scholarly journals Cannabinoid Modulation of Memory Consolidation in Rats: Beyond the Role of Cannabinoid Receptor Subtype 1

2017 ◽  
Vol 08 ◽  
Author(s):  
Patrizia Ratano ◽  
Maura Palmery ◽  
Viviana Trezza ◽  
Patrizia Campolongo
Keyword(s):  
Memory Consolidation ◽  
Cannabinoid Receptor ◽  
Receptor Subtype

scholarly journals The Central Role of Glia in Pathological Pain and the Potential of Targeting the Cannabinoid 2 Receptor for Pain Relief

2011 ◽  
Vol 2011 ◽  
pp. 1-19 ◽  
Author(s):  
Jenny L. Wilkerson ◽  
Erin D. Milligan
Keyword(s):  
Pain Relief ◽  
Cannabinoid Receptor ◽  
Receptor Subtype ◽  
Pain Processing ◽  
Neuronal Mechanisms ◽  
Cannabinoid Compounds ◽  
The Central Nervous System ◽  
Pathological Pain ◽  
Novel Therapeutic

Under normal conditions, acute pain processing consists of well-characterized neuronal signaling events. When dysfunctional pain signaling occurs, pathological pain ensues. Glial activation and their released factors participate in the mediation of pathological pain. The use of cannabinoid compounds for pain relief is currently an area of great interest for both basic scientists and physicians. These compounds, bind mainly either the cannabinoid receptor subtype 1 (CB1R) or cannabinoid receptor subtype 2 (CB2R) and are able to modulate pain. Although cannabinoids were initially only thought to modulate pain via neuronal mechanisms within the central nervous system, strong evidence now supports that CB2R cannabinoid compounds are capable of modulating glia, (e.g. astrocytes and microglia) for pain relief. However, the mechanisms underlying cannabinoid receptor-mediated pain relief remain largely unknown. An emerging body of evidence supports that CB2R agonist compounds may prove to be powerful novel therapeutic candidates for the treatment of chronic pain.

Assessment for the Role of Serotonin Receptor Subtype 3 for the Analgesic Action of Morphine at the Spinal Level

2005 ◽  
Vol 18 (2) ◽  
pp. 113
Author(s):  
Myung Ha Yoon ◽  
Hong Buem Bae ◽  
Jeong Il Choi ◽  
Seok Jae Kim ◽  
Chang Mo Kim ◽  
...  
Keyword(s):  
Serotonin Receptor ◽  
Receptor Subtype ◽  
Analgesic Action ◽  
Spinal Level ◽  
Subtype 3

The Emerging Role of the Cannabinoid Receptor Family in Peripheral and Neuro-immune Interactions

2016 ◽  
Vol 17 (16) ◽  
pp. 1834-1840 ◽  
Author(s):  
Orla Haugh ◽  
June Penman ◽  
Andrew Irving ◽  
Veronica Campbell
Keyword(s):  
Cannabinoid Receptor ◽  
Receptor Family

scholarly journals 0234 Role of Midday Naps on Episodic Memory Consolidation in Preschool Children

SLEEP ◽  
2019 ◽  
Vol 42 (Supplement_1) ◽  
pp. A97-A97
Author(s):  
Sanna Lokhandwala ◽  
Jamie Allfisher ◽  
Rebecca M C Spencer
Keyword(s):  
Preschool Children ◽  
Episodic Memory ◽  
Memory Consolidation

scholarly journals Role of Cannabinoid Receptor CB2 in HER2 Pro-oncogenic Signaling in Breast Cancer

2015 ◽  
Vol 107 (6) ◽  
Author(s):  
Eduardo Pérez-Gómez ◽  
Clara Andradas ◽  
Sandra Blasco-Benito ◽  
María M. Caffarel ◽  
Elena García-Taboada ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cannabinoid Receptor ◽  
Oncogenic Signaling

scholarly journals Diazepam-induced changes in sleep: Role of the  1 GABAA receptor subtype

2001 ◽  
Vol 98 (11) ◽  
pp. 6464-6469 ◽  
Author(s):  
I. Tobler ◽  
C. Kopp ◽  
T. Deboer ◽  
U. Rudolph
Keyword(s):  
Gabaa Receptor ◽  
Receptor Subtype ◽  
Induced Changes

Role of the Basolateral Amygdala in Memory Consolidation

2006 ◽  
Vol 985 (1) ◽  
pp. 273-293 ◽  
Author(s):  
CHRISTA K. McINTYRE ◽  
ANN E. POWER ◽  
BENNO ROOZENDAAL ◽  
JAMES L. McGAUGH
Keyword(s):  
Memory Consolidation ◽  
Basolateral Amygdala

scholarly journals Prostacyclin-IP signaling and prostaglandin E2-EP2/EP4 signaling both mediate joint inflammation in mouse collagen-induced arthritis

