Attenuation of AMPA-induced neurotoxicity by a calpain inhibitor
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Cited by (44)
Exercise mitigates calpain induced Purkinje cell loss in diabetes
2022, Life SciencesCitation Excerpt :The data suggested that induced levels of calpain-1 can be involved behind reduced levels of PCP-4. This is supported by the fact that there is less damage to Purkinje cells when calpains are inhibited [37]. Our results on calpain-1 induction by high calcium, which is accompanied by CaMKII activation followed by calmodulin, is in agreement with a study by Kim et al. that stated that CaMKII activation is associated with reduced expression of PCP-4, dysregulated, intracellular calcium handling, and proarrhythmic behavior in isolated Purkinje cells [38].
Calpain inhibitor, MDL 28170 confer electrophysiological, nociceptive and biochemical improvement in diabetic neuropathy
2015, NeuropharmacologyCitation Excerpt :DRG neurons of treated diabetic rats showed significant reduction in TTX-R INa density and altered channel kinetics in voltage-dependence of activation and steady-state inactivation suggesting a role of MDL 28170 in reversal of neuronal hyperexcitability. Calpain activation is involved in numerous acute and chronic neurological disorders, including focal brain ischemia (Siman et al., 1996), head and spinal cord trauma (Li et al., 1996a, 1996b; Saatman et al., 1996), Parkinson's and Alzheimer's disease (Mouatt-Prigent et al., 1996; Nixon et al., 1994; Ray et al., 2000a, 2000b), and peripheral neuropathies (Caner et al., 1993; LoPachin and Lehning, 1997; Meldrum and Garthwaite, 1990; Nixon, 1989; Wang, 2000). Despite its recognition in these disorders, the exact mechanism which triggers calpain activation and their specific targets remain unclear.
Involvement of calpain in AMPA-induced toxicity to rat cerebellar Purkinje neurons
2007, European Journal of PharmacologyExcitotoxicity
2007, Handbook of Clinical NeurologyCitation Excerpt :Neurotoxicity resulting from kainic acid administration in vivo is associated with calpain activation (Siman and Noszek, 1988). Calpain inhibitors are not effective against glutamate neurotoxicity in cultured cerebellar neurons (Manev et al., 1991), but they do reduce AMPA‐induced toxicity in vitro, as well as in models of cerebral ischemia (Lee et al., 1991; Caner et al., 1993; Bartus et al., 1994; Hong et al., 1994). Expression of human calpastatin in transgenic mice prevents calpain activation that is normally seen after hippocampal kainic acid injections.
Calpain inhibitor MDL 28170 protects hypoxic-ischemic brain injury in neonatal rats by inhibition of both apoptosis and necrosis
2005, Brain ResearchCitation Excerpt :The half-life of activity is approximately 2 h and maximal activity was obtained at 30 min after a single intravenous bolus injection when administered in adult rat [26]. It has been observed that MDL 28170 is effective in inhibiting the cell degeneration in vitro [1,9,10,16,43] as well as in vivo [26]. Due to the technical difficulty of measuring the activation state of calpains accurately in vivo, experiments designed to examine calpain activity often rely on measurements of the breakdown products of a calpain's preferred substrates, spectrin [32,54,59].
Activation of μ-calpain in developing cortical neurons following methylmercury treatment
2003, Developmental Brain Research