Spinal Cord Glucose Utilization Research Articles

Distribution of Spinal Sensitization Evoked by Inflammatory Pain Using Local Spinal Cord Glucose Utilization Combined with (3) H-Phorbol 12,13-Dibutyrate Binding in Rats.

Aims. Hyperalgesia following tissue injury is induced by plasticity in neurotransmission. Few investigators have considered the ascending input which activates the superficial of spinal cord. The aim was to examine neurotransmission and nociceptive processing in the spinal cord after mustard-oil (MO) injection. Both in vitro and in vivo autoradiographs were employed for neuronal activity and transmission in discrete spinal cord regions using the 14C-2-deoxyglucose method and 3H-phorbol 12,13-dibutyrate (3H-PDBu) binding sites. Methods. To quantify the hyperalgesia evoked by MO, the flinching was counted for 60 min after MO (20%, 50 μL) injection in Wistar rats. Simultaneous determination of 14C-2-deoxyglucose and 3H-PDBu binding was used for a direct observation of neuronal/metabolic changes and intracellular signaling in the spinal cord. Results. MO injection evoked an increase in flinching for 60 min. LSCGU significantly increased in the Rexed I-II with 3H-PDBu binding in the ipsilateral side of spinal cord. Discussion. We clearly demonstrated that the hyperalgesia is primarily relevant to increased neuronal activation with PKC activation in the Rexed I-II of the spinal cord. In addition, functional changes such as “neuronal plasticity” may result in increased neuronal excitability and a central sensitization.

末梢炎症性疼痛における局所脊髄ブドウ糖代謝率およびプロテインキナーゼC結合の変動

末梢炎症性疼痛における局所脊髄ブドウ糖代謝率およびプロテインキナーゼC結合の変動

2-52-09 Exercise-induced changes in the spinal cord glucose utilization

2-52-09 Exercise-induced changes in the spinal cord glucose utilization

Post-injury treatment with GM1 ganglioside reduces nociceptive behaviors and spinal cord metabolic activity in rats with experimental peripheral mononeuropathy

In a rat model of painful peripheral mononeuropathy, this study examined the effects of post-injury treatment with a monosialoganglioside, GM1, on abnormal nociceptive behaviors and spinal cord neural activity resulting from loose ligation of the rat common sciatic nerve (chronic constructive injury, CCI). Thermal hyperalgesia and spontaneous pain behaviors of CCI rats were assessed by measuring foot-withdrawal latencies to radiant heat and by rating spontaneous hind paw guarding positions, respectively. Neural activity within different regions of the spinal cord was inferred in both CCI and sham-operated rats by employing the [ 14C]-2-deoxyglucose (2-DG) autoradiographic technique to measure spinal cord glucose metabolism. Intraperitoneal (i.p.) GM1 treatment (10 mg/kg) initiated 1 h or 24 h after injury and once daily for the first 9 post-injury days reduced thermal hyperalgesia of the hind paw ipsilateral to nerve ligation and lowered spontaneous pain behavior rating scores in CCI rats. Sciatic nerve ligation reliably increased basal 2-DG metabolic activity of CCI rats in all four sampled regions (laminae I–IV, V–VI, VII, VIII–IX) of spinal cord lumbar segments (L 2–L 5) both ipsilateral and contralateral to nerve ligation 10 days after injury. Consistent with the drug's effects on spontaneous pain behaviors, 10 daily GM1 treatments (10 mg/kg, i.p.) initiated 1 h after nerve ligation reduced spinal cord 2-DG metabolic activity in laminae V–VI and VII ipsilateral to nerve ligation and in all four sampled regions contralateral to nerve ligation. This attenuation of the increased spinal cord glucose utilization that occurs in the absence of overt peripheral stimulation may reflect an influence of GM1 on increased neural activity contributing to spontaneous pain. Since gangliosides are thought to protect neurons from excitotoxic effects of excitatory amino acids, these results suggest that ganglioside treatment may result in attenuation of excitatory neurotoxicity that may occur following peripheral nerve injury. Thus, ganglioside treatment could provide a new approach to the clinical management of neuropathic pain syndromes following peripheral nerve injury.

