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Cellular/Molecular

Dopamine Excites Nucleus Accumbens Neurons through the Differential Modulation of Glutamate and GABA Release

Gregory O. Hjelmstad
Journal of Neuroscience 29 September 2004, 24 (39) 8621-8628; DOI: https://doi.org/10.1523/JNEUROSCI.3280-04.2004
Gregory O. Hjelmstad
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  •   Figure 3.
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    Figure 3.

    DA differentially modulates excitatory and inhibitory trains. A, DA preferentially inhibits early EPSCs in a train. Top traces are the average of five consecutive sweeps for control (black) and DA (gray) conditions from an example experiment. Calibration: 50 pA, 25 msec. The bar graph shows the average inhibition by DA for each EPSC in the train. *p < 0.05; repeated measures ANOVA; Student-Newman-Keuls (SNK) post hoc test. B, The effect of DA on EPSCs shows a strong frequency dependence. Circle at 0 Hz is the magnitude of inhibition of the initial EPSC. There is an overall effect of frequency on the amount of DA inhibition of the last EPSC (1-way ANOVA; p = 0.001). SNK post hoc test shows that only 25 and 50 Hz responses are not significantly different from each other. C, DA inhibits IPSCs throughout the train. Top traces are the average of five consecutive sweeps for control (black) and DA (gray) conditions from an example experiment. Calibration: 50 pA, 25 msec. The bar graph shows the average inhibition by DA for each IPSC in the train. *p < 0.05; repeated-measures ANOVA; SNK post hoc test. D, There is no significant effect of frequency on the amount of inhibition of the last IPSC in the train by DA. Circle at 0 Hz is the magnitude of inhibition of the initial IPSC. Error bars represent SEM.

  •   Figure 1.
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    Figure 1.

    EPSCs show short-term depression in response to a train. A, Example of a train of EPSCs (8 stimuli at 25 Hz) illustrating short-term depression at this synapse. Calibration: 50 pA, 25 msec. B, Average of responses for eight cells. C, In six cells in which trains of stimuli at three different frequencies were interleaved, the amount of short-term depression is frequency dependent (repeated-measures ANOVA; p < 0.001). D, Example of recovery from short-term depression. Overlay of averages of sweeps with four different recovery times (average of 8 individual responses). Dashed line represents the mean amplitude of the initial EPSC. Note that 800 msec after the train, the response has still not recovered to baseline. Calibration: 50 pA, 100 msec. E, Data from seven neurons fit with a single exponential. Error bars represent SEM.

  •   Figure 2.
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    Figure 2.

    IPSCs also show short-term depression in response to a train. A, Example of a train of IPSCs (8 stimuli at 25 Hz) illustrating short-term depression at this synapse. Calibration: 50 pA, 25 msec. B, Average of responses for eight cells. C, In six cells in which trains of stimuli at three different frequencies were interleaved, the amount of short-term depression is frequency dependent (repeated-measures ANOVA; p < 0.001). D, Example of recovery from short-term depression. Overlay of averages of sweeps with four different recovery times (average of 8 individual responses). Dashed line represents the mean amplitude of the initial IPSC. Note that by 800 msec after the train, the response has nearly recovered to baseline level. Calibration: 50 pA, 100 msec. E, Data from nine neurons fit with a single exponential. Error bars represent SEM.

  •   Figure 4.
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    Figure 4.

    Effect of DA antagonists on inhibition. A, Amount of inhibition of EPSCs by DA in the presence of the D1-selective antagonist SCH-23390 (left, 10 μm; n = 4) or the D2-selective antagonist sulpiride (right, 10 μm; n = 3). There was a significant effect of SCH-23390 (p < 0.01), but not of sulpiride, on the initial EPSC compared with controls. Dashed lines represent DA inhibition in control conditions. B, Amount of inhibition of IPSCs by DA in the presence of the D1-selective antagonist SCH-23390 (left, 10 μm; n = 3) or the D2-selective antagonist sulpiride (right, 10 μm; n = 3). There was a significant effect of SCH-23390 on both the first and last IPSC (p < 0.01 and p < 0.05, respectively). There was no significant effect of sulpiride. Error bars represent SEM.

  •   Figure 5.
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    Figure 5.

    Effect of Ca2+ channel blockers on excitatory and inhibitory trains. A, Average of five consecutive EPSCs under control conditions and in cadmium from an example experiment. B, Average inhibition of the first and last EPSC in a train after the application of a low dose (5-10 μm) of cadmium (n = 6). Both first and eighth EPSCs are significantly inhibited (p < 0.05). Calibration: 50 pA, 40 msec. C, Average of five consecutive IPSCs under control conditions and in cadmium from an example experiment. D, Average inhibition of the first and last IPSC in a 25 Hz train by cadmium. Both first and eighth IPSCs are significantly inhibited (p < 0.01). Calibration: 100 pA, 40 msec. Error bars represent SEM.

  •   Figure 6.
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    Figure 6.

    Effect of presynaptic inhibition on the recovery from short-term depression. A, The recovery from depression is slowed in the presence of cadmium (n = 4). Data were normalized to the initial IPSC in the train under control conditions. The data were fit with single exponentials. B, Bath application of DA (75 μm) also slows the time constant of recovery (n = 5). Error bars represent SEM.

  •   Figure 7.
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    Figure 7.

    Net effect of DA on trains is excitation. A, The net PSC (EPSC-IPSC normalized to the initial response in the train) versus stimulus number under control conditions and in DA indicate a shift toward excitation (hatched area). B, Membrane voltage of an integrate-and-fire model neuron with an excitatory and an inhibitory input (left) under control conditions and in DA. Conductance changes for synaptic responses were based on the example data in Figure 3 (see Materials and Methods for details).

  •   Figure 8.
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    Figure 8.

    DA increases spike probability. A, Top traces are individual traces from a cell-attached experiment during baseline (left) and in DA (right). Below is average of three experiments showing number of spikes in response to a train of eight stimuli at 25 Hz. Error bars represent SEM. B, Average probability of a spike for each stimulus in the train under control conditions (open symbols) and in DA (closed symbols). Data were calculated from a 2 min epoch represented by the arrows in A. C, IPSC recorded at +5 mV under control conditions, in the presence of DNQX (10 μm), and DNQX plus picrotoxin (100 μm). Calibration: 100 pA, 50 msec. D, The polysynaptic IPSC is determined by subtracting the IPSC recorded in DNQX from the control IPSC.

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The Journal of Neuroscience: 24 (39)
Journal of Neuroscience
Vol. 24, Issue 39
29 Sep 2004
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Dopamine Excites Nucleus Accumbens Neurons through the Differential Modulation of Glutamate and GABA Release
Gregory O. Hjelmstad
Journal of Neuroscience 29 September 2004, 24 (39) 8621-8628; DOI: 10.1523/JNEUROSCI.3280-04.2004

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Dopamine Excites Nucleus Accumbens Neurons through the Differential Modulation of Glutamate and GABA Release
Gregory O. Hjelmstad
Journal of Neuroscience 29 September 2004, 24 (39) 8621-8628; DOI: 10.1523/JNEUROSCI.3280-04.2004
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