{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T14:57:27Z","timestamp":1773673047493,"version":"3.50.1"},"reference-count":56,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2005,9]]},"abstract":"<jats:p> We investigated the mechanisms of presynaptic inhibition of GABAergic neurotransmission by group III metabotropic glutamate receptors (mGluRs) and GABA<jats:sub>B<\/jats:sub> receptors, in dopamine (DA) neurons of the substantia nigra pars compacta (SNc). Both the group III mGluRs agonist l-(+)-2-amino-4-phosphonobutyric acid (AP4, 100 \u03bcM) and the GABA<jats:sub>B<\/jats:sub> receptor agonist baclofen (10 \u03bcM) reversibly depressed the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) to 48.5 \u00b1 2.7 and 79.3 \u00b1 1.6% (means \u00b1 SE) of control, respectively. On the contrary, the frequency of action potential-independent miniature IPSCs (mIPSCs), recorded in tetrodotoxin (TTX, 1 \u03bcM) and cadmium (100 \u03bcM) were insensitive to AP4 but were reduced by baclofen to 49.7 \u00b1 8.6% of control. When the contribution of voltage-dependent calcium channels (VDCCs) to synaptic transmission was boosted with external barium (1 mM), AP4 became effective in reducing TTX-resistant mIPSCs to 65.4 \u00b1 3.9% of control, thus confirming a mechanism of presynaptic inhibition involving modulation of VDCCs. Differently from AP4, baclofen inhibited to 58.5 \u00b1 6.7% of control the frequency mIPSCs recorded in TTX and the calcium ionophore ionomycin (2 \u03bcM), which promotes Ca<jats:sup>2+<\/jats:sup>-dependent, but VDCC-independent, transmitter release. Moreover, in the presence of \u03b1-latrotoxin (0.3 nM), to promote a Ca<jats:sup>2+<\/jats:sup>-independent vesicular release of GABA, baclofen reduced mIPSC frequency to 48.1 \u00b1 3.2% of control, while AP4 was ineffective. These results indicate that group III mGluRs depress GABA release to DA neurons of the SNc through inhibition of presynaptic VDCCs, while presynaptic GABA<jats:sub>B<\/jats:sub> receptors directly impair transmitter exocytosis. <\/jats:p>","DOI":"10.1152\/jn.00171.2005","type":"journal-article","created":{"date-parts":[[2005,6,8]],"date-time":"2005-06-08T20:25:12Z","timestamp":1118262312000},"page":"1992-2003","source":"Crossref","is-referenced-by-count":22,"title":["Distinct Mechanisms of Presynaptic Inhibition at GABAergic Synapses of the Rat Substantia Nigra Pars Compacta"],"prefix":"10.1152","volume":"94","author":[{"given":"Michela","family":"Giustizieri","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Giorgio","family":"Bernardi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicola 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