D1 and D2 receptor regulation of preproenkephalin and preprodynorphin mRNA in rat striatum following acute injection of amphetamine or methamphetamine

Abstract

Our previous work has demonstrated a dose‐dependent induction of striatal preprodynorphin (PPD) in response to a single injection of the psychostimulants amphetamine (AMPH) or methamphetamine (METH). In the present study, dose‐response effects of acute administration of these stimulants on preproenkephalin (PPE) mRNA expression in the rat striatum were investigated with quantitative in situ hybridization histochemistry 3 h after injection. Acute AMPH or METH at equimolar doses (3.75, 7.5, 15, and 30 μmol/kg) significantly increased PPE mRNA expression in dorsal (caudoputamen), but not ventral (nucleus accumbens), striatum in a dose‐dependent fashion. In addition, the role of D1 and D2 dopamine receptors in mediating AMPH‐ and METH‐stimulated PPE and PPD expression was also evaluated by using subtype‐specific antagonists. Pretreatment of rats with SCH 23390 (0.1 mg/kg, i.p.), a selective D1 receptor antagonist, completely blocked acute AMPH (21 μmol/kg, i.p.)‐ or METH (21 μmol/kg, i.p.)‐induced PPE as well as PPD mRNA expression in the caudoputamen. Pretreatment with eticlopride (0.5 mg/kg, i.p.), a selective D2 receptor antagonist, also blocked PPD induction by the two stimulants, but PPE induction was unaffected. Furthermore, SCH 23390 decreased, and eticlopride elevated, constitutive PPE mRNA levels in the caudoputamen. Neither antagonist had a significant effect on the basal level of PPE or PPD mRNA in the nucleus accumbens. These results demonstrate a clear dose‐related responsiveness of PPE gene expression in striatal neurons in response to acute administration of amphetamines, although the intensity of the response is far less than that for striatal PPD. Furthermore, both D1 and D2 subtypes of dopamine receptors mediate AMPH‐ and METH‐stimulated striatal PPD mRNA expression, whereas D1 receptor activation alone mediates amphetamine‐stimulated PPE mRNA expression in the rat striatum. © 1996 Wiley‐Liss, Inc.

Acute nicotine changes dynorphin and prodynorphin mRNA in the striatum

“…Nicotine stimulates dopamine release in the striatum directly via α4 and β2 subunit-containing (α4β2*) nAChRs present on midbrain dopaminergic neurons (Gotti et al 2006) and indirectly via α7 nAChRs, expressed on glutamatergic terminals (Wonnacott et al 2005), through glutamate release and subsequent modulation of dopamine secretion by ionotropic glutamate receptors (Toth et al 1992;Sziraki et al 1998Sziraki et al , 2002Schilström et al 1998;Wonnacott et al 2000;Fu et al 2000). Direct and indirect dopamine agonists augment the expression of PD mRNA, and the levels of PD derived peptides predominantly via dopamine D1 receptors (reviewed by Trujillo et al 1993;Angulo and McEwen 1994), although D2 receptors contribute as well, and a D1/D2 synergism has been proposed (Wang and McGinty 1996a;McGinty 2007 and discussion therein). Our finding that the nicotine-induced increase of Dyn was reversed by D1-and D2-like antagonists implies that a similar mechanism operates after nicotine and suggests that dopamine is a common link for the regulation of Dyn by stimulant drugs.…”

The Role of BDNF/TrkB Signaling in Acute Amphetamine-Induced Locomotor Activity and Opioid Peptide Gene Expression in the Rat Dorsal Striatum

“…It is less likely that inhibition of kinase cascades in indirect pathway MSNs leads to suppression of AMPH-induced PPD mRNA in direct pathway neurons. The selective effect of K252a on PPD vs. PPE gene expression also diminishes the likelihood that the K252a effects are mediated by ser/thr kinases stimulated by the major striatal regulators like D1, group I metabotropic glutamate, or muscarinic receptors because antagonists of these pathways block AMPH-induced PPD and PPE gene expression (Wang and McGinty, 1996a,b, 1999; McGinty et al, 2010). Alternatively, consideration must be given to the possibility that tyrosine kinase inhibition mediated by TrkB receptors underlies these K252a effects.…”

Striatal opioid peptide gene expression differentially tracks short-term satiety but does not vary with negative energy balance in a manner opposite to hypothalamic NPY

“…Moreover, there is a substantial literature showing differential effects of these two striatal opioid peptides on dopamine function, which may also relate to the proposed motivational differences. Overall, mu agonists activate dopamine release, whereas kappa agonists decrease it (60,64,67,72). It is of interest that a fairly substantial reduction in accumbens core dynorphin was found in the brains of rats on restricted diets, also reported by Haberny and Carr (20).…”