L-CCG-l - CAS 117857-93-9
Category: Inhibitor
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Molecular Formula:
C6H9NO4
Molecular Weight:
159.14
COA:
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Targets:
mGluR
Description:
L-CCG-l is a potent group II metabotropic glutamate receptor (mGluR) agonist.
Brife Description:
group II mGluR agonist
Purity:
≥99% by HPLC
Synonyms:
(2S,1'S,2'S)-2-(Carboxycyclopropyl)glycine; (1S,2S)-2-[(S)-amino(carboxy)methyl]cyclopropane-1-carboxylic acid
MSDS:
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InChIKey:
GZOVEPYOCJWRFC-HZLVTQRSSA-N
InChI:
InChI=1S/C6H9NO4/c7-4(6(10)11)2-1-3(2)5(8)9/h2-4H,1,7H2,(H,8,9)(H,10,11)/t2-,3-,4-/m0/s1
Canonical SMILES:
C1C(C1C(=O)O)C(C(=O)O)N
1.Quisqualate induces an inward current via mGluR activation in neocortical pyramidal neurons.
Chu Z;Hablitz JJ Brain Res. 2000 Oct 6;879(1-2):88-92.
Activation of metabotropic glutamate receptors (mGluRs) has multiple effects on the excitability of pyramidal neurons in rat frontal neocortex. Synaptic transmission and intrinsic excitability are both affected. During studies of the effects of quisqualate on synaptic activity, it was observed that quisqualate also induced a slow inward current. Whole-cell patch clamp recordings were obtained from layer II/III pyramidal neurons of neocortical slices in vitro. The bath solution contained APV, CNQX and bicuculline to block ionotropic glutamate and GABA(A) receptors. At a holding potential of -70 mV, quisqualate (2 microM) induced an inward current of about 60 pA. The response was reversible upon washing. This current was associated with an increase in membrane conductance and was still seen in the presence of TTX (0.5 microM). Bath application of the nonselective mGluR antagonist, (R, S)-alpha-methyl-4-carboxyphenyglycine (MCPG, 200-500 microM) reduced the current by 70%. Other mGluR agonists (ACPD, DHPG, L-CCG-1 and L-AP4) did not induce a significant inward current at the concentrations tested. The current-voltage relation of the quisqualate-induced current was linear with a reversal potential near 0 mV suggesting involvement of nonselective cation channels.
2.A metabotropic L-glutamate receptor agonist: pharmacological difference between rat central neurones and crayfish neuromuscular junctions.
Shinozaki H;Ishida M Comp Biochem Physiol C. 1992 Sep;103(1):13-7.
1. 2S,3S,4S-2-(carboxycyclopropyl)glycine (L-CCG-I), a conformationally restricted glutamate analogue, is a potent metabotropic L-glutamate receptor agonist in the mammalian central nervous system. 2. Depolarizing actions of L-CCG-I and trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD) in the newborn rat spinal motoneurone are temperature-sensitive, and are not depressed by 3-[(+/-)-2-carboxypiperazin-4-yl] propyl-1-phosphonic acid (CPP) and/or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). 3. L-CCG-I and trans-ACPD induced oscillatory responses in Xenopus oocytes injected with rat brain mRNA. Oocytes with oscillatory responses to L-CCG-I and trans-ACPD showed reversal potential of about -20 mV, which was very close to the equilibrium potential of chloride ions. 4. In rat hippocampal synaptoneurosomes, L-CCG-I stimulated phosphoinositide hydrolysis in a concentration dependent manner. L-CCG-I was less potent than quisqualate but more potent than trans-ACPD. 5. At low concentrations, L-CCG-I did not cause any depolarization of newborn rat spinal motoneurones, but reduced substantially amplitudes of monosynaptic reflexes. 6. At the crayfish neuromuscular junction L-CCG-I, acting presynaptically, reduced the amplitude of excitatory junctional potentials.
3.The effects of DCG-IV and L-CCG-1 upon phencyclidine (PCP)-induced locomotion and behavioral changes in mice.
Tomita N;Murata M;Watanabe H;Ichikawa T;Washiyama K;Kumanishi T;Takahashi Y Ann N Y Acad Sci. 2000 Sep;914:284-91.
The behavioral changes of mice induced by acute and repeated i.p. injection of phencyclidine (PCP) were observed by measuring locomotor activity and stereotyped behavior. Then, the effects of metabotropic glutamate receptor (mGluR) agonists, DCG-IV and L-CCG-1, on the above behavioral changes induced by PCP were found. The effects of DCG-IV were very strong and completely depressed the PCP-induced hyperlocomotion. The effects of L-CCG-1 were not so strong. Repeated injection of PCP for 20 days into mice induced lower locomotor activity than that in acutely injected mice. These behavioral changes may be related with the negative symptoms of schizophrenia. In order to examine some molecular mechanisms of PCP-induced behavioral changes, Northern blot analysis of total RNA from prefrontal cortical tissues of mice treated with PCP, DCG-IV, and L-CCG-1 was carried out.
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Chemical Structure

CAS 117857-93-9 L-CCG-l

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