Figure 2.

Voltage-dependent component of evoked excitatory post-synaptic potential (EPSP)-induced SCRs. (A) Single or multiple evoked EPSPs (black), in absence of pharmacological isolation, and relative Fluo 4 traces (green). Traces are baseline-adjusted to facilitate comparison. Single EPSPs are not able to elicit detectable SCRs (left). A short EPSP train (10 Hz/1 s) is able to elicit a measurable SCR (middle). Twenty hertz/two seconds stimulation protocols elicit prolonged, slow-decaying, but not saturating, SCRs (right). (B) multiEPSP and relative SCRs recorded before (left) and after superfusion with GABA_A, GABA_B and metabotropic glutamate receptors 1 (mGlu1) receptor antagonists (SR95531, 10 μM; CGP55485, 1 μM and CPCCOEt, 1 μM; middle). Subsequent administration of AMPA and NMDA receptor antagonists (NBQX, 10 μM; D-APV, 50 μM) fully abolishes the SCR (right). Note that voltage and optical traces have different time scales. (C) The amplitude of first EPSP does not change during 10 min of synaptic stimulation with the 10 Hz/1 s protocol in presence of GABA_A–B and mGlu1 antagonists. (D) Characterization of Ih-positive, putative DAergic neurons in the ventral tegmental area (VTA) based on the electrophysiological response to bath application of the GABA_B agonist baclofen (1 μM). The inset shows the whole-cell current in response to a −95 mV step. Eight/nine neurons showing I ≥ 200 pA responded to baclofen. Ih-negative, presumed non-DAergic neurons do not respond to baclofen (blue traces).