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1  3R-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD).
2 2 inside neurones diminished the response to 1S,3R-ACPD.
3 ed the size of the inward current induced by 1S,3R-ACPD.
4 onductance, closely resembling the effect of 1S,3R-ACPD.
5 enous AMPA was not significantly affected by 1S,3R-ACPD.
6 because 4-AP occluded any further actions of 1S,3R-ACPD.
7 septal injection of the metabotropic agonist 1S,3R-ACPD.
8 shold Ca2+ currents were also suppressed by (1S,3R)-ACPD.
9 mGluR research have made use of the agonist (1S,3R)-ACPD.
10 eurons mimicked the postsynaptic effects of (1S, 3R)-ACPD.
11 nocyclopentane-trans-1,3-dicarboxylic acid [(1S, 3R)-ACPD, 0.5 nmol/side] and amphetamine (AMPH, 6.8
12 S,3R)-1-aminocyclopentane-1,3-dicarboxylate (1S,3R)-ACPD, 1), was found to possess relatively high af
13                                          The 1S,3R-ACPD (100-900 nmol) induced death of striatal neur
14 R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) (100 microM) is suppression of I(D) by accel
15 studies of ABHxD-I (6a), ABHD-VI, LY354740, (1S,3R)-ACPD, (1S, 3S)-ACPD, and l-glutamate, we conclude
16 )-1-aminocyclopentane-1,3-decarboxylic acid (1S,3R-ACPD; 200 microM), quisqualate (10 microM) and (2S
17                                          The 1S,3R-ACPD (50-200 microM)-induced inward current was as
18 nonselective group I/group II mGluR agonist (1S,3R)-ACPD ((-)-9 ED50 = 19 mg/kg, (-)-10 ED50 = 14 mg/
19                  In contrast, application of 1S,3R-ACPD, a mixed agonist at group I and group II mGlu
20                                             (1S,3R)-ACPD also depolarized trigeminal motoneurons and
21 e tested, the metabotropic glutamate agonist 1S,3R-ACPD also activated inwardly rectifying Ba2+-sensi
22 )-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD), an agonist for metabotropic glutamate recep
23                 The postsynaptic effects of (1S,3R)-ACPD and repetitive stimulation were both antagon
24 ve to 100-200 microM 4-AP was accelerated by 1S,3R-ACPD, and because 4-AP occluded any further action
25 ponse to the local application of serotonin, 1S,3R-ACPD, and CCK8S, and a rapid depolarization follow
26 dy, we investigated whether these actions of 1S,3R-ACPD are attributable to the release of calcium fr
27                               Interestingly, 1S,3R-ACPD attenuated internucleosomal DNA fragmentation
28 and require extracellular Ca2+, but that the 1S,3R-ACPD current may depend on Ca2+ influx via voltage
29 )-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) depolarized all neurones tested by activatio
30                                             (1S,3R)-ACPD depressed excitatory transmission to trigemi
31                     Moreover, Ba2+, occluded 1S,3R-ACPD effects.
32                                          The 1S,3R-ACPD exchange current requires extracellular Ca2+
33 1-amino-1,3-cyclopentane-dicarboxylic acid [(1S,3R)-ACPD], group I/II antagonist (+/-)-alpha-methyl-4
34 of the alpha,alpha-dialkyl-alpha-amino acid (1S,3R)-ACPD has been achieved using an alkylidene carben
35 -1-amino-1, 3-cyclopentanedicarboxylic acid (1S,3R-ACPD) has multiple actions on phrenic motoneurons
36 ent with the hypothesis that quisqualate and 1S,3R-ACPD in Ba2+ and Cs+ solution activate a Na(+)-Ca2
37                                              1S,3R-ACPD induced internucleosomal DNA fragmentation of
38                     Intraseptal injection of 1S,3R-ACPD induced the expression of Fos-like, Jun B-lik
39                            (S)-MCPG blocked (1S,3R)-ACPD-induced IPSC suppression and markedly reduce
40 Many other similarities between DSI and the (1S,3R)-ACPD-induced suppression of IPSCs also were found
41                                          The 1S,3R-ACPD-induced current was reduced by the heavy meta
42 a S inside neurones irreversibly blocked the 1S,3R-ACPD-induced current whilst photolysis of caged GT
43 These data suggest that the quisqualate- and 1S,3R-ACPD-induced currents are mediated through a rise
44       In the presence of Ba2+, Iacpd and the 1S,3R-ACPD-induced decrease of membrane conductance were
45 urrent evoked by baclofen (10 microM) or the 1S,3R-ACPD-induced inward current associated with decrea
46                         The quisqualate- and 1S,3R-ACPD-induced inward currents were reduced in Ca(2+
47  100 mM choline reduced the quisqualate- and 1S,3R-ACPD-induced inward currents, results consistent w
48                   These results suggest that 1S,3R-ACPD-induced reduction of inspiratory synaptic cur
49                However, in Ba2+ and Cs+, the 1S,3R-ACPD inward current amplitude was enhanced and was
50 ate-induced current was not altered, but the 1S,3R-ACPD inward current was blocked.
51 Thus, elevation of [Ca2+]i, during firing by 1S,3R-ACPD is likely attributable to enhancement of calc
52 )-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) on synaptic transmission and excitability of
53 crease in locomotor activity in response to (1S, 3R)-ACPD or AMPH when these were microinjected into
54                                We found that 1S,3R-ACPD reduced the frequency but not the amplitude o
55 1-aminocyclopentane-1S,3R-dicarboxylic acid (1S,3R-ACPD) results in contralateral rotation with delay
56 -1-aminocyclopentane-1, 3-dicarboxylic acid (1S,3R-ACPD), suggesting they are not mediated via group
57 tivated an inward current more potently than 1S,3R-ACPD, suggesting that this current is preferential
58 )-1-aminocyclopentane-1,3-dicarboxylic acid (1S, 3R-ACPD), the group I mGlu receptor selective agonis
59 ion allowed the synthesis of the amino acid (1S,3R)-ACPD to be completed.
60 abotropic glutamate receptor (mGluR) agonist 1S,3R ACPD was used to stimulate PI turnover and to dete
61                  Rotation induced by DHPG or 1S,3R-ACPD was attenuated by group I antagonists, but no
62                  Rotation induced by DHPG or 1S,3R-ACPD was attenuated by pretreatment with antagonis
63 nternucleosomal DNA fragmentation induced by 1S,3R-ACPD was attenuated by the protein synthesis inhib
64               The inward current elicited by 1S,3R-ACPD was unaffected by K+ channel blockade with ex
65                  Furthermore, the effects of 1S,3R-ACPD were inhibited by the metabotropic antagonist
66                               The effects of 1S,3R-ACPD were mimicked by the group I metabotropic ago
67                               The effects of 1S,3R-ACPD were multiple, including reduction of inspira
68 R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) were characterized in the basolateral nucleu
69 )-1-amino-1,3-cyclopentanedicarboxylic acid (1S,3R-ACPD), were studied alone and together with N-meth

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