Myeloneuropathy, neurologic toxicity, and amiodarone

Overactivation of poly(adenosine phosphate–ribose) polymerase 1 and molecular events in neuronal injury after deep hypothermic circulatory arrest: Study in a rabbit model

“…5,6 Ischemia and ischemia-reperfusion injury initiate a cascade of cellular and molecular events, of which excitotoxicity caused by overstimulation of excitory amino acids, mainly glutamate, has been a wellknown fundamental common process in all kinds of ischemic brain injury. 4,6,7 Of note, the role of excitotoxicity in neuronal injury after DHCA was demonstrated by Tseng and colleagues. 8 Apoptosis and necrosis, the possible sequelae of excitotoxicity, 9 were also identified to play a crucial role in neuronal injury after DHCA.…”

“…Although DHCA afforded a neuroprotective effect and enabled the surgeon to obtain a bloodless operative field that allowed for precise anatomic manipulation, it was always associated with immediate and late neuronal complications. [1][2][3][4] Preventing cerebral injury remains difficult because the underlying mechanisms have not been fully elucidated.…”

“…Glutamate overrelease would lead to excitotoxicity. 4 In this study cerebral microdialysis was associated with the model, which afforded an effective way to study brain molecular changes. The lactate/pyruvate and lactate/glucose ratios were significantly increased after reperfusion in the DHCA group compared with those of the CPB group, which was indicative of ischemia and energy metabolic disorder.…”

Extracellular ATP Binding to P2Y1 Receptors Prevents Glutamate-Induced Excitotoxicity: Involvement of Erk1/2 Signaling Pathway to Suppress Autophagy

“…Neuroexcitotoxicity caused by high concentration of glutamate is one of pivotal pathological features in neurodegenerative disorders [26,27]. Abnormally high concentration of glutamate stimulates the excessive activation of N-methyl-D-aspartate (NMDA) subtype of ionotropic L-glutamate receptors, subsequently results in an excessive Ca 2+ in ux, which is taken up by mitochondria and subsequently triggers excitatory biochemical processes and death pathways [28,29].…”

Peripheral role of glutamate in orofacial pain

“…Glutamate is one of the most abundant amino acids, which plays important roles in nutrition and metabolism in addition to its role in protein structure (Meldrum, 2000;Petroff, 2002;Brosnan and Brosnan, 2013). It is discovered as a neurotransmitter responsible for the excitatory action in the central nervous system (CNS) and involved in a wide variety of physiological and pathological processes such as learning, memory (Hugon et al, 1996), development, depression (Hillhouse and Porter, 2015), and neurodegeneration (Meldrum, 2000). In addition, it is well demonstrated that glutamate plays an important role in nociceptive processing not only at central synapses but also in the peripheral nervous system (PNS).…”