Research articleBromocriptine protects against delayed neuronal death of hippocampal neurons following cerebral ischemia in the gerbil
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Neuroprotective effects of dopamine D2 receptor agonist on neuroinflammatory injury in olfactory bulb neurons in vitro and in vivo in a mouse model of allergic rhinitis
2021, NeuroToxicologyCitation Excerpt :Evidence shows that dopamine D2 receptor modulates glutamate-induced neurotoxicity (Garside et al., 1996; Sawada et al., 1998). Dopamine D2 receptor agonists have shown a protective effect on the hippocampus and substantia nigra striatum after ischemia (Hall et al., 1996; Liu et al., 1995). Systemic administration of the glutamatergic agonist alginic acid resulted in the death of hippocampal cells in dopamine D2 receptor knockout mice but not wild-type mice (Bozzi and Borrelli, 2002; Bozzi et al., 2000).
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome
2021, Cell ReportsCitation Excerpt :Of the compounds identified in this study, bromocriptine showed the most compelling activity across the panel of assays, including protective effects in models of skeletal muscle calcium dysregulation, Wolfram syndrome, oxygen-glucose deprivation, T2D, and stroke. Bromocriptine was previously reported to protect hippocampal neurons from ischemic insult in gerbils (Liu et al., 1995) and was similarly reported to improve ischemia and reperfusion injury in heart (Gao et al., 2013) and kidney (Narkar et al., 2004). Ergot alkaloids, such as bromocriptine, have been postulated to cause myocardial infarction and stroke when used clinically (Larrazet et al., 1993); however, this view is controversial, as subsequent studies have found no association with ischemic injury (Arbouw et al., 2012).
Simultaneously changes in striatum dopaminergic and glutamatergic parameters following hypoxic-ischemic neuronal injury in newborn piglets
2012, European Journal of Paediatric NeurologyCitation Excerpt :Considerable evidence with microdialysis confirms that a large increase in extracellular dopamine occurs in H-I BGI,3 and interruption of the nigrostriatal pathway may relieve ischemic neuronal injury in striatum.27,28 Several studies suggested that either a dopamine D1R or D2R antagonist provided neuroprotection from H-I injury,3,32,33 whereas other studies demonstrated dopamine D2R agonists had a protective effect against both hippocampal and nigrostriatal damage after ischemia.34–36 Numerous reports have documented that excessive glutamate, through NMDA/AMPA receptors, activates the excitotoxic process.29–31
Bromocriptine methylate suppresses glial inflammation and moderates disease progression in a mouse model of amyotrophic lateral sclerosis
2011, Experimental NeurologyCitation Excerpt :It has also been shown that BRC confers protection against oxidative stress-induced cell death (Lim et al., 2008). Further, BRC exerts protective activity against ischemic neuronal insults in gerbils (Liu et al., 1995; O'Neill et al., 1998). These findings suggest that BRC could be a therapeutic agent for ALS besides Parkinson's disease.
Bromocriptine, an ergot alkaloid, inhibits excitatory amino acid release mediated by glutamate transporter reversal
2010, European Journal of PharmacologyNeuroprotection in parkinson's disease
2005, Principles of Treatment in Parkinson's Disease