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Role of Microglia in 3, 4 Methylenedioxymethamphetamine (MDMA) -Induced Neurotoxicity: A Mini Review

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MDMA (3, 4 Methylenedioxymethamphetamine) is a psychoactive drug under the amphetamine-type stimulant group. While the modulatory effects of MDMA on serotonin neurotransmission and its neurotoxicity in the central nervous system are well studied, MDMA’s effects on modulating microglial neuroimmune functions have attracted considerable attention. Resident glial cells, including microglia in the brain, are implicated in contributing to MDMA-induced neurotoxicity. In their response to the disturbances around neurons, microglia can take on the role of the first line of defence against pathogens by the production of a variety of inflammatory mediators such as tumour necrosis factor-alpha (TNF-α), interleukin (IL) 1β, IL-6, nitric oxide (NO), and reactive oxygen species (ROS). They also can act as anti-inflammatory mediators to initiate recovery from an insult. Hence, the current review illuminates MDMA-induced neurotoxicity by summarising studies reporting microglial activation after MDMA exposure in vitro and in vivo. A modulation between cytotoxic states to a neuroprotective state of microglia probably can make up an important strategy to reduce the negative impairments made by MDMA on neuronal cells by targeting microglial cells.
Title: Role of Microglia in 3, 4 Methylenedioxymethamphetamine (MDMA) -Induced Neurotoxicity: A Mini Review
Description:
MDMA (3, 4 Methylenedioxymethamphetamine) is a psychoactive drug under the amphetamine-type stimulant group.
While the modulatory effects of MDMA on serotonin neurotransmission and its neurotoxicity in the central nervous system are well studied, MDMA’s effects on modulating microglial neuroimmune functions have attracted considerable attention.
Resident glial cells, including microglia in the brain, are implicated in contributing to MDMA-induced neurotoxicity.
In their response to the disturbances around neurons, microglia can take on the role of the first line of defence against pathogens by the production of a variety of inflammatory mediators such as tumour necrosis factor-alpha (TNF-α), interleukin (IL) 1β, IL-6, nitric oxide (NO), and reactive oxygen species (ROS).
They also can act as anti-inflammatory mediators to initiate recovery from an insult.
Hence, the current review illuminates MDMA-induced neurotoxicity by summarising studies reporting microglial activation after MDMA exposure in vitro and in vivo.
A modulation between cytotoxic states to a neuroprotective state of microglia probably can make up an important strategy to reduce the negative impairments made by MDMA on neuronal cells by targeting microglial cells.

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