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. 2001 Jun 1;21(11):4090–4103. doi: 10.1523/JNEUROSCI.21-11-04090.2001

Fig. 8.

Fig. 8.

mPFC suppresses Te3-evoked monosynaptic responses in projection neurons, and this suppression is attenuated by DA receptor activation. A, Te3 stimulation (0.7 mA, 0.3 msec duration) evokes a short-latency, presumably monosynaptic response in a BLA projection neuron. B1, Overlaid traces of 20 Te3-evoked responses demonstrate a relatively narrow distribution of latencies, consistent with a monosynaptic response. The stimulation intensity can be altered to evoke an ∼50% response probability.B2, mPFC stimulation (0.6 mA, 0.3 msec duration) 20 msec before Te3 stimulation decreases the probability of Te3-evoked responses, demonstrated by fewer evoked spikes in these traces.C1, After apomorphine administration (0.5 mg/kg, i.v.), the stimulation intensity of Te3 is altered until an ∼50% response probability is regained (to 0.7 mA). C2, After apomorphine administration, mPFC stimulation 20 msec before Te3 stimulation no longer produces the potent suppression of Te3-evoked responses. D, The response probabilities for the sample traces in B1–C2 are illustrated for this neuron.E, Overall, in the neurons tested (n= 23 of 27) Te3-evoked responses are significantly attenuated by mPFC stimulation, and this attenuation is removed by apomorphine administration (n = 6/7). F, The time course of the mPFC–Te3 interaction under control conditions (F1; * indicates a p < 0.05 significant difference relative to baseline Te3-evoked response probability) and after apomorphine administration (F2).