Epidural Bupivacaine Suppresses Local Glucose Utilization in the Spinal Cord and Brain of Rats

Using the 2-[14C]deoxyglucose method, the effects of analgesic doses of epidural bupivacaine (300 micrograms) on local spinal cord glucose utilization (SP-LGU) of the cervical, thoracic, and lumbar regions and local cerebral glucose utilization (BR-LGU) in 38 brain structures were examined in conscious rats. In addition, the effects of intramuscular bupivacaine (300 micrograms) and the spinal cord transection (T2) were examined to determine whether the induced metabolic changes, if any, are related to the drug's systemic effect and/or deafferentation. Lumbar epidural bupivacaine sufficient to produce analgesia decreased SP-LGU in the thoracic (18-28%) and lumbar (21-29%) spinal cord but not in the cervical cord. Epidural bupivacaine decreased BR-LGU (15-26%) in 35 of 38 structures examined. With intramuscular bupivacaine, SP-LGU remained unchanged in almost all regions, while BR-LGU was significantly decreased (11-23%) in 23 structures. Plasma concentrations of bupivacaine in the epidural and intramuscular groups were comparable. With spinal cord transection alone, SP-LGU significantly decreased with varying degrees depending on the structure examined, but BR-LGU did not decrease in 36 of 38 structures examined. These results indicate that analgesic doses of epidural bupivacaine decrease SP-LGU, probably reflecting decreased neuronal activity of the spinal cord, and that reduced BR-LGU by epidural bupivacaine is most likely due to the drug's systemic effect rather than deafferentation.

Glucose utilization and reflex activity of the transected rat spinal cord

Spinal cord glucose utilization (SCGU) of gray and white matter was studied with the quantitative autoradiography [ 14C]2-deoxyglucose methodology, below and above a complete low thoracic transection. One day after transection, a generalized decrease in SCGU was observed in gray matter, particularly marked in the dorsal horn of the lumbar cord. A progressive increase in SCGU was observed thereafter. Values reached levels greater than those of non-transected controls by 2 and 4 weeks after the intervention in ventral horn of the lumbar cord, and ventral and dorsal horn of the cervical cord. A similar behavior of SCGU was observed in white matter of transected animals. The development of 17 lumbar reflex modalities was quantified between days 1 and 28 after spinal transection. The delay in emergence of these reflexes was related to their complexity. Correlation of reflex scores with SCGU was significant for all lumbar cord regions but linearity of this relationship was only observed in white matter. These results uncover a close relationship between SCGU and reflex activity of the spinal cord below a complete transection, particularly striking in white matter and suggests a role of the fasciculi proprii of the spinal cord in this phenomenon.

Local Spinal Cord Glucose Utilization in Conscious and Halothane-Anesthetized Rats

Local Spinal Cord Glucose Utilization in Conscious and Halothane-Anesthetized Rats

Effect of profound hypermagnesemia on spinal cord glucose utilization in rats.

The purpose of our study was to investigate the effect of hypermagnesemia on spinal metabolic rate. The 2-[14C]deoxyglucose technique was used to measure regional glucose utilization in the lumbar spinal cord of paralyzed, mechanically ventilated rats receiving 70% nitrous oxide and an intravenous infusion of either saline (n = 5) or magnesium sulfate (n = 5). Plasma magnesium concentrations were 6.75 +/- 0.5 and 0.9 +/- 0.5 mM (p less than 0.01) in hypermagnesemic and control rats, respectively. Hypermagnesemic rats were hypotensive (88 +/- 1 vs. 130 +/- 4 mm Hg, p less than 0.01) but blood pressure remained within the autoregulatory range. Glucose utilization was reduced 26-45% in spinal gray matter and 53-63% in spinal white matter during hypermagnesemia. We conclude that magnesium is a potent spinal metabolic depressant and that this action, which is unusually prominent in spinal white matter, is a plausible explanation for the recently reported beneficial effect of magnesium therapy during spinal cord ischemia.

