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In fact, a difference in experimental conditions as well as cell-type specificity of plasticity mechanisms and heterogeneity of recorded subpopulations of interneurons could have contributed to discrepancies between the findings of the above studies, e.g., whether CA1 inhibitory neurons express predominantly LTD (McMahon and Kauer, 1997) or also LTP (Taube and Schwartzkroin, 1987

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Studies have also indicated that elevated TNF- and dysregulated iron homeostasis often reinforce each other in tumor or inflammation models, collectively driving cell damage and death (120)