Norepinephrine and Serotonin Release upon Impact Injury to Rat Spinal Cord

Liu, Danxia; Valadez, Victoria; Sorkin, Linda S.; McAdoo, David J.

doi:10.1089/neu.1990.7.219

Cited by 48 publications

(12 citation statements)

References 23 publications

(26 reference statements)

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“…The secondary components of injury that are likely to have an important role in the onset of chronic pain include secondary pathophysiological processes and biochemical events that contribute to secondary injury and cell death (e.g. membrane damage, systemic and local vascular effects, infl ammation, electrolyte imbalances, altered energy metabolism, release of transmitters, excitotoxicity and activation of multiple cellular signaling pathways) [44,45,55,56] .…”

Section: Secondary Injury Cascade Following Spinal Cord Injurymentioning

confidence: 99%

Spinal Cord Injury: A Model of Central Neuropathic Pain

Yezierski

2005

Neurosignals

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The condition of pain after spinal cord injury (SCI) affects the life quality of nearly 70% of individuals with SCI. Clinical studies over the past decade have provided important insights into the complexities of the clinical and psychosocial characteristics of this debilitating consequence of SCI. The use of experimental models developed to study at-level or below-level pain has provided an appreciation for the mechanism(s) responsible for the onset and progression of these conditions. Important to the studies related to SCI pain has been the focus on the molecular, biochemical, anatomical, and functional consequences of SCI that have identified potential therapeutic targets for the design of novel treatment strategies.

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Section: Secondary Injury Cascade Following Spinal Cord Injurymentioning

confidence: 99%

Spinal Cord Injury: A Model of Central Neuropathic Pain

Yezierski

2005

Neurosignals

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“…It has since been proposed that 5-HT contributes to the posttraumatic decline of blood ow and edema seen in injured spinal cords. 13 ± 16 Microdialysis studies have shown that a spinal cord injury releases large amounts of 5-HT into extracellular spaces, 3,17,18 and we also reported that 5-HT is released from neural elements at the injury site and is transiently taken up by platelets.…”

mentioning

confidence: 72%

Effects of serotonin 1A agonist on acute spinal cord injury

Saruhashi

Matsusue

Hukuda³

2002

Spinal Cord

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Study design: We evaluated the eects of serotonin (5-HT) agonists on in vitro models of spinal cord compressive injury. Evoked potentials in injured rat spinal cords (n=24) were recorded during perfusion with 5-HT agonists. Objectives: To evaluate the therapeutic eects of 5-HT agonists on the recovery of compound action potentials in injured spinal cords. Methods: Rat dorsal columns were isolated, placed in a chamber, and injured by extradural compression with a clip. Conducting action potentials were activated by supramaximal constant current electrical stimuli and recorded during perfusion with 5-HT agonists and antagonists. Results: After inducing compression injuries, mean action potential amplitudes were reduced to 33.9+5.4% of the pre-injury level. After 120 min of perfusion with Ringer's solution, the mean amplitudes recovered to 62.8+8.4% of the pre-injury level. At a concentration of 100 mM, perfusion with tandospirone (a 5-HT1A agonist) resulted in a signi®cantly greater recovery of mean action potential amplitudes at 2 h after the injury (86.2+6.9% of pre-injury value) as compared with the control Ringer's solution (62.8+8.4% of pre-injury value, P50.05). In contrast, quipazine (a 5-HT2A agonist) accelerated the decrease of amplitude (54.5+11.7% of pre-injury value). 5-HT1A and 5-HT2A agonist did not consistently alter latencies of the action potentials. Conclusion: The 5-HT1A receptor agonist was eective for the recovery of spinal action potential amplitudes in a rat spinal cord injury model.

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“…In addition to its calcium channel antagonist properties, (S)-emopamil is a potent antagonist of serotonin-2 receptors (Szabo, 1989). Since serotonin has been suggested to play a role in ischémie CNS injury by constricting blood vessels and increasing vascular permeability after ischemia (Defeudis, 1989), spinal trauma (Liu et al, 1990), and brain injury (Pappius, 1991), (S)-emopamil may also have a protective effect on cerebral circulation after brain trauma. To this end, we have recently demonstrated that (S)-emopamil reduces regional cerebral edema, attenuates post-traumatic cognitive dysfunction, and improves functional motor recovery following fluid percussion brain injury in the rat (Okiyama et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

(S)-Emopamil Attenuates Acute Reduction in Regional Cerebral Blood Flow Following Experimental Brain Injury

Okiyama¹,

Rosenkrantz²,

Smith³

et al. 1994

Journal of Neurotrauma

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We examined the effects of (S)-emopamil, a phenylalkylamine calcium channel blocker with serotonin receptor antagonist properties, on regional cerebral blood flow (rCBF) following experimental brain injury in the rat. Animals were subjected to fluid percussion brain injury of moderate severity (2.1 atm), and received (S)-emopamil (20 mg/kg, i.p., n = 10) or saline (n = 10) at 20 minutes postinjury and 2.5 hours after the first injection of the drug. Consecutive rCBF measurements were performed: (1) prior to injury, (2) 15 minutes, (3) 90 minutes, and (4) 4 hours postinjury, using the radiolabeled microsphere technique. Brain injury produced an acute and significant reduction of rCBF at 15 minutes postinjury in all the regions examined (p < 0.05). At 90 minutes postinjury, rCBF remained significantly depressed in the forebrain regions. All brain regions showed a recovery of rCBF to normal by 4 hours following injury in saline-treated animals, with the exception of injured left parietal cortex and bilateral hippocampi, where rCBF remained significantly depressed. A significant attenuation of the trauma-induced reduction in rCBF was observed at 70 minutes after the first administration of (S)-emopamil in the forebrain regions and cerebellum (p < 0.05). Following the second (S)-emopamil injection, the significant improvement in rCBF observed in left injured cortex was maintained. These results suggest that (S)-emopamil may be efficacious in reversing post-traumatic alterations in rCBF, which may contribute to the post-traumatic pathophysiologic sequelae.

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Norepinephrine and Serotonin Release upon Impact Injury to Rat Spinal Cord

Cited by 48 publications

References 23 publications

Spinal Cord Injury: A Model of Central Neuropathic Pain

Spinal Cord Injury: A Model of Central Neuropathic Pain

Effects of serotonin 1A agonist on acute spinal cord injury

(S)-Emopamil Attenuates Acute Reduction in Regional Cerebral Blood Flow Following Experimental Brain Injury

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