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Written by ︱Shen Shiyu Editor ︱Wang Sizhen Edition ︱Zha Jiaxue Depression is one of the most common mental diseases in the world today, but its etiology is still unclear, so the current treatment methods also have many defects[1,
Recently, the relationship between neurogenesis impairment and neuroinflammation and depression has received increasing attenti.
The endocannabinoid (eCB) system plays a key role in both the maintenance of emotional homeostasis and the pathophysiology of depression [3,
As a new member of the eCB system, G protein coupled receptor 55 (GPR55) is expressed in multiple important brain regions related to emotion (hippocampus, striatum, amygdala and corte.
And it is mainly expressed on microglia, which plays an important role in maintaining a variety of normal brain functions [5-
In addition, it has been reported that GPR55 regulates anxiety-like behaviors and ameliorates impaired hippocampal neurogenesis [9, 1
However, the exact role of GPR55 in depressive behavior is uncle.
Recently, Yu Jin's research group from the School of Basic Medicine of Fudan University published a research paper entitled "The neuroprotective effects of GPR55 against hippocampal neuroinflammation and impaired adult neurogenesis in CSDS mice" in Neurobiology of Disea.
This study revealed the anti-neuroinflammatory and neurogenesis-protective roles of GPR55 in anxiety-depression-like behaviors mediated by an animal model of anxiety and depression (CSDS mode.
Associate Professor Yu Jin and Professor Zhang Yuqiu are the co-corresponding authors, and Shen Shiyu, Yu Rui and Li Wei are the co-first autho.
Chronic social defeat stress (CSDS) Chronic social defeat stress is an animal model of anxiety and depression [1
In recent years, it has been widely us.
The authors first induced the anxiety-depression-like phenotype of C57 mice using CSDS, and detected the protein and mRNA expression levels of horse GPR55 in socially frustrated mice (including insensitive mice and susceptible mic.
A significant decrease in hippocampal GPR55 protein expression was observed in susceptible mice, but Gpr55 mRNA levels were not significantly different between control and socially frustrated mice (F.
This suggests that GPR55 protein expression is affected by CSDS and is associated with social avoidance behavior, but mRNA expression is n.
In addition, the authors used RNA scope in situ hybridization to determine that Gpr55 is only expressed on microglia, but not on neurons, astrocytes, and neural stem cel.
Figure 1 Chronic social defeat stress (CSDS) induces depression and anxiety-like behaviors and reduces GPR55 protein levels in the hippocampus, but not mRNA leve.
(Image source: Shen SY et .
, Neurobiol D.
2022) Based on these results, the authors further investigated whether pretreatment with the GPR55 agonist O-1602 could hinder the emergence of CSDS-induced anxiety-depression phenotyp.
To this end, the researchers injected O-1602 30 minutes before daily social frustration in mice and found that it could significantly improve depression- and anxiety-like behaviors induced by CSDS (Figure Since depression is often accompanied by upregulation of neuroinflammation and impaired neurogenesis, the authors further investigated the effects of O-1602 on hippocampal neuroinflammation and neurogenes.
Figure 3 O-1602 can improve CSDS-induced anxiety-depression-like behavi.
(Source: Shen SY et .
, Neurobiol D.
2022) The experimental results showed that O-1602 pretreatment significantly inhibited the up-regulation of NLRP3 inflammasome expression in the hippocampal brain region of CSDS mice, and inhibited the CSDS group at the transcriptional level The up-regulated pro-inflammatory factors in CSDS indicated that activation of GPR55 could inhibit the neuroinflammatory response induced by CS.
To investigate the role of GPR55 in neurogenesis, the authors used Nestin (nestin) and DCX (doublecortin, doublecortin) to assess neurogenesis in the hippocampal brain regi.
The results showed that O-1602 could partially reverse the CSDS-induced decrease in the mean fluorescence intensity of Nestin+ and DCX+ cel.
From this, the authors speculated that activation of GPR55 could inhibit neuroinflammation and protect hippocampal neurogenes.
Due to the limited efficacy and severe side effects of many antidepressants, some patients in China tend to seek the help of traditional Chinese medicine to treat depressi.
Acupuncture is one of the main TCM treatments, and many studies have also shown that electroacupuncture (EA) can improve anxiety and depression-like behaviors [12, 1
Therefore, the authors further investigated the effect of EA on anxiety-depression-like behavior and hippocampal GPR5Specifically, 10 days after CSDS modeling, the socially frustrated mice were treated with EA for 3 wee.
