Glutamate activation of neurons within trigeminal nucleus caudalis increases adrenocorticotropin in the cat.

The role of trigeminal nucleus caudalis (Vc) in control of the autonomic and endocrine correlates of nociception was assessed in chloralose-anesthetized cats. Microinjections of the neuroexcitatory agent, L-glutamate (0.5 M), were directed at the marginal layers, at the central magnocellular portion, and at the deep magnocellular portion of Vc. Changes in the plasma concentration of adrenocorticotropin (ACTH), in mean arterial pressure, and in heart rate were examined. Glutamate excitation of neurons within the marginal layers of Vc evoked a significant (+143 +/- 52 pg/ml, P less than 0.01) increase in plasma ACTH during the 10 min postinjection sampling period. Glutamate injections into the deep magnocellular portion of Vc also increased plasma ACTH (+97 +/- 28 pg/ml, P less than 0.05), whereas activation of neurons in the central magnocellular portion of Vc had no consistent effect on plasma ACTH (-25 +/- 29 pg/ml, P greater than 0.10). Arterial pressure increased transiently after glutamate injections into the marginal layers or central magnocellular portion of Vc, whereas injections into the deep magnocellular portion of Vc did not affect arterial pressure. Heart rate increased transiently regardless of the laminar site of injection within Vc. These data indicate that activation of neurons in laminar regions of Vc that process nociceptive information cause an increase in plasma ACTH, whereas activation of neurons in laminae of Vc that process mainly non-nociceptive input have no significant influence on plasma ACTH.