Spinal cord metabolic response to noxious radiant heat stimulation of the cat hind footpad

The 2-deoxy[ 14C]glucose (2-DG) method was used to study glucose utilization in the cat lumbar spinal cord during noxious thermal stimulation to the hind footpad. Spinal cord glucose utilization in stimulated cats was twice that of control animals. Diffusely increased metabolic activity was seen in the ipsilateral dorsal horn. The highest levels of 2-DG were seen in the ipsilateral ventral horn, while a moderate increase was seen in the contralateral ventral horn.

Spinal cord glucose utilization after experimental spinal cord injury

Metabolic alterations after experimental contusion injury of the spinal cord were evaluated by determining qualitative spinal cord glucose utilization (SCGU), SCGU was determined by the 2-deoxy-D-[14C]glucose technique. An increase in SCGU occurred at the site of maximal impact in the white matter after an injury causing paraparesis and in near trauma regions after an injury causing either paraparesis or paraplegia. These findings are most likely due to anaerobic glycolysis resulting from a reduction in blood flow that still allows delivery of substrate to tissue. Although an initial increase was observed at the site of maximal impact after a paraplegia-causing injury. SCGU in the white matter demonstrated a progressive deterioration by 4 and 8 hours after injury. A failure of substrate delivery resulting from ischemia is the most likely cause for this reduction in SCGU. The somatosensory evoked potential was found to be a very sensitive indicator of the remaining functional axons at the injury site. (Neurosurgery 9:40-47, 1981)

Spinal Cord Glucose Utilization after Experimental Spinal Cord Injury

Metabolic alterations after experimental contusion injury of the spinal cord were evaluated by determining qualitative spinal cord glucose utilization (SCGU), SCGU was determined by the 2-deoxy-D-[14C] glucose technique. An increase in SCGU occurred at the site of maximal impact in the white matter after an injury causing paraparesis and in near trauma regions after an injury causing either paraparesis or paraplegia. These findings are most likely due to anaerobic glycolysis resulting from a reduction in blood flow that still allows delivery of substrate to tissue. Although an initial increase was observed at the site of maximal impact after a paraplegia-causing injury, SCGU in the white matter demonstrated a progressive deterioration by 4 and 8 hours after injury. A failure of substrate delivery resulting from ischemia is the most likely cause for this reduction in SCGU. The somatosensory evoked potential was found to be a very sensitive indicator of the remaining functional axons at the injury site.

Distribution and tissue uptake of magnesium related to its pharmacological effects.

