LOCALIZATION OF CHOLINERGIC NEURONS INVOLVED IN THE CARDIOVASCULAR-RESPONSE TO INTRATHECAL INJECTION OF CARBACHOL

Recent studies in this laboratory have demonstrated the ability of acetylcholine receptor agonists to produce systemic arterial presser responses through stimulation of spinal muscarinic receptors. In urethane-anesthetized rats a new surgical procedure was employed to permit microinjection of drugs into the cerebrospinal fluid surrounding the medulla without significant redistribution to spinal sites and vice versa. Pretreatment with intracisternal (medullary level) injection of 10 mu g of atropine significantly inhibited the expression of the presser response produced by intrathecal injection of 5 mu g of carbachol. This inhibition was due at least partly to the interruption of a medullary component of a spinobulbar pathway involving medullary muscarinic receptors. It was not due to redistribution of atropine from medullary to spinal sites since significant levels of atropine were not detected in the spinal cord after intracisternal injection of the drug. The remainder of the presser response to intrathecal carbachol after medullary muscarinic receptor blockade was most likely due to interactions within the spinal cord itself.