Literature DB >> 3668644

Photochemically induced graded spinal cord infarction. Behavioral, electrophysiological, and morphological correlates.

R Prado1, W D Dietrich, B D Watson, M D Ginsberg, B A Green.   

Abstract

Neurological and morphological outcome was evaluated in a rat model of graded spinal cord infarction initiated by a photochemical reaction. In this model, light-dye interactions induce primary microvascular stasis, resulting in consistent patterns of tissue necrosis. Four groups of rats underwent photoinduction times ranging from 30 seconds to 10 minutes. Neurological and electrophysiological functions were assessed starting 1 week after irradiation and continuing for 8 weeks. A functional neurological score was obtained by combining results from sensory and motor tasks, and electrophysiological function was evaluated from the somatosensory evoked potential recordings. In rats irradiated for short periods (30 seconds and 1 minute) mild behavioral deficits were documented. In contrast, electrical conduction was suppressed acutely in both groups; this recovered by 8 weeks to baseline or near baseline in the 30-second group but not in the 1-minute group. In rats irradiated for longer periods (5 and 10 minutes), severe behavioral and conduction abnormalities were detected at both the subacute and chronic testing periods. Although no significant difference in behavior was documented between the 5- and 10-minute groups acutely, the rats with 5-minute photoinduction time demonstrated a significant improvement in behavior over time whereas the group with 10-minute photoinduction time showed no improvement. A severe conduction block was present in both animal groups during the course of the study. Histopathological examination combined with morphometric measurements of the lesion area in cross section revealed four different degrees of spinal cord necrosis which correlated significantly with photoinduction times and neurological scores at 8 weeks. Reproducible degrees of ischemic damage to spinal cord parenchyma following primary microvascular occlusion result in a predictable sequence of behavioral and functional abnormalities, which in some cases recover with time.

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Mesh:

Year:  1987        PMID: 3668644     DOI: 10.3171/jns.1987.67.5.0745

Source DB:  PubMed          Journal:  J Neurosurg        ISSN: 0022-3085            Impact factor:   5.115


  7 in total

1.  An experimental model of intraoperative venous injury in the rat.

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2.  A novel rodent model of posterior ischemic optic neuropathy.

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Journal:  JAMA Ophthalmol       Date:  2013-02       Impact factor: 7.389

Review 3.  Translational spinal cord injury research: preclinical guidelines and challenges.

Authors:  Paul J Reier; Michael A Lane; Edward D Hall; Y D Teng; Dena R Howland
Journal:  Handb Clin Neurol       Date:  2012

4.  Rat Model of Photochemically-Induced Posterior Ischemic Optic Neuropathy.

Authors:  Yan Wang; Dale P Brown; Brant D Watson; Jeffrey L Goldberg
Journal:  J Vis Exp       Date:  2015-11-29       Impact factor: 1.355

5.  A mouse model of photochemically induced spinal cord injury.

Authors:  Min Sheng Piao; Jung-Kil Lee; Jae-Won Jang; Soo-Han Kim; Hyung-Seok Kim
Journal:  J Korean Neurosurg Soc       Date:  2009-11-30

Review 6.  The animal model of spinal cord injury as an experimental pain model.

Authors:  Aya Nakae; Kunihiro Nakai; Kenji Yano; Ko Hosokawa; Masahiko Shibata; Takashi Mashimo
Journal:  J Biomed Biotechnol       Date:  2011-03-07

7.  Behavioral improvement and regulation of molecules related to neuroplasticity in ischemic rat spinal cord treated with PEDF.

Authors:  Chary Marquez Batista; Leonardo Luis Torres Bianqui; Bruno Bonganha Zanon; Mauricio Menezes Aben Athar Ivo; Gabriela Pintar de Oliveira; Jessica Ruivo Maximino; Gerson Chadi
Journal:  Neural Plast       Date:  2014-07-03       Impact factor: 3.599

  7 in total

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