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. Author manuscript; available in PMC: 2010 Aug 2.
Published in final edited form as: Eur J Neurosci. 2008 Nov;28(10):2028–2040. doi: 10.1111/j.1460-9568.2008.06479.x

Fig. 1.

Fig. 1

Dopamine pharmacology of the effects of cocaine on VTA GABA neuron firing rate in vivo. (A) The ratemeter record shows the effects of saline and 0.5 mg/kg cocaine on a representative VTA GABA neuron with a baseline rate of ∼32 Hz. At this dose level, cocaine enhanced the firing rate of this neuron. (B) Cocaine significantly enhanced VTA GABA neuron firing rate at dose levels ≤ 0.5 mg/kg and modestly, but significantly, reduced firing rate at dose levels 1–2 mg/kg. Cocaine methiodide, which elicits cocaine's peripheral but not central effects, did not significantly alter firing rate at any dose level. Lidocaine significantly reduced firing rates at all cocaine dose levels. Methamphetamine significantly enhanced firing rate at all dose levels. *P < 0.05 and **P < 0.01. (C) Compared to saline microelectrophoresis, DA significantly increased firing rate 162% and microelectrophoretic application of the D2 antagonist eticlopride blocked DA activation. Intravenous administration of 1.0 mg/kg eticlopride blocked low-dose cocaine activation of firing rate, but not higher dose cocaine inhibition of firing rate. *P < 0.001 compared to saline control.