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The activation of nuclear factor-kappaB (NF-kappaB) leads to an increase in the expression of genes involved in important events in the central nervous system (CNS), such as development, plasticity and inflammation. It has been shown that inflammatory stimulus in the brain increases excitatory glutamatergic transmission, especially at N-methyl-D-aspartate (NMDA) receptor. These receptors have an important role in glutamate neurotoxicity and are in general coupled with the generation of nitric oxide (NO) through the activation of neuronal nitric oxide synthase (NOS). We have investigated the involvement of NMDA-NO pathway in LPS induction of NF-kappaB in CNS. Our results demonstrate that systemic LPS activates NF-kappaB in several regions of the CNS, which was partially reduced by the NMDA receptor antagonist dizolcipine (MK-801) and by the selective brain NOS inhibitor 7-Nitroindazol (7-Ni). 7-Ni effects were not synergic to MK-801 effects, suggesting that these compounds act through the same pathway. Dexamethasone caused a stronger reduction in LPS induction of NF-kappaB in CNS, demonstrating that MK-801 and 7-Ni act on a pathway that is responsible only by a fraction of the overall NF-kappaB activation. These results suggest that a considerable part of NF-kappaB activation by LPS is linked to the NMDA/NO pathway in CNS.
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http://dx.doi.org/10.1016/s0028-3908(03)00279-x | DOI Listing |
Heliyon
December 2024
Department of Biomedical Sciences, Pak Austria Fachhochschule: Institute of Applied Sciences and Technology, Haripur, Khyber Pakhtunkhwa, Pakistan.
Morphine belongs to the class of opioids and is known for its potential to cause dependence and addiction, particularly with prolonged use. Due to the associated risks, caution must be taken when prescribing and limiting its clinical use. Overexpression of N-methyl-D-aspartate (NMDA) receptors, nitric oxide and cGMP pathway has been implicated in exacerbate the development of morphine dependence and withdrawal.
View Article and Find Full Text PDFJ Appl Toxicol
October 2024
Department of Functional Biology and Health Sciences, Faculty of Biology, University of Vigo, Vigo, Spain.
Pharmacol Rep
August 2022
Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Background: Non-deleterious episodes of seizure preconditioning can efficiently increase the brain's resistance to the consequent severe status epilepticus (SE). In the present investigation, we intended to elucidate further (i) the effects of preconditioning with pentylenetetrazole (PTZ) in the lithium-pilocarpine model of SE in male rats, along with (ii) the possible contribution of opioid, N-Methyl-D-aspartate (NMDA) receptors, and nitric oxide (NO) signaling transduction.
Methods: In male Wistar rats, the SE was incited by lithium administration (127 mg/kg, ip) 20 h before pilocarpine (60 mg/kg, ip).
Fundam Clin Pharmacol
April 2022
Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Seizure occurs as a result of uncontrolled electrical disturbances within the brain. Various biomolecules such as N-methyl-D-aspartate (NMDA), nitric oxide (NO), and cAMP response element-binding protein (CREB) have been implicated in the pathophysiology of seizure. Sumatriptan is a specific 5-Hydroxytryptamine 1B/1D receptor agonist and has neuroprotective effects in various neuropsychiatric disorders.
View Article and Find Full Text PDFJ Epilepsy Res
June 2021
Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Background And Purpose: Accumulating evidence suggest that lenalidomide, a structural analog of thalidomide, has neuro-modulatory and neuroprotective properties. In the present study, we investigated effects of acute administration of lenalidomide on clonic seizure threshold in mice induced by pentylenetetrazole (PTZ) and possible role of N-methyl-D-aspartic acid receptor (NMDAR) and nitric oxide (NO) pathway.
Methods: We have utilized a clonic model of seizure in NMRI mice induced by PTZ to evaluate the potential effect of lenalidomide on seizure threshold.
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