This treatment significantly improved anxiety-depression-like behavior in CSDS mice, restored GPR55 expression in the hippocampus, and improved CSDS-induced neuroinflammation and impaired neurogenesis (F.
Figure 4 EA treatment upregulates GPR55 expression and ameliorates neuroinflammation and neurogenesis disorders in the hippocamp.
(Source: Shen SY et .
, Neurobiol D.
2022) Since the effect of EA treatment is similar to that of GPR55 agonis.
Therefore, the authors speculate that GPR55 may be involved in the antidepressant and anxiolytic effects of .
To investigate the role of GPR55 in the effect of EA treatment, the authors used the GPR55 antagonist CID16020046 during EA treatment and found that GPR55 antagonist reversed most of the antidepressant and anxiolytic effects of .
Taken together, these findings demonstrate that GPR55 plays an important role in EA-induced antidepressant and anxiolytic effec.
Figure 5 Schematic diagram of the mechanism: changes in microglial GPR55 expression with CSDS and subsequent pathological changes, such as CSDS-induced hippocampal neuroinflammation and neurogenesis disorde.
(Source: Shen SY et .
, Neurobiol D.
2022) Conclusion and discussion, inspiration and prospect This study shows that the decreased expression of hippocampal G protein-coupled receptor 55 (GPR55) is associated with chronic social frustration stress (CSDS) Activation of GPR55 reversed the detrimental effects of CSDS in relation to the social avoidance deficits induc.
Meanwhile, electroacupuncture exhibited antidepressant and anxiolytic properties through a GPR55-dependent mechanism and neuroprotective effec.
suggesting that GPR55 plays an important role in depression and anxiety (Figure Notably, in the present study, GPR55 expression was only downregulated in susceptible mice, which exhibited marked social avoidance behavior, whereas a GPR55 agonist (O-1602) was able to significantly block social avoidance behavior as well as other CSDS-induced behaviors depression and anxiety-like behavi.
This raises the question of whether alterations in GPR55 expression are associated with the development of depression and anxiety-like behaviors, and whether GPR55 activation may serve as a potential therapeutic target in patients with depression, which requires further investigati.
Link to the original text: https://d.
org/11016.
n.
202105743 Associate Professor Yu Jin and Professor Zhang Yuqiu are the co-corresponding authors, and Shen Shiyu, Yu Rui and Li Wei are the co-first autho.
Talent recruitment[1] "Logical Neuroscience" is looking for an associate editor/editor/operation position (online office) Selected previous articles[1] Science︱Reversible CD8 T cell-neuron interaction: an important mechanism of aging inhibiting nerve regeneration 【2】NeuroImage︱Luo Yuejia’s research group reveals the prefrontal control system that social information regulates risk decision 【3】Nat Neurosci | New oligodendrocytes have stronger remyelination ability after demyelination 【4】Biol Psychiatry︱Gao Tianming’s team reveals The regulatory effect of astrocytes on adult hippocampal neurogenesis and memory through the acetylcholine receptor M1 [5] Curr Biol, Chen Nannan et .
revealed that the translation of synaptic regions causes asymmetric distribution of CaMKII protein and its role in memory formation [6] ]Review of Front Aging Neurosci︱Fan Dongsheng’s team focused on the interaction between peripheral and central immune systems in amyotrophic lateral sclerosis [7]NPP︱Lu Wei’s team revealed a new mechanism of GABAA receptor auxiliary subunit phosphorylation to regulate neural behavior [8 ] Cereb Cortex︱ pattern rigidity, the role of temporal dynamics of ventromedial prefrontal cortex on rumination and depression [9] Front Aging Neurosci︱PTAFR as a novel biomarker for Alzheimer's disease diagnosis and treatment [10] PNAS ︱Feng Guoping's laboratory reveals the important role of the front-end thalamic loop in working memory Recommended for high-quality scientific research training courses [1] Practical training course for academic paper writing (Live: 20221~22) [2] Single-cell sequencing and spatial transcriptome Symposium on Scientific Data Analysis (Tencent Online Conference on June 11-12) [3] Symposium on Patch Clamp and Optogenetics and Calcium Imaging Technologies May 21-22 Tencent Conference References (swipe up and down to read) Kessler, RC and EJ Bromet, The epidemiology of depression across cultur.
