Combined neuroprotective action of adenosine A1 and cannabinoid CB1 receptors against NMDA-induced excitotoxicity in the hippocampus

Serpa, André; Pinto, Isa; Bernardino, Liliana; Cascalheira, José F.

doi:10.1016/j.neuint.2015.06.005

Cited by 15 publications

(9 citation statements)

References 20 publications

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“…Higher caspases‐3 activity in the hippocampal CA1 and CA3 regions may contribute to neuronal damage (Jafarian, Karimzadeh, Alipour, Attari, Lotfinia, Speckmann, … Gorji, ), while caspases‐3 activity was not found to be involved in the N‐methyl‐D‐aspartate (NMDA) receptor channel‐induced neuronal damage in a PTZ‐kindling model (Zaitsev, Kim, Vasilev, Lukomskaya, Lavrentyeva, Tumanova, … Magazanik, ). The extent of NMDA‐induced cell injury in the CA1 and CA3 regions was different (Ikegaya & Matsuki, ; Serpa, Pinto, Bernardino, & Cascalheira, ; Vornov, Tasker, & Coyle, ). The CA1 region appeared to be more susceptible to NMDA‐induced cytotoxicity in some previous studies (Ikegaya & Matsuki, ; Vornov, Tasker, & Coyle, ), while the CA3 region was observed to be more susceptible and only obtained neuroprotective action against NMDA‐induced excitotoxicity in a recently study (Serpa, Pinto, Bernardino, & Cascalheira, ).…”

Section: Discussionmentioning

confidence: 99%

“…The extent of NMDA‐induced cell injury in the CA1 and CA3 regions was different (Ikegaya & Matsuki, ; Serpa, Pinto, Bernardino, & Cascalheira, ; Vornov, Tasker, & Coyle, ). The CA1 region appeared to be more susceptible to NMDA‐induced cytotoxicity in some previous studies (Ikegaya & Matsuki, ; Vornov, Tasker, & Coyle, ), while the CA3 region was observed to be more susceptible and only obtained neuroprotective action against NMDA‐induced excitotoxicity in a recently study (Serpa, Pinto, Bernardino, & Cascalheira, ). Further studies need to be conducted to determine the mechanism that leads to this spatial distinct in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

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Effect of lamotrigine on epilepsy‐induced cognitive impairment and hippocampal neuronal apoptosis in pentylenetetrazole‐kindled animal model

Zhang

Wang

et al. 2016

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Purpose: Lamotrigine (LTG) is a broad-spectrum antiepileptic drug that is widely used in clinic. However, the effect of LTG on cognition and neurodegeneration during epilepsy treatment remains controversial. In this study, we compared the cognitive effects of LTG and sodium valproate in pentylenetetrazole (PTZ)-kindled animal model, and the dose dependency was tested for LTG.Methods: PTZ-kindled animals were divided into the following treatment groups: control group, treated with 3.5 mL/kg of 0.9% sodium chloride; low-dose LTG group, treated with 12.5 mg/kg of LTG; middle-dose LTG group, treated with 25 mg/kg of LTG; high-dose LTG group, treated with 50 mg/kg of LTG; VPA group, treated with 300 mg/kg of VPA. The Morris Water Maze (MWM) test commenced from the 10th day of treatment. Hippocampal cell apoptosis was determined by TUNEL staining after two weeks of treatment.Results: Compared to the vehicle-treated control group, escape latency was significantly reduced in the middle-and high-dose LTG-and VPA-treated groups on the 3rd and 4th day of the MWM test (p < .05), and spatial probe frequency was significantly improved in the middle-and high-dose LTG-and VPA-treated groups (p < .05). Furthermore, the immunohistochemical score of TUNEL positive cells significantly decreased in the hippocampal CA1 region in the middle-and high-dose LTG-and VPA-treated groups (p < .05). Conclusion:Our data suggests that LTG may ameliorate epilepsy-induced cognitive impairment and neuronal cell apoptosis during epilepsy treatment. LTG may ameliorate cognitive impairment and neuronal cell apoptosis during epilepsy treatment. K E Y W O R D Sepilepsy, cognitive impairment, pentylenetetrazole, lamotrigine, sodium valproate

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of lamotrigine on epilepsy‐induced cognitive impairment and hippocampal neuronal apoptosis in pentylenetetrazole‐kindled animal model

Zhang

Wang

et al. 2016

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“…CB1 and CB2 receptors modulate a vast variety of physiological functions including memory [10]. CB1 receptor expresses at high levels in the hippocampus [23]. Kim et al found that CB2 receptor is capable of modulating hippocampal CA1 synaptic plasticity [10].…”

