In the current study, we have characterized group I metabotropic glutamate (mGlu) receptor enhancement of 4-aminopyridine (4AP)-evoked [3H]glutamate release from rat cerebrocortical synaptosomes. The broad spectrum mGlu receptor agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid ((1S,3R)-ACPD, 10 microM) increased 4AP-evoked [3H]glutamate release (143.32+/-2.73% control) only in the presence of exogenously applied arachidonic acid; an effect reversed by the inclusion of bovine serum albumin (BSA, fatty acid free). In contrast, the selective group I mGlu receptor agonist (S)-3,5-dihydroxyphenylglycine (DHPG) potentiated (EC50 = 1.60+/-0.25 microM; Emax = 147.61+/-10.96% control) 4AP-evoked [3H]glutamate release, in the absence of arachidonic acid. This potentiation could be abolished by either the selective mGlu1 receptor antagonist (R,S)-1-aminoindan-1,5-dicarboxylic acid (AIDA, 1 mM) or the selective PKC inhibitor (Ro 31-8220, 10 microM) and was BSA-insensitive. The selective mGlu5 receptor agonist (R,S)-2-chloro-5-hydroxyphenylglycine (CHPG, 300 microM) was without effect. DHPG (100 microM) also potentiated both 30 mM and 50 mM K+ -evoked [3H]glutamate release (121.60+/-12.77% and 121.50 +/-4.45% control, respectively). DHPG (100 microM) failed to influence both 4AP-stimulated 45Ca2+ influx and 50 mM K+ -induced changes in synaptosomal membrane potential. Possible group I mGlu receptor suppression of tonic adenosine A1 receptor, group II/III mGlu receptors or GABA(B) receptor activity is unlikely since 4AP-evoked [3H]glutamate release was insensitive to the selective inhibitory receptor antagonists 8-cyclopentyl-1,3-dimethylxanthine, (R,S)-alpha-cyclopropyl-4-phosphonophenylglycine or CGP55845A, respectively. These data suggest an 'mGlu1 receptor-like' receptor potentiates [3H]glutamate release from cerebrocortical synaptosomes in the absence of exogenously applied arachidonic acid. This PKC dependent effect is unlikely to be via modulation of synaptosomal membrane potential or voltage-activated Ca2+ channels and not via a suppression of tonically active inhibitory adenosine A1 receptor, group II/III mGlu receptors or GABA(B) receptors.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0028-3908(98)00217-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dehydration increases sodium-dependent glutamate uptake by hypothalamic paraventricular nucleus synaptosomes.
Neuro Endocrinol Lett
April 2012
Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229-3900, USA.
Objectives: The purpose of this study was to identify and characterize Na+-dependent, high affinity glutamate transporter (GLUT) activity in the hypothalamic paraventricular nucleus (PVN) and to compare GLUT activity in PVN of euhydrated versus water-deprived rats.
Methods: Sprague-Dawley rats were deprived of water for two days before sacrifice. Control rats received water ad libitum.
Effects of antiepileptic drugs on glutamate release from rat and human neocortical synaptosomes.
Naunyn Schmiedebergs Arch Pharmacol
May 2011
Section of Clinical Neuropharmacology, Department of Neurosurgery, Albert-Ludwigs University, 79106, Freiburg, Germany.
Aim of this study was to learn whether the antiepileptic drugs (AEDs) carbamazepine, lamotrigine, phenytoin, gabapentin, pregabalin, levetiracetam, and valproate (all at 100 μM) presynaptically influence the neurotransmission of the excitatory transmitter glutamate. The effects of these frequently used AEDs were examined on ³H-glutamate release from superfused synaptosomes of both rat and human neocortex. Release was evoked by elevation of buffer [K(+)] from 3 to 15 mM or by the Na(+) channel activator veratridine (1, 3.
View Article and Find Full Text PDFOAT2 catalyses efflux of glutamate and uptake of orotic acid.
Biochem J
June 2011
Department of Pharmacology, University of Cologne, Gleueler Straße 24, 50931 Cologne, Germany.
OAT (organic anion transporter) 2 [human gene symbol SLC22A7 (SLC is solute carrier)] is a member of the SLC22 family of transport proteins. In the rat, the principal site of expression of OAT2 is the sinusoidal membrane domain of hepatocytes. The particular physiological function of OAT2 in liver has been unresolved so far.
View Article and Find Full Text PDFAgmatine modulates neuroadaptations of glutamate transmission in the nucleus accumbens of repeated morphine-treated rats.
Eur J Pharmacol
January 2011
Beijing Institute of Pharmacology and Toxicology, 27th Taiping Road, Beijing 100850, China.
It has been proved that agmatine inhibits opioid dependence, yet the neural mechanism remains unclear. In the present study, the effect of agmatine on the neuroadaptation of glutamate neurotransmission induced by morphine dependence, including changes of the extracellular glutamate level and glutamate receptors in the nucleus accumbens was investigated. We found that agmatine (2.
View Article and Find Full Text PDFGABA(B) receptors modulate depolarization-stimulated [³H]glutamate release in slices of the pars reticulata of the rat substantia nigra.
Eur J Pharmacol
December 2010
Departamento de Farmacología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnio Nacional, Apartado 14-740, México D.F., México.
GABA(B) receptors decrease the release of GABA from the striatal terminals within the pars reticulata of the substantia nigra by opposing the increase in the release caused by dopamine D₁ receptors. The dopamine D₁ receptors also increase the release of glutamate from subthalamic terminals in the pars reticulata. Because GABA(B) receptors decrease the glutamate release from these terminals, we have explored if the effect of GABA(B) receptors also opposed the effect of the dopamine D₁ receptors.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!