2006 ◽  
Vol 203 (2) ◽  
pp. 325-335 ◽  
Author(s):  
Tetsuya Honda ◽  
Eri Segi-Nishida ◽  
Yoshiki Miyachi ◽  
Shuh Narumiya
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Joint Inflammation ◽  
Synovial Fibroblasts ◽  
The Other ◽  
Receptor Subtype ◽  
Significant Suppression ◽  
Wild Type ◽  
Collagen Induced Arthritis

Prostaglandin (PG)I2 (prostacyclin [PGI]) and PGE2 are abundantly present in the synovial fluid of rheumatoid arthritis (RA) patients. Although the role of PGE2 in RA has been well studied, how much PGI2 contributes to RA is little known. To examine this issue, we backcrossed mice lacking the PGI receptor (IP) to the DBA/1J strain and subjected them to collagen-induced arthritis (CIA). IP-deficient (IP−/−) mice exhibited significant reduction in arthritic scores compared with wild-type (WT) mice, despite anti-collagen antibody production and complement activation similar to WT mice. IP−/− mice also showed significant reduction in contents of proinflammatory cytokines, such as interleukin (IL)-6 in arthritic paws. Consistently, the addition of an IP agonist to cultured synovial fibroblasts significantly enhanced IL-6 production and induced expression of other arthritis-related genes. On the other hand, loss or inhibition of each PGE receptor subtype alone did not affect elicitation of inflammation in CIA. However, a partial but significant suppression of CIA was achieved by the combined inhibition of EP2 and EP4. Our results show significant roles of both PGI2-IP and PGE2-EP2/EP4 signaling in the development of CIA, and suggest that inhibition of PGE2 synthesis alone may not be sufficient for suppression of RA symptoms.

The endogenous cannabinoid receptor ligand, anandamide, inhibits the motor behavior: role of nigrostriatal dopaminergic neurons

Life Sciences ◽  
1995 ◽  
Vol 56 (23-24) ◽  
pp. 2033-2040 ◽  
Author(s):  
J. Romero ◽  
L. Garcia ◽  
M. Cebeira ◽  
D. Zadrozny ◽  
J.J. Fernández-Ruiz ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Cannabinoid Receptor ◽  
Motor Behavior ◽  
Receptor Ligand ◽  
Endogenous Cannabinoid

Abstract 110: Adiponectin Inhibits TNF-a-Induced Vascular Inflammatory Response via Caveolin-Mediated Ceramidase Recruitment and Activation

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Yajing Wang ◽  
Wayne Lau ◽  
Erhe Gao ◽  
Walter Koch ◽  
Xin Ma
Keyword(s):  
Inflammatory Response ◽  
Protective Action ◽  
Receptor Subtype ◽  
Protective Actions ◽  
Nitrative Stress ◽  
S1p Receptor ◽  
Anti Inflammatory ◽  
Or Gene ◽  
First Time

Anti-inflammatory and vascular protective actions of adiponectin (APN) are well-recognized. However, many fundamental questions remain unanswered. The current study attempted to identify the APN receptor subtype responsible for APN’s vascular protective action, and investigate the role of ceramidase activation in APN anti-inflammatory signaling. Wild type (WT) or gene manipulated HUVEC were treated with TNFα in the presence and absence of APN. The effect of APN on TNFα-induced inflammatory and oxidative/nitrative stress was determined. In WT HUVEC, APN significantly reduced TNFα-induced ICAM-1 expression and attenuated TNFα-induced superoxide and peroxynitrite formation (P<0.01). These anti-inflammatory actions were virtually abolished by AdipoR1-, but not AdipoR2-, knockdown (KD). Treatment with APN significantly increased neutral ceramidase (nCDase) activity (3.7-fold, P<0.01). AdipoR1-KD markedly (P0.05), reduced APN-induced nCDase activation. More importantly, siRNA mediated nCDase-KD markedly blocked the effect of APN upon TNFα-induced ICAM-1 expression (P0.05), and modestly inhibited APN anti-inflammatory effect (P87% of APN-induced nCDase activation was lost. Whereas APN treatment failed to inhibit TNFα-induced ICAM-1 expression, treatment with S1P or SEW (S1P receptor agonist) remained effective in Cav1-KD cells in reducing TNFα-induced ICAM-1 expression (P<0.01). AdipoR1 and Cav1 co-localized and co-precipitated in HUVECs. APN treatment did not affect this interaction. Moreover, re-expression of WT Cav1 in Cav1-KD cells restored nCDase activation in response to APN (P<0.01 vs. vehicle), whereas re-expression of a mutated Cav1 blocking AdipoR1/Cav1 interaction failed to restore APN-mediated nCDase activation. Finally, there is weak basal Cav1/nCDase interaction, which significantly increased following APN treatment. These results demonstrate for the first time that APN inhibits TNFα-induced inflammatory response via Cav1-mediated ceramidase recruitment and activation in an AdipoR1- dependent fashion.

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