ライフサイエンスコーパス: MCPG

1 MCPG by itself did not affect basal levels of either gen

2 MCPG in the doses given did not significantly affect the

3 Metabolites of hypoglycin A, MCPG, or both were detected in 48 [66%] of 73 urine spec

4 Although MCPG does antagonize the actions of the synthetic mGluR

5 BQX; (d) NMDA + MK-801; (e) AMPA; (f) AMPA + MCPG; (g) AMPA + MK-801; and (h) AMPA + NBQX.

6 ntagonists, i.e., NMDA + NBQX/MCPG or AMPA + MCPG/MK-801, was not significantly different from that p

7 farpur associated with both hypoglycin A and MCPG toxicity.

8 ns ranged from 12.4 mug/g to 152.0 mug/g and MCPG ranged from 44.9 mug/g to 220.0 mug/g.

9 ACPD reduced firing rate, and MCPG plus CPPG had an opposite effect, indicating that m

10 HPG, abolished by the competitive antagonist MCPG, and partially inhibited by mGluR1-selective allost

11 cking action of the group I mGluR antagonist MCPG [(RS)-alpha-methyl-4-carboxyphenylglycine, 50-500 m

12 The non-selective mGluR antagonist MCPG produced a dose-dependent inhibition of the cardiac

13 was blocked by the mGlu receptor antagonist MCPG.

14 NA in a small region, and mGluR antagonists (MCPG) did not affect localization.

15 esence of 4-AP required the presence of both MCPG and the ionotropic glutamate receptor antagonist ky

16 etitive stimulation were both antagonized by MCPG, suggesting that mGluRs were similarly activated in

17 ease evoked by mGluR agonists was blocked by MCPG, AIDA, 4-CPG, MPEP, and LY367385, a profile consist

18 This 3HPG effect was blocked by MCPG.

19 nhibitory effect of L-CCG-I was prevented by MCPG and by the group II/III mGluR antagonist (RS)-alpha

20 , (R, S)-alpha-methyl-4-carboxyphenyglycine (MCPG, 200-500 microM) reduced the current by 70%.

21 gonists alpha-methyl-4-carboxyphenylglycine (MCPG) and 1-aminoindan-1,5-dicarboxylic acid (AIDA) but

22 agonist alpha-methyl-4-carboxyphenylglycine (MCPG) and/or (RS)-alpha-cyclopropyl-4-phosphonophenylgly

23 ith (S)-alpha-methyl-4-carboxyphenylglycine (MCPG) did not result in shorter average spine length.

24 agonist alpha-methyl-4-carboxyphenylglycine (MCPG) does not block the actions of glutamate or APB.

25 ompound alpha-methyl-4-carboxyphenylglycine (MCPG) has been widely used to test the role of PI-couple

26 agonist alpha-methyl-4-carboxyphenylglycine (MCPG) strongly attenuated LTP, resulting in a response i

27 (R, S)-alpha-methyl-4-carboxyphenylglycine (MCPG) was infused into the hippocampus 30 min before fea

28 QX) and alpha-methyl-4-carboxyphenylglycine (MCPG) were evaluated against neuronal injury produced by

29 f (+/-)-alpha-methyl-4-carboxyphenylglycine (MCPG), a metabotropic glutamate receptor (mGluR) antagon

30 st, (S)-alpha-methyl-4-carboxyphenylglycine (MCPG), into the dorsal striatum at 10 but not 0.4 nmol s

31 agonist alpha-methyl-4-carboxyphenylglycine (MCPG).

32 ntagonist (S)-Methyl-4-carboxyphenylglycine (MCPG).

33 st (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG; 500 microM) and by the selective mGluR1/5 antagoni

34 ist (+)-alpha-methyl-4-carboxyphenylglycine (MCPG; 500 microM).

35 (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG; 1000 microM) but was greatly enhanced by the acety

36 P) attenuated LTP to a similar degree as did MCPG in wild-type slices, but MPEP did not alter the red

37 t (RS)-alpha-methyl-4-carboxyphenyl-glycine (MCPG).

38 However, MCPG at a dose of 5.0 microg/0.2 microl/side impaired th

39 However, MCPG did prevent the stimulation-dependent regulation of

40 etabotropic glutamate receptors (kynurenate, MCPG, CPPG and MAP4).

41 hypoglycin A or methylenecyclopropylglycine (MCPG), naturally-occurring fruit-based toxins that cause

42 f-EPSP is blocked by antagonists of mGluRs (MCPG) and PKC (calphostin-C, tamoxifen), suggesting that

43 inappropriate antagonists, i.e., NMDA + NBQX/MCPG or AMPA + MCPG/MK-801, was not significantly differ

44 rent drug combinations: (a) NMDA; (b) NMDA + MCPG; (c) NMDA + NBQX; (d) NMDA + MK-801; (e) AMPA; (f)

45 Addition of MCPG to the bath did not block EPSPs produced by stimula

46 results show that pretraining antagonism of MCPG-sensitive mGluRs in the hippocampus impaired contex

47 y, a nociception test indicated that dose of MCPG infused into the BLA did not affect the footshock s

48 d either vehicle or three different doses of MCPG (0.2, or 1.0, or 5.0 microg/0.2 microl/side, respec

49 No significant effects of MCPG were found on spontaneous or amphetamine-stimulated

50 ained intact despite pretraining infusion of MCPG.

51 (+/-)-alpha-methyl-4-carboxy-phenylglycine (MCPG), and group III agonist L-2-amino-4-phosphonobutano

52 (S)-MCPG blocked (1S,3R)-ACPD-induced IPSC suppression and m

53 rrent was inhibited reversibly by 1 mM (R,S)-MCPG or the non-competitive mGluR1 antagonist CPCCOEt (2

54 ist S-alpha-methyl-4-carboxyphenylglycine (S-MCPG).

55 se studies were based on the assumption that MCPG blocks the actions of glutamate at PI-coupled mGluR

56 In addition, we find that MCPG fails to block the NMDA receptor-dependent forms of

57 Our results indicate that MCPG, when infused into the BLA of rats prior to the tra

58 Activation of the MCPG-sensitive mGluRs is required for the upregulation o

59 etamine was not altered by pretreatment with MCPG.

60 Treating rats with MCPG did not affect context- or tone-specific fear durin