title: Excitatory modulation by a spinal cholinergic system of a descending sympathoexcitatory pathway in rats.
abstract: Earlier studies have demonstrated that an excitatory cardiovascular response can be produced through activation of a spinal cholinergic system in rats. The present study was performed to determine whether this excitatory cardiovascular response was elicited through cholinergic potentiation of a descending spinal sympathoexcitatory pathway. Application of the cholinesterase inhibitor, neostigmine, directly to the surface of the spinal cord elicited increases in heart rate selectively when neostigmine was applied to upper thoracic segments (Th1-Th4), whereas all thoracic segments participated in the generation of the associated hypertensive response. The injection of a direct cholinergic agonist, carbachol, into an upper thoracic segment (Th2) produced tachycardic and pressor responses but only pressor responses when injected into a lower segment (Th11). Tachycardic responses occurred after injection of carbachol into the intermediolateral nucleus, a site between the intermediolateral nucleus and the central canal, the right lower dorsal horn and the ventral horn. At the Th11 level, carbachol increased blood pressure only when injected into sites between the intermediolateral nucleus and central canal. The pressor response, induced by electrical stimulation of the descending spinal sympathetic tract, was markedly potentiated at all stimulus strengths after intrathecal (i.t.) injection of neostigmine and this potentiation was antagonized by atropine. The accompanying tachycardic response to electrical stimulation was not affected when low stimulus strengths were employed but means increases in the heart rate, obtained in response to larger stimulus intensities, were eliminated after administration of neostigmine. These results are consistent with the presence of an intrinsic spinal cholinergic sympathoexcitatory pathway, possibly relegated to interneurons, which elicits cardiovascular responses, at least in part through potentation of descending sympathetic influences.
authors.affiliation: Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912-2300.
authors.forename: H
authors.initials: H
authors.lastname: Takahashi
authors.forename: J J
authors.initials: JJ
authors.lastname: Buccafusco
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002217:Carbachol / Q000494:pharmacology; D002802:Cholinesterases / Q000378:metabolism; D004525:Efferent Pathways / Q000187:drug effects / Q000502:physiology; D004558:Electric Stimulation; D006339:Heart Rate / Q000187:drug effects; D007278:Injections, Spinal; D008297:Male; D009388:Neostigmine / Q000008:administration & dosage / Q000494:pharmacology; D010275:Parasympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D013238:Stereotaxic Techniques
chemical_list: D009388:Neostigmine; D002217:Carbachol; D002802:Cholinesterases