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.
|Number of pages||11|
|Journal||Journal of Neuroscience|
|Publication status||Published - Sep 1 1998|
- Dopamine neurons
- Excitatory postsynaptic currents
- L-type calcium channels
ASJC Scopus subject areas