6533b7dcfe1ef96bd12733b6

RESEARCH PRODUCT

Interaction Between Uridine and GABA-Mediated Inhibitory Transmission: Studies In Vivo and In Vitro

Vincenzo La BellaP. GuarneriRosa GuarneriFederico Piccoli

subject

MaleSynaptic MembranesNeurotransmissionPharmacologyBicucullineInhibitory postsynaptic potentialHippocampusSynaptic Transmissiongamma-Aminobutyric acidchemistry.chemical_compoundThalamusGABA receptorSeizuresIn vivomedicineAnimalsCyclic GMPUridinegamma-Aminobutyric AcidNeurotransmitter AgentsBicucullineReceptors GABA-AUridineIn vitroFrontal LobeRatsnervous systemNeurologychemistryBiochemistryNeurology (clinical)medicine.drug

description

Na+-independent [3H]gamma-aminobutyric acid (GABA) binding to membrane preparations from frontal cortex, hippocampus, and thalamus is competitively inhibited by the in vitro addition of a naturally occurring pyrimidinic compound, uridine. Moreover, the intraperitoneal injection of uridine produces a dose-related decrease in the cerebellar content of cyclic GMP and antagonizes its increase elicited by bicuculline. The pyrimidinic compound also shows an antagonism toward bicuculline-induced seizures. The relationship between the anti-convulsant actions of uridine and GABA-mediated inhibitory neurotransmission is discussed in terms of an activation of GABA receptor function by the naturally occurring pyrimidinic compound.

yearjournalcountryeditionlanguage
1985-11-01Epilepsia
https://doi.org/10.1111/j.1528-1157.1985.tb05709.x