Received: JAccepted: OctoPublished: October 29, 2010Ĭopyright: © 2010 Jeong et al. Feany, Brigham and Women's Hospital, Harvard Medical School, United States of America Similarly, in the cortex, ATP-induced neuron-damage area detected at 3 h did not increase for up to 7 d.Ĭitation: Jeong H-K, Ji K-m, Kim B, Kim J, Jou I, Joe E-h (2010) Inflammatory Responses Are Not Sufficient to Cause Delayed Neuronal Death in ATP-Induced Acute Brain Injury. Importantly, the total number of dopaminergic neurons in the SNpc at 3 h (∼80% of that in the contralateral side) did not decrease further at 7 d. Monocytes rather expressed CD68, a marker of phagocytic activity. Interestingly, neither activated microglia nor monocytes expressed iNOS, a major neurotoxic inflammatory mediator. Monocytes filled the damaged core after neurons and microglia died. In the penumbra region, morphologically activated microglia arranged around the injury sites. We defined as the core region the area where both TH + and Iba-1 + cells acutely died, and as the penumbra the area surrounding the core where Iba-1 + cells showed activated morphology.

ATP acutely caused death of microglia as well as neurons in a similar area within 3 h. Inflammatory responses and their effects on neuronal damage were investigated by immunohistochemistry, electron microscopy, quantitative RT-PCR, and stereological counting, etc.

Acute neuronal damage was induced by stereotaxic injection of ATP into the substantia nigra pars compacta (SNpc) and the cortex of the rat brain.

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