Though not as extensively studied, there is also supporting evidence that Meth may produce cell death, in addition to damaging DA and 5HT terminals. Increases in terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), a marker for apoptotic cell death, has been reported after exposure to Meth in the prefrontal cortex and striatum (Kadota and Kadota, 2004, Cadet et al., 2005, Zhu et al., 2006b). This cell death has been identified in different subpopulations of GABA-interneurons. Within the hippocampus, cell death of calbindin-containing GABA interneurons has been demonstrated after Meth and Methcontributes to the death of parvalbumin containing striatal GABA interneurons (Zhu et al., 2006a, Kuczenski et al., 2007). Mitochondrial damage and endoplasmic reticulum stress have been associated with this Meth-induced apoptosis (Cadet et al., 2005). Specifically, Meth has been shown to produce apoptosis through increases in caspase-3 activity and the Fas/FasL cell death pathways (Jayanthi et al., 2005). Meth also produces DNA damage and alterations in the expression of Bcl-2 related genes, which may contribute to GABA
interneuron cell death (Jayanthi et al., 2001, Jeng et al., 2006).
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