Dopaminergic regulation of striatal proenkephalin mrna and prodynorphin mrna: Contrasting effects of d1 and d2 antagonists
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2021, Early Human DevelopmentAdaptive changes in the expression of central opioid receptors in mice lacking the dopamine D2 receptor gene
2008, NeuroscienceCitation Excerpt :Interestingly, we have demonstrated in genetically modified mice (Clarke et al., 2003) that the absence of dynorphin in the basal ganglia led to a pronounced up-regulation of kappa receptors in the nucleus accumbens and substantia nigra but not in the caudate-putamen. Although the data concerning changes in preprodynorphin mRNA expression after chronic blockade of D2 receptors are contradictory (Morris et al., 1988; Trujillo et al., 1990; Jiang et al., 1990; Fox et al., 1994; Daunais and McGinty, 1996; Mavridis and Besson, 1999), it has been consistently shown that D2 antagonists blocked the increase in striatal preprodynorphin levels induced by dopaminergic compounds (Daunais and McGinty, 1996, Sivam, 1996; Wang and McGinty, 1996). To date, only one study has examined in D2R−/− mice the expression of preprodynorphin mRNA and has focused on the striatum in which no apparent change has been observed (Baik et al., 1995).
Chronic 3,4-dihydroxyphenylalanine treatment induces dyskinesia in aphakia mice, a novel genetic model of Parkinson's disease
2007, Neurobiology of DiseaseCitation Excerpt :Dynorphin is localized to D1 expressing striatal neurons of the direct pathway to SN, while enkephalin is in D2 expressing striatal neurons of the indirect pathway to the globus pallidus (Gerfen et al., 1990; Steiner and Gerfen, 1998; Nadjar et al., 2006). The expression of the precursor of dynorphin, prodynorphin, is under the tonic activation of D1 receptors, but the enkephalin precursor, proenkephalin, is under the tonic suppression of D2 receptors (Morris et al., 1988). Reports of striatal prodynorphin expression following unilateral acute 6-OHDA toxic lesion have been inconsistent, either no change (Morris et al., 1989) or a decrease in level (Gerfen et al., 1990, 1991; Cenci et al., 1998).
The influence of group III metabotropic glutamate receptor stimulation by (1S,3R,4S)-1-aminocyclo-pentane-1,3,4-tricarboxylic acid on the parkinsonian-like akinesia and striatal proenkephalin and prodynorphin mRNA expression in rats
2007, NeuroscienceCitation Excerpt :The weakest antiparkinsonian effect of the intranigral injection of ACPT-1 compared with its intrapallidal and intrastriatal effects is not surprising, in view of the fact that group III mGluRs are also situated on striatonigral GABAergic efferents (Bradley et al., 1999b; Kosinski et al., 1999); hence the activation of these receptors counteracts the antiparkinsonian effect via SNr stimulation (Wittmann et al., 2001). The results of our study that reveal a haloperidol-induced increase in striatal PENK mRNA expression are in line with the commonly known data indicating that this compound directly influences striatal enkephalin biosynthesis by blocking D2 receptors (Tang et al., 1983; Morris et al., 1988; Angulo, 1992; Mavridis and Besson, 1999). Contrary to the above-reported effect, haloperidol does not affect striatal PDYN mRNA expression.