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Inhibitory and excitatory effects of adenosine on spontaneous locomotor activity in mice
LIFE SC
5'-N-ethylcarboxamido[8-3H]adenosine binds to two different adenosine receptors in membranes from the cerebral cortex of the rat
5-Hydroxytriptamine-14C and Dexamphetamine-14C uptake by fundal sarcolemma preparations and the problem of the common receptor.
An NK1 receptor-dependent component of the slow excitation recordered intracellularly from rat motoneirones following dorsal root stimulation
Demethyldiazepam and chlor-demethyldiazepam administered by different routes: comparative evaluation of hypnogenic and anticonvulsivant activities.
Depressive effects of Chamomilla recutita (L.) Rausch, tubular flowers, on Central Nervous System in mice.
Strain-related differences in adenosine receptor density and in behavioral sensitivity to adenosine analogs in mice
ADENOSINE-A1 RECEPTOR-MEDIATED INHIBITION OF EVOKED GLUTAMATE RELEASE IS COUPLED TO CALCIUM INFLUX DECREASE IN GOLDFISH BRAIN SYNAPTOSOMES
Abstract
Binding of [3H]cyclohexyladenosine (CHA) to the cellular fractions and P2 subfractions of the goldfish brain was studied. The A1 receptor density was predominantly in synaptosomal membranes. In goldfish brain synaptosomes (P2), 30 mM K+ stimulated glutamate, taurine and GABA release in a Ca2+-dependent fashion, whereas the aspartate release was Ca2+-independent. Adenosine, R-phenylisopropyladenosine (R-PIA) and CHA (100 μM) inhibited K+-stimulated glutamate release (31%, 34% and 45%, respectively). All of these effects were reversed by the selective adenosine A1 receptor antagonist, 8-cyclopentyltheophylline (CPT). In the same synaptosomal preparation, K+ (30 mM) stimulated Ca2+ influx (46.8±6.8%) and this increase was completely abolished by pretreatment with 100 nM ω-conotoxin. Pretreatment with 100 μM R-PIA or 100 μM CHA, reduced the evoked increase of intra-synaptosomal Ca2+ concentration, respectively by 37.7±4.3% and 39.7±9.0%. A possible correlation between presynaptic A1 receptor inhibition of glutamate release and inhibition of calcium influx is discussed
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