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Increased levels of the metabotropic glutamate receptor mGluR5 have been observed in the hippocampus and basal ganglia of a transgenic (Tg) mouse model of PD, indicating that α-synuclein may directly interact with mGluR5 to cause overactivation of this receptor, leading to excitotoxic cell death [17]
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An early phase, common to both cultivars, is characterized by activation of core antioxidant defenses that buffer the oxidative burst associated with microspore isolation and osmotic/starvation stress, thereby enabling cell survival and entry into developmental reprogramming
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