  
Memory Performance ◽  
Fear Memory ◽  
Peroxiredoxin 6 ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Anxiety Response ◽  
Anxiety Behavior

Stress can elicit glucocorticoid release to promote coping mechanisms and influence learning and memory performance. Individual memory performance varies in response to stress, and the underlying mechanism is not clear yet. Peroxiredoxin 6 (PRDX6) is a multifunctional enzyme participating in both physiological and pathological conditions. Several studies have demonstrated the correlation between PRDX6 expression level and stress-related disorders. Our recent finding indicates that lack of the Prdx6 gene leads to enhanced fear memory. However, it is unknown whether PRDX6 is involved in changes in anxiety response and memory performance upon stress. The present study reveals that hippocampal PRDX6 level is downregulated 30 min after acute immobilization stress (AIS) and trace fear conditioning (TFC). In human retinal pigment epithelium (ARPE-19) cells, the PRDX6 expression level decreases after being treated with stress hormone corticosterone. Lack of PRDX6 caused elevated basal H2O2 levels in the hippocampus, basolateral amygdala, and medial prefrontal cortex, brain regions involved in anxiety response and fear memory formation. Additionally, this H2O2 level was still high in the medial prefrontal cortex of the knockout mice under AIS. Anxiety behavior of Prdx6−/− mice was enhanced after immobilization for 30 min. After exposure to AIS before a contextual test, Prdx6−/− mice displayed a contextual fear memory deficit. Our results showed that the memory performance of Prdx6−/− mice was impaired when responding to AIS, accompanied by dysregulated H2O2 levels. The present study helps better understand the function of PRDX6 in memory performance after acute stress.

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