Dual role of glutamatergic neurotransmission on amyloid β1–42 aggregation and neurotoxicity in embryonic avian retina

Protective effects of ginsenoside Rg2 against glutamate-induced neurotoxicity in PC12 cells

“…The results showed a strong positive reaction of A␤ in PC12 cells treated by glutamate for 24 h, whereas weak positive reactions were found in ginsenoside Rg 2 -treated and control groups. Our data support the theory of glutamate inducing the formation of A␤ (Louzada et al, 2001), and, in this way can be involved in the pathomechanism of AD.…”

Amyloid-β Decreases Nitric Oxide Production in Cultured Retinal Neurons: A Possible Mechanism for Synaptic Dysfunction in Alzheimer’s Disease?

“…We have previously reported that Ab-induced death of retinal neurons requires long-term ([24 h) exposure times [9,10]. Exposure of retinal neuronal cultures to 1 mM glutamate or 20 lM Ab for 15 min caused similar inhibition of NO production (43 and 62% reductions, respectively; Fig.…”

“…Retinas from different species have been used to study excitotoxicity mediated by excitatory amino acids [37]. Retinal neurons have been shown to be sensitive to the neurotoxicity of Ab [9,10] and recent studies have suggested that Ab-induced neurotoxicity may be directly relevant to the onset and development of retinal pathology, including glaucoma and macular degeneration [38,39]. In addition, AD patients may exhibit extensive retinal abnormalities that have been linked to the deposition of amyloid peptide in retinal tissue [40].…”

“…Pharmacological blockade of ionotropic (NMDA and non-NMDA) glutamate receptors blocks Ab-induced death of retinal neurons in culture [9] and cell surface expression of glutamate receptors is required for Ab toxicity [10]. In harmony with the notion that overactivation of excitatory glutamate receptors plays an important role in Ab toxicity, recent studies have shown that agonists of inhibitory GABA A receptors block neuronal death induced by Ab in retinal, cortical and hippocampal neurons [10,32,34].…”

“…It has long been known that Ab aggregates are toxic to neurons both in vitro and in vivo (for early studies, see [7,8]). Although the mechanisms of Ab-induced neurotoxicity are still incompletely understood, considerable evidence indicates that toxicity is, at least in part, related to aberrant activation of glutamate receptors, notably N-methyl-D-aspartate (NMDA) receptors [9][10][11][12]. In fact, previous reports from our group have shown that both NMDA and non-NMDA receptor antagonists blocked neuronal death induced by Ab [9,10].…”