Antagonistic effects of stimulation of the paramedian reticular nucleus in the rat medulla oblongata and of amphetamine on locomotor activity and striatal release of dopamine-like material.
The effects of stimulation of the paramedian reticular nucleus (PRN) in the rat medulla oblongata on both amphetamine-induced locomotor activity and striatal release of dopamine-like material were assessed. PRN stimulation (by intra-PRN injection of the excitatory amino acid, kainic acid) decreased vertical motion and total distance travelled, and increased postural freezing, in freely moving rats. On the other hand, a small dose (e.g. 1.25 mg/kg, i.p.) of amphetamine increased locomotor activity (including horizontal motion, vertical motion, total distance travelled and lines crossed counts), increased the number of turnings (both clockwise and anti-clockwise), induced locomotor stereotypy (including both gamma value and number of trip types), and inhibited postural freezing. The changes in activity induced by amphetamine administration were suppressed following PRN stimulation. In vivo voltammetric data revealed that electrical stimulation of the PRN decreased the release of dopamine-like material in the corpus striatum. This effect could be mimicked by intra-PRN injection of kainic acid in anesthetized rats. In contrast, i.p. administration of amphetamine increased the release of dopamine-like material in the corpus striatum. Furthermore, the enhanced release of dopamine-like material induced by amphetamine was attenuated by simultaneous stimulation of the PRN. The results reported here indicate that PRN stimulation decreases the striatal dopamine release and results in attenuation of the amphetamine-induced locomotor activity responses in rats.[1]References
- Antagonistic effects of stimulation of the paramedian reticular nucleus in the rat medulla oblongata and of amphetamine on locomotor activity and striatal release of dopamine-like material. Lin, M.T., Chuang, S.F., Li, Y.C., Young, M.S., Chai, C.Y. Naunyn Schmiedebergs Arch. Pharmacol. (1993) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
