Human platelets express the synaptic markers VGLUT1 and 2 and release glutamate following aggregation

Distinct Plasma Profile of Polar Neutral Amino Acids, Leucine, and Glutamate in Children with Autism Spectrum Disorders

“…Among these three types of preparations, platelet-poor plasma provides the most accurate appraisal of AA levels, since serum is contaminated with products of coagulation and concomitant platelet, leukocyte and erythrocyte activation, whereas platelet-rich plasma that has been frozen and thawed is contaminated with intra-platelet contents due to platelet lysis. Since platelets contain several AA, including glutamate and aspartate (Rolf et al 1993;Tremolizzo et al 2006), the use of platelet-poor plasma, but not of other preparations, minimizes non-specific AA release during sample preparation. Extracellular GLU is regarded as a potentially important factor in the etiology of ASD due to its excitotoxic capacity in the brain (Blaylock and Strunecka 2009).…”

The potential role of glutamate in the current diabetes epidemic

“…Interestingly, in both these conditions, increased glutamate levels are inversely correlated with lymphocytic activity [136] and hyperglutamatemia has been implicated in the pathogenesis of immunosuppression [136][137][138]. Hyperglutamatemia is common in neurodegenerative diseases and in particular in stroke patients [139][140][141] where it has been ascribed to an increased release of glutamate by the activated platelets [139,140]. In multiple sclerosis, increased glutamate levels have been associated with a mutation of the glutamate transporter GLT1 [142].…”

“…Amyotrophic lateral sclerosis [143][144][145], Parkinson's disease [146], epilepsy [147], autism [148], migraine [149], and depression [150] are also associated with increased circulating glutamate levels. Interestingly, hyperglutamatemia has been shown also in patients with rheumatoid arthritis [151] where, as in stroke patients, it has been related to the increased release of glutamate by the activated platelets [139,140]. The relevance of the hyperglutamatemia observed under different pathological conditions to disease manifestation and natural history is not always clear but indicates an important area of investigation.…”

“…T cells may directly impair BBB function and induce an encephalomyelitis-like disease [185]. The impaired BBB function might increase the load of glutamate in the CNS [185] and worsen neurotoxicity that, in turn, might increase plasma glutamate levels [139][140][141][142][143][144][145][146][147]. Hyperglutamatemia affects the immune system [136][137][138]186] and might also exert a suppressive function on regulatory T cells as glutamate decreases Interleukin-10 secretion by peripheral blood lymphocytes of subjects with autoimmune thyroiditis [187].…”

Temporomandibular Joint Bone Tissue Resorption in Patients with Early Rheumatoid Arthritis Can Be Predicted by Joint Crepitus and Plasma Glutamate Level

“…Glutamate participates in normal bone turn over and bone tissue remodeling [9, 10] The glutamate level has been reported to be elevated in plasma [11] and synovial tissues in RA [12], probably as a result of release from activated thrombocytes [13, 14]. Continuous thrombocyte activation in the synovial tissues might be accomplished by proinflammatory cytokines such as tumor necrosis factor (TNF) since thrombocytes express cytokine receptors [15].…”