scholarly journals Sustained corticosterone rise in the prefrontal cortex is a key factor for chronic stress-induced working memory deficits in mice

2019 ◽  
Vol 10 ◽  
pp. 100161 ◽  
Author(s):  
Gaelle Dominguez ◽  
Nadia Henkous ◽  
Thomas Prevot ◽  
Vincent David ◽  
Jean-Louis Guillou ◽  
...  
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Memory Deficits ◽  
Key Factor

General discussion

1996 ◽  
Vol 351 (1346) ◽  
pp. 1481-1482 ◽  
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Frontal Lobe ◽  
Experimental Psychology ◽  
Experimental Studies ◽  
Memory Deficits ◽  
Cortical Lesions ◽  
Short Term ◽  
Memory Processes ◽  
University Of Oxford

L. Weiskrantz ( Department of Experimental Psychology, University of Oxford, South Parks Road, Oxford OX1 3UD, U. K.). I have tried to link what we have heard from experimental studies in humans with what we have heard from experimental studies in monkeys concerning functions of the prefrontal cortex. The obvious difference is that in my experience, patients with posterior cortical lesions are often those with shortterm memory deficits (such as patient KF), whereas you have to work very hard with frontal lobe lesioned patients to see profound impairments of that kind. This provides an obvious contrast with experimental studies in monkeys which suggest a role for the prefrontal cortex in just such simple short-term or working memory processes. I was wondering if any of the speakers would care to comment on this rather obvious distinction between human and monkey work that has been presented so far?

Cotinine reduces depressive-like behavior, working memory deficits, and synaptic loss associated with chronic stress in mice

2014 ◽  
Vol 268 ◽  
pp. 55-65 ◽  
Author(s):  
J. Alex Grizzell ◽  
Alexandre Iarkov ◽  
Rosalee Holmes ◽  
Takahashi Mori ◽  
Valentina Echeverria
Keyword(s):  
Working Memory ◽  
Chronic Stress ◽  
Memory Deficits ◽  
Synaptic Loss

scholarly journals Ketamine disrupts naturalistic coding of working memory in primate lateral prefrontal cortex networks

2021 ◽  
Author(s):  
Megan Roussy ◽  
Rogelio Luna ◽  
Lyndon Duong ◽  
Benjamin Corrigan ◽  
Roberto A. Gulli ◽  
...  
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Spatial Working Memory ◽  
Memory Task ◽  
Memory Deficits ◽  
Lateral Prefrontal Cortex ◽  
Neuronal Populations ◽  
Neuronal Types ◽  
Fast Spiking ◽  
Selective Working

AbstractKetamine is a dissociative anesthetic drug, which has more recently emerged as a rapid-acting antidepressant. When acutely administered at subanesthetic doses, ketamine causes cognitive deficits like those observed in patients with schizophrenia, including impaired working memory. Although these effects have been linked to ketamine’s action as an N-methyl-D-aspartate receptor antagonist, it is unclear how synaptic alterations translate into changes in brain microcircuit function that ultimately influence cognition. Here, we administered ketamine to rhesus monkeys during a spatial working memory task set in a naturalistic virtual environment. Ketamine induced transient working memory deficits while sparing perceptual and motor skills. Working memory deficits were accompanied by decreased responses of fast spiking inhibitory interneurons and increased responses of broad spiking excitatory neurons in the lateral prefrontal cortex. This translated into a decrease in neuronal tuning and information encoded by neuronal populations about remembered locations. Our results demonstrate that ketamine differentially affects neuronal types in the neocortex; thus, it perturbs the excitation inhibition balance within prefrontal microcircuits and ultimately leads to selective working memory deficits.

scholarly journals The dynamics of disordered dialogue: Prefrontal, hippocampal and thalamic miscommunication underlying working memory deficits in schizophrenia

2018 ◽  
Vol 2 ◽  
pp. 239821281877182 ◽  
Author(s):  
David A Kupferschmidt ◽  
Joshua A Gordon
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Cognitive Function ◽  
Spatial Working Memory ◽  
Memory Deficits ◽  
Brain Regions ◽  
Brain Network ◽  
Rodent Models ◽  
Neural Interaction ◽  
Preclinical Work

The prefrontal cortex is central to the orchestrated brain network communication that gives rise to working memory and other cognitive functions. Accordingly, working memory deficits in schizophrenia are increasingly thought to derive from prefrontal cortex dysfunction coupled with broader network disconnectivity. How the prefrontal cortex dynamically communicates with its distal network partners to support working memory and how this communication is disrupted in individuals with schizophrenia remain unclear. Here we review recent evidence that prefrontal cortex communication with the hippocampus and thalamus is essential for normal spatial working memory, and that miscommunication between these structures underlies spatial working memory deficits in schizophrenia. We focus on studies using normal rodents and rodent models designed to probe schizophrenia-related pathology to assess the dynamics of neural interaction between these brain regions. We also highlight recent preclinical work parsing roles for long-range prefrontal cortex connections with the hippocampus and thalamus in normal and disordered spatial working memory. Finally, we discuss how emerging rodent endophenotypes of hippocampal- and thalamo-prefrontal cortex dynamics in spatial working memory could translate into richer understanding of the neural bases of cognitive function and dysfunction in humans.

scholarly journals Chronic stress impairs prefrontal cortex-dependent response inhibition and spatial working memory.

2012 ◽  
Vol 126 (5) ◽  
pp. 605-619 ◽  
Author(s):  
Agnieszka Mika ◽  
Gabriel J. Mazur ◽  
Ann N. Hoffman ◽  
Joshua S. Talboom ◽  
Heather A. Bimonte-Nelson ◽  
...  
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Response Inhibition ◽  
Spatial Working Memory
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