MSOP is a selective group III metabotropic glutamate receptor antagonist with apparent KD of 51 μM for the L-AP4-sensitive presynaptic mGluR.
In the presence of 200 μM MSOP, a rightward parallel shift of the dose-response curve to L-AP4 is observed, with an apparent KD calculated as 51±6 μM (n=3). MSOP is shown to be selective for the L-APC sensitive presynaptic mGluR, the apparent KD for the interaction of MSOP with the (1S, 3S)-ACPD sensitive receptor calculated as greater than 700 μM (n=3)[1].
It is found that TBOA-induced antinociceptive effects are significantly blocked by intrathecal co-administration of MSOP (second phase of formalin model: F3,16=30.96, P<0.001; CFA model: F3,16=30.77, P<0.001). As expected, intrathecal TBOA (10 μg) reduces the number of formalin-induced flinches and shakes by 47% of the value in the saline-treated group in the second phase (P<0.001) and blocked the CFA-induced decrease in ipsilateral paw withdrawal latency by 60% of the value in the saline-treated group (P=0.01). The number of formalin-induced flinches in the second phase in the group treated with MSOP and TBOA is increased by 56% (P=0.04) of the value in the TBOA-treated group. CFA-induced paw withdrawal latency in the group treated with MSOP and TBOA is decreased by 86% (P=0.03) of the value in the TBOA-treated group[2].
References:
[1]. Thomas NK, et al. alpha-Methyl derivatives of serine-O-phosphate as novel, selective competitive metabotropic glutamate receptor antagonists. Neuropharmacology. 1996 Jun;35(6):637-42.
[2]. Myron Yaster, et al. Effect of inhibition of spinal cord glutamate transporters on inflammatory pain induced by formalin and complete Freund’s adjuvant. Anesthesiology. 2011 Feb; 114(2): 412–423.