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PubMed1994

Dynorphin A-induced rat spinal cord injury: evidence for excitatory amino acid involvement in a pharmacological model of ischemic spinal cord injury.

Dynorphin A reduced lumbosacral blood flow, elevated cerebrospinal fluid lactic acid concentrations and caused flaccid hindlimb paralysis and striking neuropathological changes after its injection into the spinal subarachnoid space in rats. Coadministration of the vasodilator hydralazine substantially eliminated the paralytic, anaerobic metabolic and neuropathological responses to dynorphin A. In contrast, in concentrations up to 1 mM, dynorphin A did not alter the viability of cultured rat spinal cord neurons. Thus, it appears that this peptide lacks direct neurotoxic effects and that neuronal injuries in vivo result primarily from ischemia associated with dynorphin A-induced blood flow reductions. NMDA receptor antagonists significantly improved recovery from dynorphin A-induced hindlimb paralysis, and substantially eliminated neuropathological changes without attenuating the acute blood flow reductions or lactic acid elevations. Additionally, glutamate and aspartate concentrations were increased significantly in spinal cord cerebrospinal fluid samples removed during the time that peptide-induced spinal cord blood flow reductions were observed. In contrast, neither amino acid concentration was elevated in media removed after 1-hr exposure of spinal cord neuronal cell cultures to 100 microM concentrations of dynorphin A. These results indicate that the paralysis and spinal cord injuries produced in rats after spinal subarachnoid injection of dynorphin A result predominantly from spinal cord ischemia, and further identify excitatory amino acids and N-methyl-D-aspartate receptor mechanisms as important mediators in this injury model.

Amino Acids↗
PubMed2000

Inhibition of spinal nociceptive responses after intramuscular injection of capsaicin involves activation of noradrenergic and opioid systems.

Extracellular recordings of wide dynamic range neurones in the dorsal horn driven by electrical stimulation of the sciatic nerve were performed in intact urethane-anaesthetized Sprague-Dawley rats. The electrically evoked neuronal responses were defined as A- and C-fibres responses according to latencies, and the effect of a deep nociceptive conditioning stimulus induced by 200 microg capsaicin (8-methyl-N-vanillyl-6-noneamide) injected into the contralateral gastrocnemius-soleus muscle was studied for at least 30 min. Independent of the size and location of the receptive field of the neurone under study, a clear inhibition of the neuronal responses was observed. The electrically evoked C-fibre responses were inhibited to 53% of baseline 15-30 min after injection of capsaicin. This inhibition was only slightly attenuated by 125 nmol of the alpha-adrenoceptor antagonist phentolamine or 250 nmol of the opioid receptor antagonist naloxone applied directly onto the spinal cord when the two compounds were administered separately 5 min before capsaicin. In contrast, when a mixture of the two compounds was given 5 min before capsaicin, the effect of capsaicin was completely abolished. These results indicate that activation of the capsaicin-sensitive afferents in the gastrocnemius-soleus muscle inhibits the electrically evoked C-fibre responses in the dorsal horn by activating noradrenergic and opioidergic inhibitory systems. Moreover, our data indicate that the activation of these two systems following injection of capsaicin has a sub-additive inhibitory effect on the wide dynamic range neurones in the spinal cord. We conclude that only one of these systems is sufficient for the inhibition to occur.

Adrenergic alpha-Antagonists↗
PubMed1999

Antinociception after both peripheral and intrathecal injection of oxotremorine is modulated by spinal nitric oxide.

