Schematic illustrating the vSub and the mPFC interactions to the NAc. A, The NAc receives concomitant information from the mPFC and the vSub that are under dynamic regulation of the DA system from the VTA; DA facilitates vSub afferent input via D1 receptors and attenuates mPFC input via D2 receptors. B, Inhibition of the mPFC by TTX attenuates the ability of the vSub to drive spike firing in the NAc. In addition to a direct drive from the vSub, a contribution of the vSub–mPFC–NAc indirect pathway is necessary for the activation of the NAc by the vSub. C, If tetanic stimulation is first applied to the vSub, inactivation of the mPFC fails to affect the vSub–NAc pathway, suggesting that once the vSub–NAc pathway is enhanced via LTP, the mPFC is no longer required to drive spike firing. LTP in the vSub is apparently under the influence of D2 receptors expressed in the accumbens (dashed arrow). D, When the D2 receptor antagonist sulpiride is injected before the tetanic stimulation is applied to the vSub–NAc pathway, inactivation of mPFC reverses the vSub–NAc LTP. This suggests that D2 blockade restored the requirement of an intact vSub–mPFC–NAc pathway to enable direct activation of NAc by the vSub.
