Central nuclei and spinal pathways in feedback inhibitory spinal cord potentials in ketamine-anaesthetized rats

Abstract

It has been suggested that heterosegmentally activated slow positive potentials (HSP), recorded from the spinal cord of rat and humans, are feedback inhibitory potentials. The present study was carried out to define ascending and descending spinal tracts and the sites of central nuclei involved in the production of these HSP, and the effects of ketamine on these central nuclei. The spinal cords in ketamine-anaesthetized rats were transected to determine the ascending and descending tracts involved in the production of hindpaw (HP) and forepaw (FP) HSP, respectively. Lesions of the brain at various levels were performed stereotactically during ketamine anaesthesia. Dorsal one-third resection of the cord at the T8-9 level did not affect HSP significantly, while contralateral lesion of the dorsal two-thirds of the cord decreased FP-HSP but not HP-HSP during ketamine. Bilateral transection of the ventral one-third of the cord abolished both HSP. Ablation of the cerebral cortex, cerebellum, thalamus, midbrain and pons did not affect HSP significantly. However, transection of the middle medulla decreased, while transection of the most caudal part of the medulla completely abolished both HSP. Ketamine decreased HSP even in the medulla-spinal cord preparation and the segmental slow positive wave in spinalized animals. In ketamine-anaesthetized rats, ascending and descending spinal tracts involved in the production of HP-HSP and FP-HSP are located bilaterally in the ventrolateral quadrant and in the contralateral lateral funiculus and ventrolateral quadrant, respectively. Principal central nuclei feeding back HSP might be situated diffusely in the medulla down to the caudal part. Ketamine is suggested to suppress these inhibitory feedback potentials predominantly at, and partly even below, the level of the medulla.

The Effects of Isoflurane on Conditioned Inhibition by Dorsal Column Stimulation

“…Spinal transection by surgery and administration of drugs have proved this theory (17)(18)(19). Anesthetics are suggested to block the descending inhibitory action and thus modulate neuronal activities in the dorsal horn (17)(18)(19).…”

“…This study, however, demonstrated that the P2 wave was always inhibited by DCS. These different results may be due to the effects of ketamine on supraspinal structures, distinct from the wakeful state (19), because the effects of DCS on the N1 wave Figure 2. The effects of isoflurane and spinal cord transection on the conditioned inhibition of the segmental spinal cord potential (sgSCP) by dorsal column stimulation (DCS).…”

“…Anesthetic and surgical procedures were similar to those described in our previous studies (17)(18)(19). The study was performed on 22 male Sprague-Dawley rats weighing 330 -400 g. After an intraperitoneal injection of 120 mg/kg of ketamine hydrochloride with 0.1 mg/kg of atropine sulfate, intratracheal intubation was made through a tracheotomized orifice and connected to a Harvard animal ventilator (Harvard Apparatus, Holliston, MA).…”

“…Preliminary experiments had demonstrated that the electroencephalogram and somatosensory evoked potentials from the skull showed no significant changes with stable arterial blood pressure throughout several hours at this infusion rate of ketamine (17)(18)(19). A cannula was also inserted into the urinary bladder for monitoring urine volume.…”

“…The DCS from the posterior epidural space at upper spinal levels produces inhibition of the segmentally evoked negative wave (N1) and potentiation of the P2 wave after a transient inhibition in humans (16). There have been several reports about the effects of anesthetics on segmentally evoked SCPs (8,9,13,(17)(18)(19). Influences of the supraspinal structures on spinal sensory transmission in the spinal cord can be tested through the investigation of the modulatory actions of DCS by recording segmental SCPs (segSCPs) (16,18), because the N1 and P2 of segSCP are thought to reflect the synchronized activity of dorsal horn neurons and primary afferent depolarization (PAD), respectively (8 -13).…”