Detail of "157381-42-5"

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Epileptogenesis in vivo enhances the sensitivity of inhibitory presynaptic metabotropic glutamate receptors in basolateral amygdala neurons in vitro

Epileptogenesis in vivo enhances the sensitivity of inhibitory presynaptic metabotropic glutamate receptors in basolateral amygdala neurons in vitro. Neugebauer, Volker; Keele, N. Bradley; Shinnick-Gallagher, Patricia ( Department of Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, TX 77555-1031, USA). Journal of Neuroscience, 17(3), 983-995 (English) 1997 Society for Neuroscience. CODEN: JNRSDS. ISSN: 0270-6474. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 1 Modulation of excitatory synaptic transmission by presynaptic metabotropic glutamate receptors (mGluRs) was examd. in brain slices from control rats and rats with amygdala-kindled seizures. Using whole-cell voltage-clamp and current-clamp recordings, this study shows for the first time that in control and kindled basolateral amygdala neurons, two pharmacol. distinct presynaptic mGluRs mediate depression of synaptic transmission. Moreover, in kindled neurons, agonists at either group II- or group III-like mGluRs exhibit a 28- to 30-fold increase in potency and suppress synaptically evoked bursting. The group II mGluR agonist (2S,3S,4S)-2-(carboxycyclopropyl)glycine (L-CCG) dose-dependently depressed monosynaptic EPSCs evoked by stimulation in the lateral amygdala with EC50 values of 36 nM (control) and 1.2 nM (kindled neurons). The group III mGluR agonist L-2-amino-4-phosphonobutyrate (L-AP4) was less potent, with EC50 values of 297 nM (control) and 10.8 nM (kindled neurons). The effects of L-CCG and L-AP4 were fully reversible. Neither L-CCG (0.0001-10 mM) nor L-AP4 (0.001-50 mM) caused membrane currents or changes in the current-voltage relationship. 157141-16-7 and 157381-42-5 which are cas registry numbers of chemicals are mentioned. The novel mGluR antagonists (2S,3S,4S)-2-methyl-2-(carboxycyclopropyl)-glycine (MCCG; 100 mM) and (S)-2-methyl-2-amino-4-phosphonobutyrate (MAP4; 100 mM) selectively reversed the inhibition by L-CCG and L-AP4 to 81.3% and 65.3% of predrug, resp. MCCG and MAP4 (100-300 mM) themselves did not significantly affect synaptic transmission. The exquisite sensitivity of agonists in the kindling model of epilepsy and the lack of evidence for endogenous receptor activation suggest that presynaptic group II- and group III-like mGluRs might be useful targets for suppression of excessive synaptic activation in neurol. disorders such as epilepsy. .