Figure 9.

Diagrammatic representation of the differential control of Prl release by AEA in male, OVX, and OVX-E rats. As can be seen, AEA acts on CB1 receptors on TIDA neurons to increase release of DA into portal vessels, which reaches the lactotropes to inhibit Prl release by action on D2 DA receptors in male rats (A), whereas in OVX animals, AEA also acts on the DA neurons, but this time the action on the CB1 receptor causes inhibition of DA release slightly decreasing inhibitory DA control over Prl release, but with little effect on Prl release. In OVX-E animals, AEA neurons activate CB1 receptors on DA neurons to inhibit DA release, resulting in a reduction in DA inhibitory tone on the lactotrope; however, because the effect on Prl is not matched by a larger decrease in DA tone, other transmitters are probably partially responsible for the elevated Prl in the OVX-E animals under resting or AEA-stimulated conditions. The inhibitor of AEA action lowered basal Prl and blocked the action of AEA in the OVX-E animals, indicating that AEA is a synaptic transmitter that acts on CB1 receptors to increase plasma Prl in OVX-E rats. 3V, third ventricle; AEAN, AEA neuron; CB1 R, CB1 receptors; DAN, dopaminergic neuron; PV, hypophyseal portal veins; ME, median eminence; D2 R, DA type 2 receptors; LAC, lactotropes; +, increase; −, decrease; ∼, little or no change.