Article Figures & Data
Figures
- Fig. 1.
Histology. A, Schematic of coronal sections of the rat brain (Paxinos and Watson, 1997) showing representative placements of electrochemical electrodes (squares) and location of extracellular single-unit recording electrodes (circles) recorded from control rats and rats whose data are presented in Figure 3A–C.Numbers correspond to millimeters from bregma.B, Photograph of a representative placement of a stimulating electrode in the BLA. Arrow highlights the location of stimulating electrode placements. Opt, Optic tract.
- Fig. 2.
Tetanic stimulation of BLA afferents increases mesoaccumbens DA oxidation currents and enhances BLA-evoked spiking activity in NAc neurons. A, Mean changes in DA oxidation currents in the NAc recorded by chronoamperometry. ** denote significant difference from baseline (white circle) atp < 0.05. Error bars (+ SEM) are placed on those time points that were included in the data analysis. B, Mean percentage change (+SEM) in BLA-evoked spiking activity recorded from NAc neurons in the same animals from which the chronoamperometic recordings were obtained. Squares represent percentage change in BLA-evoked spiking probability normalized to the spike probability obtained 2 min before tetanus. Arrowheadsindicate time points at which trains of 2 Hz BLA stimulation were administered. ** denote significance versus baseline spike probability at p < 0.01. C, Peristimulus–time histograms showing the typical response from a NAc neuron 2 min before and 2, 10, and 20 min after BLA tetanus. This neuron displayed a baseline spiking probability of 0.54 (800 μA stimulation current). After BLA tetanus (gray bar), the spiking probability of the neuron was increased to nearly 1.0.Arrows represent time points when BLA stimulation was administered.
- Fig. 3.
Potentiation of BLA-evoked spiking activity in NAc neurons is dependent on both D1 and NMDA receptors.Symbols represent mean percentage change (+SEM) in BLA-evoked spiking activity of NAc neurons. A, Change in BLA-evoked spiking activity under control conditions (black squares, same as Fig. 2B), after treatment with the D1 receptor antagonist SCH23390 (0.5 mg/kg; black circles), and the D2 receptor antagonist sulpiride (5.0 mg/kg; white circles).Arrow indicates time point of drug injection.B, Change in BLA-evoked spiking activity recorded from NAc neurons after 25 min of 2 Hz stimulation in the absence of drug and for another 25 min after injection of SCH23390. Black circles represent time points when trains of 2 Hz stimulation were delivered to the BLA. In this experiment, no tetanus of the BLA was administered. Neither repeated trains of 2 Hz stimulation over 25 min nor injections of SCH23390 produced any significant change in evoked activity. C, Change in BLA-evoked spiking from control neurons (black squares, same as Fig.2B), after pretreatment with the NMDA receptor antagonist CPP (1.0 mg/kg; black squares).D, Change in BLA-evoked spiking activity after post-tetanus injection of SCH23390 (black circles) or CPP (gray squares). Arrowindicates time point when the drugs were administered (3 min after tetanus). * and ** denote significance from baseline spiking probabilities at p < 0.05 and 0.01, respectively.
- Fig. 4.
Individual data. A, Peristimulus–time histograms showing the typical response from a NAc neuron that was treated with SCH23390 iontophoretically (+40 nA) at time points 2 min before and 2, 10, and 20 min after BLA tetanus. This neuron displayed a baseline spiking probability of 0.34 (220 μA stimulation current). After BLA tetanus (gray bar), there was no potentiation of evoked-spiking activity.B, Peristimulus–time histograms showing the typical response from a NAc neuron recorded from an animal that had received intravenous administration of CPP (1.0 mg/kg) 10 min before tetanus. Histograms were taken from time points 2 min before and 2, 10, and 20 min after BLA tetanus. This neuron displayed a baseline spiking probability of 0.52 (480 μA stimulation current). After BLA tetanus (gray bar), there was no potentiation of evoked-spiking activity. For A and B,arrows represent time points when BLA stimulation was administered.