The present study investigated the role of spinal nitric oxide (NO) in the antinociception induced by intraperitoneal (i.p.) and intrathecal (i.th.) injection of oxotremorine. The experiments were carried out on male Wistar rats, which had cannulas chronically implanted in the lumbar enlargement of the spinal cord. Antinociceptive effects were evaluated using a tail-flick and a paw pressure test. To raise the spinal NO level, the rats received the NO donor, 3-morpholino-sydnonimine (SIN-1, 10 and 100 microg/5 microl); to lower the NO level, the inhibitor of NO synthase, N-nitro-L-arginine methyl ester (L-NAME, 50 and 400 microg/5 microl), was administered. Both those substances were injected i.th. Systemic injections of oxotremorine (0.02 and 0.1 mg/kg) produced a significant increase in the thermal nociceptive threshold, while the mechanical threshold was affected only by the higher dose (0.1 mg/kg) of the muscarinic agonist. I.th. injections of oxotremorine (0.1 ng, 1 ng, 1 microg/5 microl) produced significant antinociception in both those tests. I.th. administration of SIN-1 in doses which themselves did not affect the nociceptive threshold antagonized both the peripheral and central oxotremorine antinociception. I.th. administration of L-NAME (50 and 400 microg/5 microl) did not change the nociceptive threshold, but dose-dependently potentiated the effects of oxotremorine injected i.p. in both tests; however, the effect of i.th. administration of oxotremorine was potentiated only in the tail-flick test. Our results demonstrate that irrespective of the way of its injection, the antinociceptive effect of oxotremorine is modulated by activity of the spinal NO. Moreover, our results further support the hypothesis that NO present in the spinal cord exerts pronociceptive effects.

Animals↗
PubMed1989

Spinocerebellar projections from spinal border cells in the cat as studied by anterograde transport of wheat germ agglutinin-horseradish peroxidase.

The cerebellar projections of spinal border cells, which give rise to crossed ascending axons, were studied in the lower lumbar segments by the anterograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) in the cat. Prior to the injections, the spinal cord was lesioned rostral and ipsilateral to the WGA-HRP injections to eliminate labeling of the ipsilaterally ascending axons. Following injections of WGA-HRP into the L4-L6 segments, labeled terminals were seen in sublobules Ib-Vf of the anterior lobe, sublobules VIf-VIe, lobule VIII, the paramedian lobule, and crus II. More than 90% of the total number of labeled terminals were in the anterior lobe; the projections were predominantly ipsilateral to their cells of origin (about 90% or more labeled terminals of the total number in each of sublobules IIb-Va). Many labeled terminals were seen ipsilaterally in sublobules IIb (11.1-17.5% of the total number), IIIa (11.7-12.9%), IIIb (16.1-17.6%), IVa (8.8-10.8%), IVb (6.2-10.5%), and Va (9.7-10.3%). In the posterior lobe, labeled terminals were numerous only in sublobule C of the ipsilateral paramedian lobule (2.7-4.9%). The projection fields in the horizontal plane of the lobules were reconstructed from a series of cross-sections through each lobule. In the anterior lobe, labeled terminals were distributed in four major areas. In sublobules IIa-IVa, area 1 was located between 1.0 and 2.0 mm lateral to the midline in zones B-C1 of Voogd; area 2, between 2.0 and 3.0 mm lateral to the midline in zones C1-C2; area 3, between 3.0 and 4.0 mm in zones C2-C3; and area 4, lateral to 4.0 mm from the midline in zone C3. These areas extended apicobasally in the apical to middle parts of the lobules. On the rostral side of sublobule C1 of the ipsilateral paramedian lobule, the projection areas extended in the entire apicobasal and the mediolateral axis of the sublobule, except in the most lateral part. The present results suggest that the SBCs project to specific areas in the cerebellar lobules.

Afferent Pathways↗
PubMed2003

Accidental intrathecal mercury application.

