Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats
Identifieur interne : 000321 ( Ncbi/Curation ); précédent : 000320; suivant : 000322Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats
Auteurs : Kristin Dupre [États-Unis] ; Corinne Ostock [États-Unis] ; Karen Jaunarajs [États-Unis] ; Thomas Button [États-Unis] ; Lisa Savage [États-Unis] ; William Wolf [États-Unis] ; Christopher Bishop [États-Unis]Source :
- Experimental neurology [ 0014-4886 ] ; 2011.
Abstract
Serotonin 1A receptor (5-HT1AR) agonists reduce both L-DOPA- and D1 receptor (D1R) agonist-mediated dyskinesia, but their anti-dyskinetic mechanism of action is not fully understood. Given that 5-HT1AR stimulation reduces glutamatergic neurotransmission in the dopamine-depleted striatum, 5-HT1AR agonists may diminish dyskinesia in part through modulation of pro-dyskinetic striatal glutamate levels. To test this, rats with unilateral medial forebrain bundle dopamine or sham lesions were primed with L-DOPA (12 mg/kg + benserazide, 15 mg/kg, sc) or the D1R agonist SKF81297 (0.8 mg/kg, sc) until abnormal involuntary movements (AIMs) stabilized. On subsequent test days, rats were treated with vehicle or the 5-HT1AR agonist ±8-OH-DPAT (1.0 mg/kg, sc), followed by L-DOPA or SKF81297, or intrastriatal ±8-OH-DPAT (7.5 or 15 mM), followed by L-DOPA. In some cases, the 5-HT1AR antagonist WAY100635 was employed to determine receptor-specific effects.
Url:
DOI: 10.1016/j.expneurol.2011.02.012
PubMed: 21352823
PubMed Central: 3100430
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<front><div type="abstract" xml:lang="en"><p id="P1">Serotonin 1A receptor (5-HT<sub>1A</sub>
R) agonists reduce both L-DOPA- and D1 receptor (D1R) agonist-mediated dyskinesia, but their anti-dyskinetic mechanism of action is not fully understood. Given that 5-HT<sub>1A</sub>
R stimulation reduces glutamatergic neurotransmission in the dopamine-depleted striatum, 5-HT<sub>1A</sub>
R agonists may diminish dyskinesia in part through modulation of pro-dyskinetic striatal glutamate levels. To test this, rats with unilateral medial forebrain bundle dopamine or sham lesions were primed with L-DOPA (12 mg/kg + benserazide, 15 mg/kg, sc) or the D1R agonist SKF81297 (0.8 mg/kg, sc) until abnormal involuntary movements (AIMs) stabilized. On subsequent test days, rats were treated with vehicle or the 5-HT<sub>1A</sub>
R agonist ±8-OH-DPAT (1.0 mg/kg, sc), followed by L-DOPA or SKF81297, or intrastriatal ±8-OH-DPAT (7.5 or 15 mM), followed by L-DOPA. In some cases, the 5-HT<sub>1A</sub>
R antagonist WAY100635 was employed to determine receptor-specific effects. <italic>In vivo</italic>
microdialysis was used to collect striatal samples for analysis of extracellular glutamate levels during AIMs assessment. Systemic and striatal ±8-OH-DPAT attenuated L-DOPA-induced dyskinesia and striatal glutamate efflux while WAY100635 reversed ±8-OH-DPAT’s effects. Interestingly, systemic ±8-OH-DPAT diminished D1R-mediated AIMs without affecting glutamate. These findings indicate a novel anti-dyskinetic mechanism of action for 5-HT<sub>1A</sub>
R agonists with implications for the improved treatment of Parkinson’s disease.</p>
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