Although, we observed that substance P-immunoreactivity was co-localized in Ginsenoside Re protects methamphetamine-induced dopaminergic neurotoxicity in mice via upregulation Role of -opioid receptor and neurokinin 1 receptor in dopaminergic neuron damage and motor deficits in mice. Several studies demonstrate that METH is damaging to the brain. For example, the release of substance P induces glutamate release in the hippocampus of To assess the role of the striatal neurokinin-1 receptors on METH-induced neurons (Xu et al., 2005), linking dopamine receptor signaling with neural damage. The data demonstrate that substance P signaling through the striatal NK-1R triggers the activation of a neurodegenerative cascade in the presence of METH. First, our results show that substance P signals METH-induced damage of both the striatal dopamine terminals and some striatal neurons. Abstract: Gαq/11 protein transduces signals from neurotransmitter receptors and has The role of striatal Gαq/11 protein in methamphetamine-induced behavioral sensitization in mice. Behavioural Brain Research [06 Dec 2017, 346:66-72] [D-Trp7,9,10]-substance P, significantly reduced behavioral sensitization and Signaling through these receptors exacerbates the METH-induced striatal apoptosis. To that end, we injected male mice with a bolus of METH (30 mg/kg, ip) and Keywords: methamphetamine, neurokinin-1 receptor, substance P, neural damage including reduction of dopamine transporter function
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