Elsevier

Pediatric Neurology

Volume 17, Issue 2, September 1997, Pages 139-143
Pediatric Neurology

Original article
Changes in AMPA glutamate and dopamine D2 receptors in hypoxic-ischemic basal ganglia necrosis

https://doi.org/10.1016/S0887-8994(97)00087-8Get rights and content

Abstract

Changes in the AMPA glutamate receptor subunits (GluR1, 2–3, and 4) and dopamine D2 receptor (D2R) were investigated in 16 cases of hypoxic-ischemic basal ganglia necrosis (BGN) by immunohistochemistry. Immunoreactivity to GluR1, 2–3, and 4 was observed in the cytoplasm and dendrites of small and large neurons in the basal ganglia. Neuronal immunoreactivity to GluR1, 2–3, and 4 was decreased in cases with acute BGN as compared with that in age-matched controls, the areas of decreased immunoreactivity corresponding to the damaged regions observed on hematoxylin and eosin staining. Glia in the basal ganglia exhibited immunoreactivity to GluR4 in 4 patients with acute BNG, 3 of the 4 surviving for 12 to 35 days. In addition, neuronal immunoreactivity to D2R was also decreased in cases of acute BGN, the decrease being similar to that of GluR1, 2–3, and 4. Our results suggest that excitotoxicity mediated by GluR1, 2–3, and 4 is involved in the pathogenesis of hypoxic-ischemic neuronal damage, and that GluR4 expressed in glia of the BG in the late stage of hypoxic-ischemic injury may participate in the delayed and long-term response of the glia to injury. The decrease in neuronal D2R may be related to downregulated synthesis of the D2R protein induced by the decrease in GluR1–4 in the basal ganglia.

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