The behavioral and anatomical effects of MgCl2 therapy in an electrolytic lesion model of cortical injury in the rat

Michael R. Hoane, Timothy M. Barth

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Magnesium has been shown to be involved with the processes associated with brain injury and its use in animal models of brain injury has received considerable attention. The present paper reviews the use of MgCl2 therapy to facilitate behavioral recovery and to reduce subcortical degeneration in an electrolytic lesion model of cortical injury in the rat. Several studies were performed which compared the effectiveness of MgCl2 to other established neuroprotective agents, examined the preoperative administration of MgCl2, and examined the effectiveness of MgCl2 in a lesion model that produces chronic behavioral impairments. The results from these studies indicate that MgCl2 therapy is effective in facilitating recovery of function and limiting subcortical degeneration, is as effective as other neuroprotective agents, and can induce recovery of function in a chronic lesion model. These results suggest that MgCl2 therapy is effective in facilitating recovery of function in an electrolytic lesion model of cortical injury.

Original languageEnglish (US)
Pages (from-to)51-63
Number of pages13
JournalMagnesium Research
Volume14
Issue number1-2
StatePublished - Dec 1 2001
Externally publishedYes

Fingerprint

Magnesium Chloride
Rats
Recovery of Function
Wounds and Injuries
Recovery
Neuroprotective Agents
Brain Injuries
Brain
Therapeutics
Magnesium
Animals
Animal Models

Keywords

  • Brain injury
  • Magnesium
  • Recovery of function
  • Secondary brain injury
  • Sensorimotor behavior
  • Striatum

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Clinical Biochemistry

Cite this

The behavioral and anatomical effects of MgCl2 therapy in an electrolytic lesion model of cortical injury in the rat. / Hoane, Michael R.; Barth, Timothy M.

In: Magnesium Research, Vol. 14, No. 1-2, 01.12.2001, p. 51-63.

Research output: Contribution to journalArticle

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