Kinin B1 receptor mediates memory impairment in the rat hippocampus

2016 ◽  
Vol 397 (4) ◽  
pp. 353-364 ◽  
Author(s):  
Káris Ester Dong-Creste ◽  
Ticiana Baraldi-Tornisielo ◽  
Ariadiny Lima Caetano ◽  
Fernand Gobeil ◽  
Wagner Ricardo Montor ◽  
...  
Keyword(s):  
Tissue Damage ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Inhibitory Avoidance ◽  
Long Term Memory ◽  
Guide Cannula ◽  
Physiological Concentration ◽  
B1 Receptor ◽  
Kinin B1 Receptor ◽  
Short And Long Term

Abstract The bradykinin (BK) receptors B1R and B2R are involved in inflammatory responses and their activation can enhance tissue damage. The B2R is constitutively expressed and mediates the physiologic effects of BK, whereas B1R expression is induced after tissue damage. Recently, they have been involved with Alzheimer’s disease, ischemic stroke and traumatic brain injury (TBI). In this study, we investigated the role of bradykinin in short and long-term memory consolidation (STM and LTM). It was observed that bilateral injection of BK (300 pmol/μl) disrupted the STM consolidation but not LTM, both evaluated by inhibitory avoidance test. The STM disruption due to BK injection was blocked by the previous injection of the B1R antagonist des-Arg10-HOE140 but not by the B2R antagonist HOE140. Additionally, the injection of the B1 agonist desArg9-BK disrupted STM and LTM consolidation at doses close to physiological concentration of the peptide (2.3 and 37.5 pmol, respectively) which could be reached during tissue injury. The presence of B1R located on glial cells around the implanted guide cannula used for peptide injection was confirmed by immunofluorescence. These data imply in a possible participation of B1R in the STM impairment observed in TBI, neuroinflammation and neurodegeneration.

scholarly journals DNGR-1 in dendritic cells limits tissue damage by dampening neutrophil recruitment

Science ◽  
2018 ◽  
Vol 362 (6412) ◽  
pp. 351-356 ◽  
Author(s):  
Carlos del Fresno ◽  
Paula Saz-Leal ◽  
Michel Enamorado ◽  
Stefanie K. Wculek ◽  
Sarai Martínez-Cano ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Tissue Damage ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Necrotizing Pancreatitis ◽  
Neutrophil Recruitment ◽  
Dead Cell ◽  
Cross Presentation ◽  
Conventional Type

Host injury triggers feedback mechanisms that limit tissue damage. Conventional type 1 dendritic cells (cDC1s) express dendritic cell natural killer lectin group receptor-1 (DNGR-1), encoded by the gene Clec9a, which senses tissue damage and favors cross-presentation of dead-cell material to CD8+ T cells. Here we find that DNGR-1 additionally reduces host-damaging inflammatory responses induced by sterile and infectious tissue injury in mice. DNGR-1 deficiency leads to exacerbated caerulein-induced necrotizing pancreatitis and increased pathology during systemic Candida albicans infection without affecting fungal burden. This effect is B and T cell–independent and attributable to increased neutrophilia in DNGR-1–deficient settings. Mechanistically, DNGR-1 engagement activates SHP-1 and inhibits MIP-2 (encoded by Cxcl2) production by cDC1s during Candida infection. This consequently restrains neutrophil recruitment and promotes disease tolerance. Thus, DNGR-1–mediated sensing of injury by cDC1s serves as a rheostat for the control of tissue damage, innate immunity, and immunopathology.

INVOLVEMENT OF cAMP/PKA SIGNALING PATHWAY IN SHORT-AND LONG-TERM MEMORY OF INHIBITORY AVOIDANCE

2002 ◽  
Author(s):  
MONICA R. M. VIANNA ◽  
PATRICIA ARDENGHI ◽  
PATRICIA PEREIRA ◽  
LUCIANA A. IZQUIERDO ◽  
DANIELA M. BARROS ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inhibitory Avoidance ◽  
Long Term Memory ◽  
Term Memory ◽  
Short And Long Term

scholarly journals Resolution of Inflammation in Acute Graft-Versus-Host-Disease: Advances and Perspectives

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 75
Author(s):  
Layara Roberta Ferreira Duarte ◽  
Vanessa Pinho ◽  
Barbara Maximino Rezende ◽  
Mauro Martins Teixeira
Keyword(s):  
Graft Versus Host Disease ◽  
Tissue Damage ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Inflammatory Diseases ◽  
Resolution Of Inflammation ◽  
Hematopoietic Stem ◽  
Host Disease ◽  
Graft Versus Host ◽  
Potential Use

Inflammation is an essential reaction of the immune system to infections and sterile tissue injury. However, uncontrolled or unresolved inflammation can cause tissue damage and contribute to the pathogenesis of various inflammatory diseases. Resolution of inflammation is driven by endogenous molecules, known as pro-resolving mediators, that contribute to dampening inflammatory responses, promoting the resolution of inflammation and the recovery of tissue homeostasis. These mediators have been shown to be useful to decrease inflammatory responses and tissue damage in various models of inflammatory diseases. Graft-versus-host disease (GVHD) is a major unwanted reaction following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and is characterized by an exacerbated inflammatory response provoked by antigen disparities between transplant recipient and donor. There is no fully effective treatment or prophylaxis for GVHD. This review explores the effects of several pro-resolving mediators and discusses their potential use as novel therapies in the context of GVHD.

Short- and long-term memory tasks predict working memory performance, and vice versa.

2019 ◽  
Vol 73 (2) ◽  
pp. 79-93 ◽  
Author(s):  
Ian Neath ◽  
Jean Saint-Aubin ◽  
Tamra J. Bireta ◽  
Andrew J. Gabel ◽  
Chelsea G. Hudson ◽  
...  
Keyword(s):  
Working Memory ◽  
Memory Performance ◽  
Long Term Memory ◽  
Term Memory ◽  
Short And Long Term

The Improvement of Short- and Long-term Memory of Young Children by BF-7

2010 ◽  
Vol 39 (3) ◽  
pp. 376-382 ◽  
Author(s):  
Do-Hee Kim ◽  
Ok-Hyeon Kim ◽  
Joo-Hong Yeo ◽  
Kwang-Gill Lee ◽  
Geum-Duck Park ◽  
...  
Keyword(s):  
Young Children ◽  
Long Term Memory ◽  
Term Memory ◽  
Short And Long Term
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