Group III mGluR Function and Physiology Sample Clauses

Group III mGluR Function and Physiology. Group III mGluR activation has been shown to reduce the release of vesicular and non-vesicular glutamate. Previous studies have shown that local perfusion of L-AP4, a non-selective group III mGluR agonist, lowered extracellular glutamate levels in many brain regions, including the nucleus accumbens (NAc) (Anwyl, 1999; Cartmell and Xxxxxxx, 2000; Hu et al., 1999; Kogo et al., 2004; Panatier et al., 2004; Xi et al., 2003). Additionally, mGluR4b and/or mGluR7 were shown to regulate in vivo extracellular glutamate in the nucleus accumbens by inhibiting non-vesicular glutamate release via the PKA-dependent modulation of cysteine-glutamate exchange (Xi et al., 2003). This is very important because the basal levels of in vivo extracellular glutamate are largely independent of vesicular release (Xxxxxxxxx et al., 2003; Xi et al., 2003). Group III mGluRs are therefore able to modulate glutamate locally at each synapse via regulation of voltage-gated Ca+ channels and on larger scale via the glial cysteine-glutamate transporter (Xi et al., 2003).