Annu Rev Public Health, 201 34:.
119-3 Richards,.
, Prevalence and clinical course of depression: a revi.
Clin Psychol Rev, 201 31( 7):.
1117-2 Lutz,.
, et .
, The endocannabinoid system in guarding against fear, anxiety and stre.
Nat Rev Neurosci, 201 16(12):.
705-1 Micale,.
, et .
, Endocannabinoid system and mood disorders: priming a target for new therapi.
Pharmacol Ther, 201 138(1):.
18-3Ryberg,.
, et .
, The orphan receptor GPR55 is a novel cannabinoid recept.
British Journal of Pharmacology, 200 152(7):.
1092-110 Liu,.
, et .
, GPR55: from orphan to metabolic regulator? Pharmacol Ther, 201 145:.
35-4 Marichal-Cancino , BA, et .
, Advances in the Physiology of GPR55 in the Central Nervous Syst.
Current Neuropharmacology, 201 15(5):.
771-77 Xiang,.
, et .
, Activation of GPR55 attenuates cognitive impairment , oxidative stress, neuroinflammation, and synaptic dysfunction in a streptozotocin-induced Alzheimer's mouse mod.
Pharmacol Biochem Behav, 202 214:.
17334 Hill, JD, et .
, Activation of GPR55 induces neuroprotection of hippocampal neurogenesis and immune responses of neural stem cells following chronic, systemic inflammati.
Brain Behav Immun, 201
76:.
165-181Shi, QX, et .
, The novel cannabinoid receptor GPR55 mediates anxiolytic-like effects in the medial orbital cortex of mice with acute stre.
Molecular Brain, 201 11Golden, SA, et .
.
, A standardized protocol for repeated social defeat stress in mice (vol 6, pg 1183, 201
Nature Protocols, 201 10(4):.
643-641Yue,.
, et .
, Electro- Acupuncture Alleviates Chronic Unpredictable Stress-Induced Depressive- and Anxiety-Like Behavior and Hippocampal Neuroinflammation in Rat Model of Depressi.
Front Mol Neurosci, 201 11:.
141 Liu,.
, et .
,Electroacupuncture attenuates the decrease of hippocampal progenitor cell proliferation in the adult rats exposed to chronic unpredictable stre.
Life Sci, 200 81(21-22):.
1489-9 End of this paper
Recently, the relationship between neurogenesis impairment and neuroinflammation and depression has received increasing attenti.
The endocannabinoid (eCB) system plays a key role in both the maintenance of emotional homeostasis and the pathophysiology of depression [3,
As a new member of the eCB system, G protein coupled receptor 55 (GPR55) is expressed in multiple important brain regions related to emotion (hippocampus, striatum, amygdala and corte.
And it is mainly expressed on microglia, which plays an important role in maintaining a variety of normal brain functions [5-
In addition, it has been reported that GPR55 regulates anxiety-like behaviors and ameliorates impaired hippocampal neurogenesis [9, 1
However, the exact role of GPR55 in depressive behavior is uncle.
Recently, Yu Jin's research group from the School of Basic Medicine of Fudan University published a research paper entitled "The neuroprotective effects of GPR55 against hippocampal neuroinflammation and impaired adult neurogenesis in CSDS mice" in Neurobiology of Disea.
This study revealed the anti-neuroinflammatory and neurogenesis-protective roles of GPR55 in anxiety-depression-like behaviors mediated by an animal model of anxiety and depression (CSDS mode.
Associate Professor Yu Jin and Professor Zhang Yuqiu are the co-corresponding authors, and Shen Shiyu, Yu Rui and Li Wei are the co-first autho.
Chronic social defeat stress (CSDS) Chronic social defeat stress is an animal model of anxiety and depression [1
In recent years, it has been widely us.
The authors first induced the anxiety-depression-like phenotype of C57 mice using CSDS, and detected the protein and mRNA expression levels of horse GPR55 in socially frustrated mice (including insensitive mice and susceptible mic.
A significant decrease in hippocampal GPR55 protein expression was observed in susceptible mice, but Gpr55 mRNA levels were not significantly different between control and socially frustrated mice (F.
This suggests that GPR55 protein expression is affected by CSDS and is associated with social avoidance behavior, but mRNA expression is n.
In addition, the authors used RNA scope in situ hybridization to determine that Gpr55 is only expressed on microglia, but not on neurons, astrocytes, and neural stem cel.
