L-type calcium channels mediate a slow excitatory synaptic transmission in rat midbrain dopaminergic neurons

Antonello Bonci, Pernilla Grillner, Nicola B. Mercuri, Giorgio Bernardi

Research output: Contribution to journalArticlepeer-review

Abstract

Patch pipettes were used to record whole-cell synaptic currents under voltage-clamp in dopaminergic neurons in slices of rat substantia nigra pars compacta and ventral tegmental area. We report that dihydropyridines (DHPs), L-type Ca2+ channel antagonists, depressed a slow EPSC (EPSC(slow)) evoked by a train of focally delivered electrical stimuli. In fact, the amplitude of the EPSC(slow) was reduced by the DHP antagonists nifedipine (1-100 μM), nimodipine (1-100 μM), and isradipine (30 nM-100 μM) in a concentration- dependent and reversible manner. On the other hand, Bay-K 8644 (1 μM), an L- type Ca2+ channel agonist, increased the EPSC(slow). The DHPs depressed the EPSC(slow) only when the high-frequency stimulation that was used to evoke this synaptic current lasted >70 msec. On the other hand, Bay-K 8644 increased the amplitude of the EPSC(slow) only when it was evoked by a train 2+ channels was changed by holding the neurons at - 100, -60, and +30 mV. Finally, a DHP-sensitive component of the EPSC(slow), could even be detected after the blockade of N-, Q-, and P-type Ca2+ channels by the combination of ω-conotoxin GVIA, ω-agatoxin IVA, and ω- conotoxin MVIIC. Taken together, these results indicate that under certain patterns of synaptic activity, L-type Ca2+ channels regulate the synaptic release of excitatory amino acids on the dopaminergic neurons of the ventral mesencephalon.

Original languageEnglish
Pages (from-to)6693-6703
Number of pages11
JournalJournal of Neuroscience
Volume18
Issue number17
Publication statusPublished - Sep 1 1998

Keywords

  • Dihydropyridines
  • Dopamine neurons
  • Electrophysiology
  • Excitatory postsynaptic currents
  • L-type calcium channels
  • Midbrain

ASJC Scopus subject areas

  • Neuroscience(all)

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