Timothy M Barth

Publications (2)6.09 Total impact

• Article: Systemic lipopolysaccharide plus MPTP as a model of dopamine loss and gait instability in C57Bl/6J mice.

  Stefanie L Byler, Gary W Boehm, Jonathan D Karp, Rachel A Kohman, Andrew J Tarr, Timothy Schallert, Timothy M Barth
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  ABSTRACT: In most environmental models of Parkinson's disease (PD), a single neurodegenerative agent is introduced to cause nigrostriatal dopamine depletion. However, cell loss in human PD often might derive, at least in part, from multiple toxins or vulnerabilities, any one of which alone does not inevitably lead to chronic dopamine depletion. In the present research, male C57BL/6J mice were systemically administered the inflammatory bacterial endotoxin, lipopolysaccharide (LPS) and the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) alone or in combination and the behavior as well as striatal dopamine levels were compared to saline-treated mice. Mice in the combination (LPS+MPTP) group, but not in the single-factor groups, showed both dopamine depletion and parkinsonian symptoms, i.e., reduced stride length, at 4 months post-injection. MPTP alone acutely reduced striatal dopamine levels but this effect was transient as striatal dopamine recovered to normal levels after time (4 months). The LPS-only group showed no dopamine depletion or reduced stride length. These data are consistent with the view that nigrostriatal dopamine neurons might succumb after time to multiple toxic agents that independently may have only a transient, adverse effect.
  Behavioural brain research 12/2008; 198(2):434-9. · 3.22 Impact Factor
• Article: The window of opportunity for administration of magnesium therapy following focal brain injury is 24 h but is task dependent in the rat.

  Michael R Hoane, Timothy M Barth
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  ABSTRACT: The present study was conducted to establish the window of opportunity for the administration of a regimen of MgCl2 pharmacotherapy following focal injury to the brain. Rats were subjected to unilateral electrolytic lesions of the sensorimotor cortex (SMC) and administered a regimen of MgCl2 (1.0 mmol/kg) or 0.9% saline (1.0 ml/kg) beginning either 15 min, 8 h or 24 h after injury. Subsequent injections were administered 24 and 72 h after the initial treatment. Behavioral testing assessed recovery of function on several sensorimotor behaviors for 24 days following injury. The results of the present study suggest that treatment with a regimen of MgCl2 significantly facilitated recovery of function on the forelimb-->forelimb and vibrissae-->forelimb placing tests when administered 15 min, 8 h or 24 h after injury compared with saline-treated rats. Recovery of locomotor placing was significantly facilitated at 15 min and 8 h but not at 24 h compared with saline-treated rats. In addition, the ability of MgCl2 to limit neuronal loss in the ipsilateral ventral posterior lateral (VPL) nucleus of the thalamus was seen at only the 15-min treatment interval. These results suggest that the window of opportunity for MgCl2 pharmacotherapy is 24 h, task dependent and is much shorter for protecting neurons in the VPL.
  Physiology & Behavior 06/2002; 76(2):271-80. · 2.87 Impact Factor