Figure 1 Chronic social defeat stress (CSDS) induces depression and anxiety-like behaviors and reduces GPR55 protein levels in the hippocampus, but not mRNA leve.
(Image source: Shen SY et .
, Neurobiol D.
2022) Based on these results, the authors further investigated whether pretreatment with the GPR55 agonist O-1602 could hinder the emergence of CSDS-induced anxiety-depression phenotyp.
To this end, the researchers injected O-1602 30 minutes before daily social frustration in mice and found that it could significantly improve depression- and anxiety-like behaviors induced by CSDS (Figure Since depression is often accompanied by upregulation of neuroinflammation and impaired neurogenesis, the authors further investigated the effects of O-1602 on hippocampal neuroinflammation and neurogenes.
Figure 3 O-1602 can improve CSDS-induced anxiety-depression-like behavi.
(Source: Shen SY et .
, Neurobiol D.
2022) The experimental results showed that O-1602 pretreatment significantly inhibited the up-regulation of NLRP3 inflammasome expression in the hippocampal brain region of CSDS mice, and inhibited the CSDS group at the transcriptional level The up-regulated pro-inflammatory factors in CSDS indicated that activation of GPR55 could inhibit the neuroinflammatory response induced by CS.
To investigate the role of GPR55 in neurogenesis, the authors used Nestin (nestin) and DCX (doublecortin, doublecortin) to assess neurogenesis in the hippocampal brain regi.
The results showed that O-1602 could partially reverse the CSDS-induced decrease in the mean fluorescence intensity of Nestin+ and DCX+ cel.
From this, the authors speculated that activation of GPR55 could inhibit neuroinflammation and protect hippocampal neurogenes.
Due to the limited efficacy and severe side effects of many antidepressants, some patients in China tend to seek the help of traditional Chinese medicine to treat depressi.
Acupuncture is one of the main TCM treatments, and many studies have also shown that electroacupuncture (EA) can improve anxiety and depression-like behaviors [12, 1
Therefore, the authors further investigated the effect of EA on anxiety-depression-like behavior and hippocampal GPR5Specifically, 10 days after CSDS modeling, the socially frustrated mice were treated with EA for 3 wee.
This treatment significantly improved anxiety-depression-like behavior in CSDS mice, restored GPR55 expression in the hippocampus, and improved CSDS-induced neuroinflammation and impaired neurogenesis (F.
Figure 4 EA treatment upregulates GPR55 expression and ameliorates neuroinflammation and neurogenesis disorders in the hippocamp.
(Source: Shen SY et .
, Neurobiol D.
2022) Since the effect of EA treatment is similar to that of GPR55 agonis.
Therefore, the authors speculate that GPR55 may be involved in the antidepressant and anxiolytic effects of .
To investigate the role of GPR55 in the effect of EA treatment, the authors used the GPR55 antagonist CID16020046 during EA treatment and found that GPR55 antagonist reversed most of the antidepressant and anxiolytic effects of .
Taken together, these findings demonstrate that GPR55 plays an important role in EA-induced antidepressant and anxiolytic effec.
Figure 5 Schematic diagram of the mechanism: changes in microglial GPR55 expression with CSDS and subsequent pathological changes, such as CSDS-induced hippocampal neuroinflammation and neurogenesis disorde.
(Source: Shen SY et .
, Neurobiol D.
2022) Conclusion and discussion, inspiration and prospect This study shows that the decreased expression of hippocampal G protein-coupled receptor 55 (GPR55) is associated with chronic social frustration stress (CSDS) Activation of GPR55 reversed the detrimental effects of CSDS in relation to the social avoidance deficits induc.
Meanwhile, electroacupuncture exhibited antidepressant and anxiolytic properties through a GPR55-dependent mechanism and neuroprotective effec.
suggesting that GPR55 plays an important role in depression and anxiety (Figure Notably, in the present study, GPR55 expression was only downregulated in susceptible mice, which exhibited marked social avoidance behavior, whereas a GPR55 agonist (O-1602) was able to significantly block social avoidance behavior as well as other CSDS-induced behaviors depression and anxiety-like behavi.
This raises the question of whether alterations in GPR55 expression are associated with the development of depression and anxiety-like behaviors, and whether GPR55 activation may serve as a potential therapeutic target in patients with depression, which requires further investigati.
Link to the original text: https://d.
org/11016.
n.
