CCK-induced inhibition of presympathetic vasomotor neurons: dependence on subdiaphragmatic vagal afferents and central NMDA receptors in the rat

Anthony J. M. Verberne , Daniela M. Sartor Am J Physiol Regul Integr Comp Physiol. 2004 Oct;287(4):R809-16. Epub 2004 May 20 “Systemic administration of cholecystokinin (CCK) inhibits a subpopulation of rostral ventrolateral medulla (RVLM) presympathetic vasomotor neurons”. The authors investigated whether the above effects are mediated by 1)Subdiaphragmatic vagal afferents. To test this, Lidocaine, a topical anesthetic was applied to the subdiaphragmatic branches of the vagus before and after injections of CCK, phenylbiguanide and phenylephrine. Application of lidocaine abolished the neuronal responses to CCK. 2) Central N-methyl-D-aspartic acid (NMDA) receptors. To test this, NMDA receptor antagonist, dizocilpine was given systemically. Central NMDA receptor blockade reduced the CCK induced inhibition of the RVLM presympathetic neuronal discharge. The authors suggest that CCK receptors located on subdiaphragmatic vagal afferents mediate the actions of CCK on the discharge of RVLM presympathetic vasomotor neuron. Also, central NMDA receptors mediates CCK-induced sympathoinhibition. Madhan