A. Abuirmeileh, A. Harkavyi, A. Kingsbury, R. Lever and P. S. Whitton, “The CRF-Like Peptide Urocortin Greatly Attenuates Loss of Extracellular Striatal Dopamine in Rat Models of Parkinson’s Disease by Activating CRF(1) Receptors,” European Journal of Pharmacology, Vol. 604, No. 1-3, 2009, pp. 45-50.
http://dx.doi.org/10.1016/j.ejphar.2008.11.009

has been cited by the following article:

• TITLE: Involvement of CRH Receptors in the Neuroprotective Action of R-Apomorphine in the Striatal 6-OHDA Rat Model

  AUTHORS: Mustafa Varçin, Eduard Bentea, Steven Roosens, Yvette Michotte, Sophie Sarre

  KEYWORDS: Apomorphine; Gene Expression; Inflammation; Neuroprotection; Parkinson’s Disease; Striatal 6-Hydroxydopamine Rat Model

  JOURNAL NAME: Neuroscience and Medicine, Vol.4 No.4, December 27, 2013

  ABSTRACT: The dopamine D1-D2 receptor agonist, R-apomorphine, has been shown to be neuroprotective in different models of Parkinson’s disease. Different mechanisms of action for this effect have been proposed, but not verified in the striatal 6-hydroxydopamine rat model. In this study, the expression of a set of genes involved in 1) signaling, 2) growth and differentiation, 3) neuronal regeneration and survival, 4) apoptosis and 5) inflammation in the striatum was measured after a subchronic R-apomorphine treatment (10 mg/kg/day, subcutaneously, during 11 days) in the striatal 6-hydroxydopamine rat model. The expression of 84 genes was analysed by using the rat neurotrophins and receptors RT2 ProfilerTM PCR array. The neuroprotective effects of R-apomorphine in the striatal 6-hydroxydopamine model were confirmed by neurochemical and behavioural analysis. The expression data suggest the observed neuroprotection involved the alteration of the gene and the protein expression levels of the anti-inflammatory corticotropin releasing hormone receptor (CRHR) 1 and the pro-inflammatory CRHR2 receptor confirming its potential anti-inflammatory action.