202105743 Associate Professor Yu Jin and Professor Zhang Yuqiu are the co-corresponding authors, and Shen Shiyu, Yu Rui and Li Wei are the co-first autho.
Talent recruitment[1] "Logical Neuroscience" is looking for an associate editor/editor/operation position (online office) Selected previous articles[1] Science︱Reversible CD8 T cell-neuron interaction: an important mechanism of aging inhibiting nerve regeneration 【2】NeuroImage︱Luo Yuejia’s research group reveals the prefrontal control system that social information regulates risk decision 【3】Nat Neurosci | New oligodendrocytes have stronger remyelination ability after demyelination 【4】Biol Psychiatry︱Gao Tianming’s team reveals The regulatory effect of astrocytes on adult hippocampal neurogenesis and memory through the acetylcholine receptor M1 [5] Curr Biol, Chen Nannan et .
revealed that the translation of synaptic regions causes asymmetric distribution of CaMKII protein and its role in memory formation [6] ]Review of Front Aging Neurosci︱Fan Dongsheng’s team focused on the interaction between peripheral and central immune systems in amyotrophic lateral sclerosis [7]NPP︱Lu Wei’s team revealed a new mechanism of GABAA receptor auxiliary subunit phosphorylation to regulate neural behavior [8 ] Cereb Cortex︱ pattern rigidity, the role of temporal dynamics of ventromedial prefrontal cortex on rumination and depression [9] Front Aging Neurosci︱PTAFR as a novel biomarker for Alzheimer's disease diagnosis and treatment [10] PNAS ︱Feng Guoping's laboratory reveals the important role of the front-end thalamic loop in working memory Recommended for high-quality scientific research training courses [1] Practical training course for academic paper writing (Live: 20221~22) [2] Single-cell sequencing and spatial transcriptome Symposium on Scientific Data Analysis (Tencent Online Conference on June 11-12) [3] Symposium on Patch Clamp and Optogenetics and Calcium Imaging Technologies May 21-22 Tencent Conference References (swipe up and down to read) Kessler, RC and EJ Bromet, The epidemiology of depression across cultur.
Annu Rev Public Health, 201 34:.
119-3 Richards,.
, Prevalence and clinical course of depression: a revi.
Clin Psychol Rev, 201 31( 7):.
1117-2 Lutz,.
, et .
, The endocannabinoid system in guarding against fear, anxiety and stre.
Nat Rev Neurosci, 201 16(12):.
705-1 Micale,.
, et .
, Endocannabinoid system and mood disorders: priming a target for new therapi.
Pharmacol Ther, 201 138(1):.
18-3Ryberg,.
, et .
, The orphan receptor GPR55 is a novel cannabinoid recept.
British Journal of Pharmacology, 200 152(7):.
1092-110 Liu,.
, et .
, GPR55: from orphan to metabolic regulator? Pharmacol Ther, 201 145:.
35-4 Marichal-Cancino , BA, et .
, Advances in the Physiology of GPR55 in the Central Nervous Syst.
Current Neuropharmacology, 201 15(5):.
771-77 Xiang,.
, et .
, Activation of GPR55 attenuates cognitive impairment , oxidative stress, neuroinflammation, and synaptic dysfunction in a streptozotocin-induced Alzheimer's mouse mod.
Pharmacol Biochem Behav, 202 214:.
17334 Hill, JD, et .
, Activation of GPR55 induces neuroprotection of hippocampal neurogenesis and immune responses of neural stem cells following chronic, systemic inflammati.
Brain Behav Immun, 201
76:.
165-181Shi, QX, et .
, The novel cannabinoid receptor GPR55 mediates anxiolytic-like effects in the medial orbital cortex of mice with acute stre.
Molecular Brain, 201 11Golden, SA, et .
.
, A standardized protocol for repeated social defeat stress in mice (vol 6, pg 1183, 201
Nature Protocols, 201 10(4):.
643-641Yue,.
, et .
, Electro- Acupuncture Alleviates Chronic Unpredictable Stress-Induced Depressive- and Anxiety-Like Behavior and Hippocampal Neuroinflammation in Rat Model of Depressi.
Front Mol Neurosci, 201 11:.
141 Liu,.
, et .
,Electroacupuncture attenuates the decrease of hippocampal progenitor cell proliferation in the adult rats exposed to chronic unpredictable stre.
Life Sci, 200 81(21-22):.
1489-9 End of this paper
