title: [Regulation of 3H-dopamine release by presynaptic GABA and glutamate heteroreceptors in the synaptosomes of the rat nucleus accumbens].
abstract: The influence of GABA, muscimol, delta-aminolevulinic acid (DALA), baclofen and L-glutamate on K+-evoked release of 3H-dopamine (3H-DA) from the rat brain n. accumbens crude synaptosomal fraction was studied in superfusion experimental conditions. Both GABA-receptor agonists--GABA and muscimol (50 microM) depressed the 3H-DA release by bicuculline- and picrotoxin-sensitive manner. On the contrary, glutamate, DALA and baclofen led to the increase in 3H-DA efflux independently of the presence of GABA-receptor antagonists. While the action of glutamate was antagonized by glutamate-receptor blocker--glutamic acid diethyl ester (GDEE), the effects of DALA and baclofen were suppressed upon adding to superfusion medium of GABA uptake inhibitors (nipecotic acid and 2,4-diaminobutyric acid) but not GDEE. The data obtained demonstrate that 3-H-DA secretion from n. accumbens is inhibited by GABA- and stimulated by glutamate-heteroreceptors. At the same time the mechanism of interaction between baclofen, DALA and GABA-uptake blockers effects with 3H-DA release needs special investigations.
mesh_terms: D000818:Animals; D004298:Dopamine / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism*; D008297:Male; D009714:Nucleus Accumbens / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism*; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism*; D012686:Septal Nuclei / Q000378:metabolism*; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism*; D014316:Tritium
chemical_list: D005971:Glutamates; D011963:Receptors, GABA-A; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter; D014316:Tritium; D004298:Dopamine
vernacular_title: Reguliatsiia vysvobozhdeniia 3H-dofamina presinapticheskimi geteroretseptorami GAMK i glutamata v sinaptosomakh prilezhashchego iadra mozga.