scholarly journals Constellation of HCN Channels and cAMP Regulating Proteins in Dendritic Spines of the Primate Prefrontal Cortex: Potential Substrate for Working Memory Deficits in Schizophrenia

2012 ◽  
Vol 23 (7) ◽  
pp. 1643-1654 ◽  
Author(s):  
Constantinos D. Paspalas ◽  
Min Wang ◽  
Amy F.T. Arnsten
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Dendritic Spines ◽  
Memory Deficits ◽  
Hcn Channels ◽  
Potential Substrate

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?

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 Downregulation of HCN1 Channels in Hippocampus and Prefrontal Cortex in Methamphetamine Re-Exposed Mice With Enhanced Working Memory

2019 ◽  
pp. 107-117 ◽  
Author(s):  
Mei Zhou ◽  
Kuan Lin ◽  
Yuanren Si ◽  
Qin R ◽  
Lin Chen ◽  
...  
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Protein Expression ◽  
Memory Function ◽  
Morris Water Maze Test ◽  
Hcn Channels ◽  
Protein Expressions ◽  
Important Regulator ◽  
Hcn1 Channels

The hyperpolarization-activated cyclic-nucleotide-gated non-selective cation (HCN) channels play a potential role in the neurological basis underlying drug addiction. However, little is known about the role of HCN channels in methamphetamine (METH) abuse. In the present study, we examined the changes in working memory functions of METH re-exposed mice through Morris water maze test, and investigated the protein expression of HCN1 channels and potential mechanisms underlying the modulation of HCN channels by Western blotting analysis. Mice were injected with METH (1 mg/kg, i.p.) once per day for 6 consecutive days. After 5 days without METH, mice were re-exposed to METH at the same concentration. We found that METH re-exposure caused an enhancement of working memory, and a decrease in the HCN1 channels protein expression in both hippocampus and prefrontal cortex. The phosphorylated extracellular regulated protein kinase 1/2 (p-ERK1/2), an important regulator of HCN channels, was also obviously reduced in hippocampus and prefrontal cortex of mice with METH re-exposure. Meanwhile, acute METH exposure did not affect the working memory function and the protein expressions of HCN1 channels and p-ERK1/2. Overall, our data firstly showed the aberrant protein expression of HCN1 channels in METH re-exposed mice with enhanced working memory, which was probably related to the down-regulation of p-ERK1/2 protein expression.

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

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.

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