Properties of a projection pathway from the medial preoptic nucleus to the midbrain periaqueductal gray of the rat and its role in the regulation of cardiovascular function

In this study we examined (1) the effect of stimulation of the MPO on the firing activity of neurons in the FAG, (2) the role of glutamic acid in this interaction and, (3) whether reversible blockade of neuronal activity in the FAG by lidocaine can alter the effect of stimulation of the MPO on arterial blood pressure. Single pulse stimulation of the MPO produced a biphasic response in 2/32 cells and inhibited 3/32 cells. Train electrical stimulation excited 21/54 cells and inhibited 12/54 cells. The latencies to the onset of the excitatory and the inhibitory effects were not different, but the duration of the excitatory effect was slightly longer than that of the inhibitory effect. Chemical stimulation of the MPO excited 17/97 cells and inhibited 16/97 cells. The latency to onset of the excitatory response to stimulation of the MPO was longer but the duration was shorter than that of the inhibitory response. In 83% of the animals (29/35), stimulation of the MPO produced a decrease in mean arterial pressure (MAP). The duration of the response was 196.9 +/- 20.9 s and the average decrease in the MAP was 18.2 +/- 1.4 mmHg. Application of KYN blocked the excitatory response to stimulation of the MPO in 8/16 cells and the inhibitory response of 3/10 cells. Injection of lidocaine into the FAG by itself had no effect on the arterial blood pressure. However, in all animals (n = 10) lidocaine totally or significantly reduced the magnitude of the blood pressure change produced by stimulation of the MPO in a reversible manner. These studies electrophysiologically confirm a pathway between the MPO and the FAG that is, in part, under glutamatergic control. In addition, our results demonstrate that stimulation of the MPO produces a distinctive depressor effect that is mediated through the PAG.