MSOP - CAS 66515-29-5
Category: Inhibitor
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MSOP is a selective group III metabotropic glutamate receptor (mGluR) antagonist. MSOP exhibits an apparent KD of 51 μM for the L-AP4-sensitive presynaptic mGluR on primary afferent terminals in spinal cord compared to > 700 μM for the (1S,3S)-ACPD-sensitive presynaptic mGlu in the same system. MSOP has no effect on postsynaptic mGlu receptors or on ionotropic glutamate receptors on neonatal rat motoneurons.
Brife Description:
group III mGluR antagonist
(RS)-α-Methylserine-O-phosphate; Alpha-MSOP; Alpha-methylserine-O-phosphate; 2-amino-2-methyl-3-phosphonooxypropanoic acid
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1.Neuroprotective effects of group III mGluR in traumatic neuronal injury.
Faden AI;Ivanova SA;Yakovlev AG;Mukhin AG J Neurotrauma. 1997 Dec;14(12):885-95.
We have used an in vitro trauma model to examine the effects of modulation of group III metabotropic glutamate receptors (mGluR) on post-traumatic neuronal cell death. Rat cortical neuronal/glial cultures were subjected to standardized mechanical injury using a punch that delivers 28 parallel cuts to 96-well culture plates, resulting in approximately 50% neuronal cell loss in untreated cultures. RT-PCR demonstrated expression of mRNA for mGluR4, mGluR6, mGluR7, and mGluR8 in uninjured cultures as well as in adult rat brain. Treatment with the group III agonists L-(+)-2-amino-4-phosphonobutyric acid (L-AP4) or L-serine-O-phosphate (L-SOP) resulted in dose-dependent neuroprotection. In contrast, treatment with the group III antagonists alpha-methyl-AP4 (MAP4) or (RS)-alpha-methylserine-O-phosphate (MSOP) caused dose-dependent exacerbation of injury, which was significantly attenuated by L-AP4 or L-SOP. The neuroprotective actions of L-AP4 or L-SOP were markedly reduced by the cyclic AMP analog 8-CPT-cAMP (500 microm), which by itself had no effects at this concentration. Moreover, treatment with L-AP4 or L-SOP reduced basal cyclic AMP levels. Treatment with the NMDA antagonist MK 801 decreased post-traumatic cell death by 45% at optimal concentrations; combined treatment with MK 801 and group III agonists showed a significant enhancement of neuroprotection as compared to treatment with the NMDA antagonist alone.
2.Cardiovascular responses to activation of metabotropic glutamate receptors in the nTS of the rat.
Viard E;Sapru HN Brain Res. 2002 Oct 18;952(2):308-21.
Although several agonists and antagonists for different subtypes of metabotropic glutamate receptors (mGLURs) have become available in recent years, detailed information regarding their selectivity is not complete in the in vivo animal models. The purpose of the present investigation was to study the cardiovascular effects of microinjections of some of these mGLUR agonists and antagonists into the nucleus tractus solitarius (nTS). Microinjections (100 nl) of EC(50) concentrations of 3,5-DHPG (0.005 mM; mGLUR(1) agonist), APDC (17.3 mM; mGLUR(2/3) agonist), PPG (11.7 mM; mGLUR(8) agonist) and L-AP(4) (1 mM; mGLUR(4) agonist) into the nucleus tractus solitarius of urethane-anesthetized male Wistar rats elicited depressor and bradycardic responses which may be mediated by pre- and/or postsynaptic mechanisms. The blocking effect of mGLUR antagonists used here was not specific for any one type of glutamate receptors (GLURs). For example, AIDA (50 mM; mGLUR(1) antagonist) blocked the effects of EC(50) concentrations of 3,5-DHPG, and PPG. LY341495 (135 mM; mGLUR(2/3) antagonist) blocked all of the mGLURs and ionotropic GLURs. EGLU, APICA and MCCG (250 mM each; mGLUR(2/3) antagonists) blocked the effects of APDC, NMDA and AMPA.
3.Characterisation of mGluRs which modulate nociception in the PAG of the mouse.
Maione S;Marabese I;Leyva J;Palazzo E;de Novellis V;Rossi F Neuropharmacology. 1998 Dec;37(12):1475-83.
The contribution of metabotropic glutamate receptors (mGluRs) to the modulation of nociception by the periaqueductal gray (PAG) matter was investigated in mice. Intra-PAG microinjection of (IS,3R)-ACPD, an agonist of groups I and II mGluRs, as well as (S)-3,5-DHPG, a selective agonist of group I mGluRs, increased the latency of the nociceptive reaction (NR) in the hot plate test. (RS)-AIDA, an antagonist of group I mGluRs, antagonized the effect of (S)-3,5-DHPG, but changed the effect induced by (1S,3R)-ACPD in that a decrease in the latency for the NR could now be observed. L-CCG-I and L-SOP, which are agonists of groups II and III mGluRs respectively, decreased the latency of the NR. (2S)-alpha-EGlu and (RS)-alpha-MSOP, which are antagonists of groups II and III mGluRs, respectively, antagonized the effect of L-CCG-I and L-SOP. (RS)-AIDA and (RS)-alpha-MSOP alone decreased and increased, respectively, the latency of the NR with the highest doses used. (2S)-alpha-EGlu alone did not change significantly the latency of the NR. Intra-PAG microinjection of LH, an agonist of ionotropic glutamate receptors, induced a dose-dependent analgesia which was blocked by pretreatment with DL-AP5, a selective antagonist of NMDA receptors.
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CAS 66515-29-5 MSOP

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