Abstract
Abnormal glutamate neurotransmission has been implicated in the pathophysiology of schizophrenia. In the present study we investigated two potential neuronal glutamatergic markers, the Excitatory Amino Acid Transporter 3 (EAAT3) and the Vesicular Glutamate Transporter 1 (VGluTl), in post-mortem striatal tissue from control subjects and from subjects with schizophrenia (n= 15 per group). We also investigated the possible influence of chronic antipsychotic administration (typical and atyp ical) on striatal VGluTl expression in the rat brain. We found deficits in EAAT3 in all striatal regions examined in schizophrenia when compared to controls. Following correction for confounding factors (post-mortem interval), these deficits only remained significant in the caudate nucleus (p = 0.019). We also found significant deficits in VGluTl in the caudate nucleus (p = 0.009) in schizophrenia. There were no significant differences in VGluTl in the striatum of antipsychotic treated rats when compared to their vehicle treated controls.
These authors contributed equally to the work
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Nudmamud-Thanoi, S., Piyabhan, P., Harte, M., Cahir, M., Reynolds, G. (2007). Deficits of neuronal glutamatergic markers in the caudate nucleus in schizophrenia. In: Gerlach, M., Deckert, J., Double, K., Koutsilieri, E. (eds) Neuropsychiatric Disorders An Integrative Approach. Journal of Neural Transmission. Supplementa, vol 72. Springer, Vienna. https://doi.org/10.1007/978-3-211-73574-9_34
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DOI: https://doi.org/10.1007/978-3-211-73574-9_34
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