By Farabee M.

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Example text

At this time, the contributions of striatal or subthalamic mGluRs to the antiparkinsonian effects of group II mGluR agonists have not been directly evaluated. Although the antiparkinsonian actions of group II mGluR agonists have been demonstrated in certain behavioral models of PD, systemic administration of LY379268 fails to reverse motor deficits caused by chronic reserpine treatment or unilateral 6-hydroxydopamine lesion (Murray et al. 2002), raising concerns that this therapy may not be useful in a chronic state of dopamine depletion.

2002). In vivo microdialysis studies have shown that local administration of group II mGluR antagonists in the striatum increases extracellular glutamate levels, suggesting that these receptors tonically inhibit glutamate release (Cozzi et al. 1997). Further studies have revealed that extracellular glutamate derived from cysteine-glutamate antiporter activity is the main source of glutamate responsible for the tonic activation of striatal group II mGluRs (Baker et al. 2002). In contrast to the reversible inhibition of excitatory transmission in rat brain slices, activation of group II mGluRs at the mouse corticostriatal synapse causes an LTD of excitatory transmission that persists after drug-washout (Kahn et al.

2005; De Leonibus et al. 2009). Interestingly, combined blockade of mGluR5 and A2A adenosine receptors produces very robust antiparkinsonian effects (Coccurello et al. 2004; Kachroo et al. 2005), possibly due to the interaction of these receptors in the striatal neurons that give rise to the indirect pathway. Several mechanisms could mediate the antiparkinsonian effects of mGluR5 antagonism. Direct-site infusion of group I mGluR agonists into the rat striatum increases activity of the indirect pathway while reducing motor activity (Kearney 10 Dopamine–Glutamate Interactions in the Basal Ganglia et al.

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