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Protein kinase C inhibition differentially affects 3,4-methylenedioxymethamphetamine-induced dopamine release in the striatum and prefrontal cortex of the rat.
Brain Res 2004; 1013(2):168-73BR

Abstract

The acute administration of 3,4-methylenedioxymethamphetamine (MDMA) elevates extracellular concentrations of dopamine (DA) and serotonin (5-HT) in the rat striatum and medial prefrontal cortex (mPFC). The release of DA induced by MDMA is thought to involve both transporter and impulse-mediated processes. Furthermore, the impulse-dependent release of DA in the striatum elicited by MDMA appears to involve 5-HT2 receptor activation. Since 5-HT2 receptors are known to utilize protein kinase C (PKC) for intracellular signaling, we examined the effects of modulators of PKC activity on DA release stimulated by MDMA. Reverse dialysis of the PKC inhibitors bisindolylmaleimide I (BIM; 30 microM) or chelerythrine chloride (100 microM) through a microdialysis probe significantly attenuated the MDMA (10 mg/kg, i.p.)-induced increase in the extracellular concentration of DA in the striatum. In contrast, BIM did not significantly alter the increase in the extracellular concentration of DA in the striatum elicited by amphetamine (5 mg/kg, i.p.). Reverse dialysis of a PKC activator, phorbol 12,13-dibutyrate (PDBu) (0.5 microM), through the microdialysis probe into the striatum, significantly increased MDMA-induced DA release. In contrast to the inhibitory effects of the PKC inhibitors on MDMA-induced DA release in the striatum, intracortical infusion of BIM enhanced MDMA-induced release of DA in the mPFC. These data suggest that PKC-mediated signaling pathways differentially modulate MDMA-induced DA release from mesocorticolimbic and nigrostriatal neurons.

Authors+Show Affiliations

College of Pharmacy, University of Cincinnati, 3223 Eden Avenue, Cincinnati, OH 45267, USA.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15193525

Citation

Nair, Sunila G., and Gary A. Gudelsky. "Protein Kinase C Inhibition Differentially Affects 3,4-methylenedioxymethamphetamine-induced Dopamine Release in the Striatum and Prefrontal Cortex of the Rat." Brain Research, vol. 1013, no. 2, 2004, pp. 168-73.
Nair SG, Gudelsky GA. Protein kinase C inhibition differentially affects 3,4-methylenedioxymethamphetamine-induced dopamine release in the striatum and prefrontal cortex of the rat. Brain Res. 2004;1013(2):168-73.
Nair, S. G., & Gudelsky, G. A. (2004). Protein kinase C inhibition differentially affects 3,4-methylenedioxymethamphetamine-induced dopamine release in the striatum and prefrontal cortex of the rat. Brain Research, 1013(2), pp. 168-73.
Nair SG, Gudelsky GA. Protein Kinase C Inhibition Differentially Affects 3,4-methylenedioxymethamphetamine-induced Dopamine Release in the Striatum and Prefrontal Cortex of the Rat. Brain Res. 2004 Jul 9;1013(2):168-73. PubMed PMID: 15193525.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protein kinase C inhibition differentially affects 3,4-methylenedioxymethamphetamine-induced dopamine release in the striatum and prefrontal cortex of the rat. AU - Nair,Sunila G, AU - Gudelsky,Gary A, PY - 2004/04/01/accepted PY - 2004/6/15/pubmed PY - 2004/8/26/medline PY - 2004/6/15/entrez SP - 168 EP - 73 JF - Brain research JO - Brain Res. VL - 1013 IS - 2 N2 - The acute administration of 3,4-methylenedioxymethamphetamine (MDMA) elevates extracellular concentrations of dopamine (DA) and serotonin (5-HT) in the rat striatum and medial prefrontal cortex (mPFC). The release of DA induced by MDMA is thought to involve both transporter and impulse-mediated processes. Furthermore, the impulse-dependent release of DA in the striatum elicited by MDMA appears to involve 5-HT2 receptor activation. Since 5-HT2 receptors are known to utilize protein kinase C (PKC) for intracellular signaling, we examined the effects of modulators of PKC activity on DA release stimulated by MDMA. Reverse dialysis of the PKC inhibitors bisindolylmaleimide I (BIM; 30 microM) or chelerythrine chloride (100 microM) through a microdialysis probe significantly attenuated the MDMA (10 mg/kg, i.p.)-induced increase in the extracellular concentration of DA in the striatum. In contrast, BIM did not significantly alter the increase in the extracellular concentration of DA in the striatum elicited by amphetamine (5 mg/kg, i.p.). Reverse dialysis of a PKC activator, phorbol 12,13-dibutyrate (PDBu) (0.5 microM), through the microdialysis probe into the striatum, significantly increased MDMA-induced DA release. In contrast to the inhibitory effects of the PKC inhibitors on MDMA-induced DA release in the striatum, intracortical infusion of BIM enhanced MDMA-induced release of DA in the mPFC. These data suggest that PKC-mediated signaling pathways differentially modulate MDMA-induced DA release from mesocorticolimbic and nigrostriatal neurons. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/15193525/Protein_kinase_C_inhibition_differentially_affects_34_methylenedioxymethamphetamine_induced_dopamine_release_in_the_striatum_and_prefrontal_cortex_of_the_rat_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006899304005499 DB - PRIME DP - Unbound Medicine ER -