Section: Discussionmentioning

confidence: 99%

Combined Neuroprotective Action of JWH-015 and AM251 in the CA1 Hippocampal Area of Transient Global Cerebral Ischemia

Shiasi¹,

Mortezaee²,

Abolhassani³

et al. 2017

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Transient global cerebral ischemia (TGCI) induces by bilateral common carotid artery occlusion (BCCAO), and it mediates neuronal cell death of the CA1 hippocampal area. AM251 is a cannabinoid receptors type 1 (CB1) blocker that has been known to be protective against transient focal cerebral ischemia. JWH-015 is a selective agonist of CB2 and activator of CB1 that is involved in promotion of neuronal recovery and survival. The role of combined application of JWH-015 with AM251 in the rat model of GCI has been surveyed in this study. Male Wistar rats underwent 20 min of ischemia followed by reperfusion. Then, 1 mg/kg JWH-015 and 2 mg/kg AM251 were administered through caudal vein. The groups were control, sham, ischemia, vehicle, AM251, JWH-015 and AM251 + JWH-015. Animals were sacrificed at 14 days after reperfusion. The AM251 + JWH-015 group showed a significant increase in the protein expressions of AKT1, Bad 14-3-3, Bcl-2 and Bcl-XL, but it showed a considerable decrease in the protein expressions of Bad and JNK1/2 (p ≤ 0.05 vs. AM251, and JWH-015 groups). The AM251 + JWH-015 group had a significant higher number of alive cells and lower number of TUNEL-positive cells in the CA1 hippocampal area, and it also had a considerable improvement of spatial memory (p ≤ 0.05 vs. AM251, and JWH-015 groups). The results of this study showed that combined application of AM251 and JWH-015 could be neuroprotective against detrimental effects of ischemia probably via suppression of neuronal apoptosis and maintenance of their survival.

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“…Adenosine is generated in response to cell stress and cell injury and its concentration increases during episodes of hypoxia and inflammation (Lopes, Sebastião, & Ribeiro, ), as those occurring upon stroke or in brain tumours. Adenosine plays a regulatory role in the nervous system by decreasing neurotransmitter release and synaptic transmission, including excitatory synaptic transmission (Dias, Rombo, Ribeiro, Henley, & Sebastião, ; Dunwiddie & Hoffer, ; Pinto, Serpa, Sebastião, & Cascalheira, ; Serpa, Ribeiro, & Sebastião, ), protecting against neurotoxic insults (Ribeiro, Sebastião, & Mendonça, ; Serpa, Pinto, Bernardino, & Cascalheira, ) and modulating synaptic plasticity (Dias et al, ; Santschi, Zhang, & Stanton, ). Most of these adenosine actions are mediated by activation of G‐protein‐coupled adenosine receptors located at the extracellular membrane, specifically A 1 , A 2A , A 2B and A 3 receptors (Dias et al, ; Serpa, Sara, Ribeiro, Sebastião, & Cascalheira, ; Serpa, Sebastião, & Cascalheira, ).…”

Section: Introductionmentioning

confidence: 99%

Adenosine inhibits human astrocyte proliferation independently of adenosine receptor activation

Marcelino

Nogueira

Santos

et al. 2019

Journal of Neurochemistry

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are Co-senior authors. Abbreviations Used:: ABT 702, 4-Amino-5-(3-bromophenyl)-7-(6-morpholinopyridin-3-yl)pyrido[2,3-d]pyrimidine; ADA, adenosine deaminase; ADK, adenosine kinase; DPCPX, 8-cyclopentyl-1,3-dipropylxanthine; HA, Human astrocytes; ITU, 5-iodotubercidin; LDH, lactate dehydrogenase; AbstractBrain adenosine concentrations can reach micromolar concentrations in stressful situations such as stroke, neurodegenerative diseases or hypoxic regions of brain tumours. Adenosine can act by receptor-independent mechanism by reversing the reaction catalysed by S-adenosylhomocysteine (SAH) hydrolase, leading to SAH accumulation and inhibition of S-adenosylmethionine (SAM)-dependent methyl-

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Combined neuroprotective action of adenosine A1 and cannabinoid CB1 receptors against NMDA-induced excitotoxicity in the hippocampus

Cited by 15 publications

References 20 publications

Effect of lamotrigine on epilepsy‐induced cognitive impairment and hippocampal neuronal apoptosis in pentylenetetrazole‐kindled animal model

Effect of lamotrigine on epilepsy‐induced cognitive impairment and hippocampal neuronal apoptosis in pentylenetetrazole‐kindled animal model

Combined Neuroprotective Action of JWH-015 and AM251 in the CA1 Hippocampal Area of Transient Global Cerebral Ischemia

Adenosine inhibits human astrocyte proliferation independently of adenosine receptor activation

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