Neurotoxic-related changes in tyrosine hydroxylase, microglia, myelin, and the blood-brain barrier in the caudate-putamen from acute methamphetamine exposure

摘要: Changes in the histological morphology of caudate-putamen (CPu) were determined after a high-dose methamphetamine (METH) exposure an effort to elucidate whether BBB disruption plays role CPu neurotoxicity. This was accomplished by evaluating tyrosine hydroxylase immunoreactivity (TH-IR), isolectin B4 reactivity, Black Gold II (BG-II) and Fluoro-Jade C (FJ-C) staining, mouse immunoglobulin G (IgG-IR) adult male mice at 90-min, 4-h, 12-h, 1-day, 3-day post-METH exposure. The IgG-IR indicated that only modestly altered time points neurodegeneration occurred dependent on hyperthermia status epilepticus. modest changes observed perivascular areas immunoglobulins present some microglia 1 day or more METH. first signs damage swellings TH-IR axons, myelin damage, few degenerating neurons 4-h post-METH. loss but not seizures neurodegeneration, virtually absent throughout within 12 h. Surprisingly, FJ-C labeling (degenerating) axons seen regions pronounced somatic independent loss. Microglial activation did occur until In summary, major does directly contribute neurotoxicity this single METH However, seizure activity produced exacerbated amygdalar can significantly increase (but affect dopamine (DA) terminal damage). course microglial indicates response and/or damaged DA terminals TH-IR.