The authors present a case of accidental intrathecal mercury application. A 69-year-old white woman was admitted to our department with suspected meningitis following surgery for spinal stenosis at another hospital. Postoperatively, she had developed a cerebro-spinal fluid (CSF) fistula with a subcutaneous cavity. Local wound irritation had been suspected and, unfortunately, mercury-containing disinfectant was injected into the cavity. Within 24 h the patient demonstrated acute neurological deterioration due to meningitis and encephalitis and was admitted to our clinic with suspected meningitis due to postoperative CSF fistula. Lumbar puncture revealed desinfectant-stained, non-bloody CSF, while lumbar MRI demonstrated the large lumbar subcutaneous cavity. Additionally, CSF fistula was visualized on MRI. Laboratory examination revealed extremely high mercury levels in CSF, blood and urine. Treatment consisted in insertion of a lumbar drainage to wash out the mercury. The patient underwent medical detoxication using chelating agents (DMPS: RS-2,3-dimercapto-1-propansulfonacid, DMSA: meso-2,3-dimercaptosuccinatacid). Surgery was performed in order to close the cavity and the fistula. Postoperatively, the patient was admitted to the intensive care unit and remained intubated for 3 days. Within 4 weeks after surgery, she demonstrated good recovery. Eighteen months after intoxication, polyneuropathy and slight neuropsychological deficiencies were detectable.

Aged↗
PubMed1979

Is the pressor response to strychnine centrally mediated?

Intravenous administration of strychnine (0.003-0.300 mg . kg-1) to curarized, chloralosed dogs induced hypertension and tachycardia. In spinal cord-transected dogs, intravenous administration of strychnine no longer elicited a rise in blood pressure and heart rate. Intracisternal injections of strychnine also produced hypertension and tachycardia but at lower doses. Similar results were obtained after intrathecal administration of strychnine in doses significantly different from those effective on intravenous and intracisternal administration. These findings suggest that the central nervous system may be involved in the haemodynamic changes induced by strychnine, but did not allow the site of action to be located.

Animals↗
PubMed1993

Inhibition of nitric oxide synthase enhances morphine antinociception in the rat spinal cord.

NG-nitro-L-arginine methyl ester (L-NAME, 400-1500 micrograms), administered intrathecally (ith.), elicits a slight but dose-related antinociception in rats, assessed by tail-flick and paw pressure tests. L-NAME (400 micrograms) and morphine (0.5 microgram) coadministered ith. elicit a profound and long-lasting antinociception, which is abolished by ith. administration of 3-morpholino-sydnonimine (SIN-1, 100 micrograms). Hemoglobin (266 micrograms) administered ith. also slightly potentiates morphine antinociception. These results suggest that nitric oxide (NO) is involved in spinal nociceptive events, and that the increased production of NO following the nociceptive input may diminish the efficiency of opioid antinociception in the spinal cord.

Amino Acid Oxidoreductases↗
PubMed1986

The effects of morphine administered intrathecally on the somatosympathetic reflex discharges in anesthetized cats.

The effect of intrathecally applied morphine or naloxone on the sympathetic A and C reflexes evoked by stimulation of somatic myelinated A and unmyelinated C afferent nerves was investigated in anesthetized cats. Intrathecal application of morphine in the lumbar spinal region depressed the C reflex elicited by stimulation of a hindlimb nerve (superficial peroneal, SP) without affecting the C reflex elicited by stimulation of a forelimb nerve (radial, RA). Also, intrathecal application of naloxone in the lumbar spinal region was found to reverse the intravenous morphine-induced depression of the C reflex elicited by stimulation of the SP nerve. The present results suggest that selective depression of morphine on the somatosympathetic C reflex is mediated at the spinal cord level.

Animals↗
PubMed1988

Reversal of the antinociceptive effects of intrathecally administered serotonin in the rat by a selective 5-HT3 receptor antagonist.

The ability of the highly selective 5-HT3 receptor antagonist ICS 205-930 (3 alpha-tropanyl-1H-indole-3-carboxylic acid ester) to block the increase in tail flick (TFL) and hot plate latencies (HPL) produced by intrathecally (i.t.) administered serotonin (5-HT) was examined in pargyline pretreated rats. ICS 205-930 (0.1 microgram, i.t.) blocked the ability of 5-HT (200 micrograms) to increase TFL and HPL. Significant hyperalgesia, as measured by a decrease in TFL and HPL compared to saline controls, also resulted from either the coadministration of ICS 205-930 (10 micrograms) and 5-HT (200 micrograms) or from ICS 205-930 (100 micrograms) alone. These data suggest an important role for 5-HT3 receptors in modulating spinal nociceptive responses.

Animals↗