ARTICLESDistribution and tissue uptake of magnesium related to its pharmacological effectsMI Hilmy, and GG SomjenMI Hilmy, and GG SomjenPublished Online:01 Feb 1968https://doi.org/10.1152/ajplegacy.1968.214.2.406MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByStructural and functional disorders of hippocampus following ischemia/reperfusion in lower limbs and kidneysNeuroscience, Vol. 358Magnesium sulfate treatment for juvenile ferrets following induction of hydrocephalus with kaolin27 April 2016 | Fluids and Barriers of the CNS, Vol. 13, No. 1Special Treatments in Epilepsy10 January 2013Magnesium Sulfate for the Treatment of EclampsiaStroke, Vol. 40, No. 4Ion Regulation in the Brain: Implications for Pathophysiology29 June 2016 | The Neuroscientist, Vol. 8, No. 3Prevention of eclampsiaSeminars in Perinatology, Vol. 23, No. 1Magnesium Attenuates a Striatal Dopamine Increase Induced by Anoxia in the Neonatal Rat Brain: An in Vivo Microdialysis StudyPediatric Research, Vol. 41, No. 6The Effects of Plasma and Brain Magnesium Concentrations on Lidocaine-Induced Seizures in the RatAnesthesia & Analgesia, Vol. 83, No. 6Anticonvulsant effects of magnesium sulfate in hippocampal-kindled ratsJournal of Biomedical Science, Vol. 2, No. 1Oral magnesium intake reduces permanent hearing loss induced by noise exposureAmerican Journal of Otolaryngology, Vol. 15, No. 1Effect of Magnesium Sulfate on Eicosanoid Levels in Women with Pregnancy-Induced Hypertension7 July 2009 | Hypertension in Pregnancy, Vol. 13, No. 1Transfer of maternally administered magnesium sulfate into the fetal compartment of the rat: Assessment of amniotic fluid, blood, and brain concentrationsAmerican Journal of Obstetrics and Gynecology, Vol. 169, No. 2The effect of magnesium sulfate on maternal retinal blood flow in preeclampsia: A randomized placebo-controlled studyAmerican Journal of Obstetrics and Gynecology, Vol. 167, No. 6Peripheral magnesium sulfate enters the brain and increases the threshold for hippocampal seizures in ratsAmerican Journal of Obstetrics and Gynecology, Vol. 167, No. 6Effect of magnesium sulfate on maternal brain blood flow in preeclampsia: A randomized, placebo-controlled studyAmerican Journal of Obstetrics and Gynecology, Vol. 167, No. 3Anticonvulsant effects of magnesium sulfate on hippocampal seizures: Therapeutic implications in preeclampsia-eclampsiaAmerican Journal of Obstetrics and Gynecology, Vol. 166, No. 4Management of Severe Preeclampsia and EclampsiaCritical Care Clinics, Vol. 7, No. 4Effects of acute hypermagnesemia on the threshold for lidocaine-induced seizures in the ratAmerican Journal of Obstetrics and Gynecology, Vol. 164, No. 2Excess Mg2+ and Central Nervous System MetabolismParenteral magnesium sulfate fails to control electroshock and pentylenetetrazol seizures in miceEpilepsy Research, Vol. 4, No. 3Action of magnesium sulfate in the treatment of preeclampsia-eclampsia.Stroke, Vol. 20, No. 9Eclampsia: A Pediatric Neurologic Problem2 July 2016 | Journal of Child Neurology, Vol. 4, No. 1Effect of profound hypermagnesemia on spinal cord glucose utilization in rats.Stroke, Vol. 19, No. 6PHENYTOIN INFUSION IN SEVERE PRE-ECLAMPSIAThe Lancet, Vol. 329, No. 8547Zn2+, not Ca2+, is the most effective cation for activation of dolichol kinase of mammalian brain.Journal of Biological Chemistry, Vol. 260, No. 29Magnesium and seizure controlAmerican Journal of Obstetrics and Gynecology, Vol. 136, No. 1Effect of Magnesium on Epileptic Foci5 November 2007 | Epilepsia, Vol. 19, No. 1Maternal and postnatal hypermagnesemia and the meconium plug syndromeJournal of Pediatric Surgery, Vol. 11, No. 2Feeding following intraventricular injection of Ca++, Mg++ or pentobarbital in pigsPharmacology Biochemistry and Behavior, Vol. 3, No. 5Control of post-anaesthetic shiveringCanadian Anaesthetists’ Society Journal, Vol. 21, No. 5Cold stress induced changes in the uptake and distribution of radiolabelled magnesium in the brain and pituitary of the ratExperientia, Vol. 30, No. 8EFFECT OF STRESS ON THE UPTAKE OF RADIOLABELLED CALCIUM IN THE PITUITARY GLAND AND THE BRAIN OF THE RATJournal of Neurochemistry, Vol. 22, No. 5The effect of magnesium sulfate on anoxia and resuscitation in the neonateAmerican Journal of Obstetrics and Gynecology, Vol. 109, No. 3Anaesthetic action of magnesium ionsCanadian Anaesthetists’ Society Journal, Vol. 15, No. 6Effects of magnesium and calcium on neurones in the central nervous systemBrain Research, Vol. 9, No. 1 More from this issue > Volume 214Issue 2February 1968Pages 406-413 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.214.2.406PubMed5639567History Published online 1 February 1968 Published in print 1 February 1968 Metrics