scholarly journals Activation of the basolateral amygdala induces long-term enhancement of specific memory representations in the cerebral cortex

2013 ◽  
Vol 101 ◽  
pp. 8-18 ◽  
Author(s):  
Candice M. Chavez ◽  
James L. McGaugh ◽  
Norman M. Weinberger
2012 ◽  
Vol 24 (5) ◽  
pp. 1173-1190 ◽  
Author(s):  
Kerstin Jost ◽  
Patrick H. Khader ◽  
Peter Düsel ◽  
Franziska R. Richter ◽  
Kristina B. Rohde ◽  
...  

Remembering is more than an activation of a memory trace. As retrieval cues are often not uniquely related to one specific memory, cognitive control should come into play to guide selective memory retrieval by focusing on relevant while ignoring irrelevant information. Here, we investigated, by means of EEG and fMRI, how the memory system deals with retrieval interference arising when retrieval cues are associated with two material types (faces and spatial positions), but only one is task-relevant. The topography of slow EEG potentials and the fMRI BOLD signal in posterior storage areas indicated that in such situations not only the relevant but also the irrelevant material becomes activated. This results in retrieval interference that triggers control processes mediated by the medial and lateral PFC, which are presumably involved in biasing target representations by boosting the task-relevant material. Moreover, memory-based conflict was found to be dissociable from response conflict that arises when the relevant and irrelevant materials imply different responses. The two types of conflict show different activations in the medial frontal cortex, supporting the claim of domain-specific prefrontal control systems.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.


Author(s):  
Vanessa Kogel ◽  
Stefanie Trinh ◽  
Natalie Gasterich ◽  
Cordian Beyer ◽  
Jochen Seitz

AbstractAstrocytes are the most abundant cell type in the brain and crucial to ensure the metabolic supply of neurons and their synapse formation. Overnutrition as present in patients suffering from obesity causes astrogliosis in the hypothalamus. Other diseases accompanied by malnutrition appear to have an impact on the brain and astrocyte function. In the eating disorder anorexia nervosa (AN), patients suffer from undernutrition and develop volume reductions of the cerebral cortex, associated with reduced astrocyte proliferation and cell count. Although an effect on astrocytes and their function has already been shown for overnutrition, their role in long-term undernutrition remains unclear. The present study used primary rat cerebral cortex astrocytes to investigate their response to chronic glucose starvation. Cells were grown with a medium containing a reduced glucose concentration (2 mM) for 15 days. Long-term glucose starvation increased the expression of a subset of pro-inflammatory genes and shifted the primary astrocyte population to the pro-inflammatory A1-like phenotype. Moreover, genes encoding for proteins involved in the unfolded protein response were elevated. Our findings demonstrate that astrocytes under chronic glucose starvation respond with an inflammatory reaction. With respect to the multiple functions of astrocytes, an association between elevated inflammatory responses due to chronic starvation and alterations found in the brain of patients suffering from undernutrition seems possible.


2008 ◽  
Vol 1 (3) ◽  
pp. 320-321
Author(s):  
R.L.J. Meesen ◽  
K. Cuypers ◽  
S.P. Swinnen ◽  
O. Levin

1992 ◽  
Vol 16 (3-4) ◽  
pp. 345-352 ◽  
Author(s):  
Peter S. Eriksson ◽  
Björn Carlsson ◽  
Olle G.P. Isaksson ◽  
Elisabeth Hansson ◽  
Lars Rönnbäck

2000 ◽  
Vol 191 (7) ◽  
pp. 1149-1166 ◽  
Author(s):  
Louise J. McHeyzer-Williams ◽  
Melinda Cool ◽  
Michael G. McHeyzer-Williams

The mechanisms that regulate B cell memory and the rapid recall response to antigen remain poorly defined. This study focuses on the rapid expression of B cell memory upon antigen recall in vivo, and the replenishment of quiescent B cell memory that follows. Based on expression of CD138 and B220, we reveal a unique and major subtype of antigen-specific memory B cells (B220−CD138−) that are distinct from antibody-secreting B cells (B220+/−CD138+) and B220+CD138− memory B cells. These nonsecreting somatically mutated B220− memory responders rapidly dominate the splenic response and comprise >95% of antigen-specific memory B cells that migrate to the bone marrow. By day 42 after recall, the predominant quiescent memory B cell population in the spleen (75–85%) and the bone marrow (>95%) expresses the B220− phenotype. Upon adoptive transfer, B220− memory B cells proliferate to a lesser degree but produce greater amounts of antibody than their B220+ counterparts. The pattern of cellular differentiation after transfer indicates that B220− memory B cells act as stable self-replenishing intermediates that arise from B220+ memory B cells and produce antibody-secreting cells on rechallenge with antigen. Cell surface phenotype and Ig isotype expression divide the B220− compartment into two main subsets with distinct patterns of integrin and coreceptor expression. Thus, we identify new cellular components of B cell memory and propose a model for long-term protective immunity that is regulated by a complex balance of committed memory B cells with subspecialized immune function.


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