A Bile Acid Protects against Motor and Cognitive Deficits and Reduces Striatal Degeneration in the 3-Nitropropionic Acid Model of Huntington's Disease

Keene, C. Dirk; Rodrigues, Cecília M. P.; Eich, Tacjana; Linehan-Stieers, Cheryle; Abt, Anna; Kren, Betsy T.; Steer, Clifford J.; Low, Walter C.

doi:10.1006/exnr.2001.7755

Cited by 114 publications

(92 citation statements)

References 62 publications

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Section: Discussionsupporting

confidence: 93%

“…It is consistent with the studies of Keene et al [21] , who reported that 3-NP treated rats exhibited increased activity levels in the retest at 6 months following the injections. Keene et al suggested that the increased activity was related to the cognitive impairment, due to the findings that cognition intact rat would habituate the environment, which resulted in reduced overall activity [21] . However, other researchers analyzed that the increased activity might be a consequence of the animals' preservative behavior, which could be interpreted as an inability to inhibit ongoing action [17] .…”

Section: Discussionsupporting

confidence: 93%

“…In rat and mouse strains, Lewis rat and C57BL/6 mouse were reported to respond poorly to 3-NP toxicity [19,20] . The impaired cognitive performance following 3-NP treatment could be detected in Wistar and Sprague-Dawley rats [9,21,22] , but not seen in Lewis rats [17,22] . Therefore, we postulate that genetic factors might influence the cognitive performance following 3-NP intoxication.…”

Section: Discussionmentioning

confidence: 81%

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No spatial memory deficit exists in Kunming mice that recently recovered from motor defects following 3-nitropropionic acid intoxication

Zhu

et al. 2009

Neurosci. Bull.

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Objective Numerous studies have described both motor defects and cognitive impairments in several strains of rodents following 3-nitropropionic acid (3-NP) intoxication. In the present study, we investigated spatial recognition memory in Kunming mice that just recovered from motor defects induced by 3-NP. Methods Mouse model was made by systemic subacute 3-NP treatment, and spatial recognition memory was measured through the Y-maze Test, a simple two-trial recognition test. Results (1) On day 15 following 3-NP treatment, affected Kunming mice did not show motor defects in the Rotarod test and presented normal gait again. (2) In the following Y-maze test after 1h interval, the percentage (90.0%) of mice showing novel arm preference in 3-NP treatment group was significantly higher than the random chance level (50%), although it was only slightly higher than that (83.3%) in control group. On day 45 after 3-NP treatment, mice failed to choose unfamiliar novel arm as first choice, and the same occured in the control group. (3) For both post-intoxicated (on day 15 and day 45 following 3-NP treatment) and control groups, the duration in the novel arm and the frequency of entering it, were longer and higher compared with familiar start and other arms. For these mice that recently recovered from motor defects following 3-NP intoxication, no spatial memory deficits were observed through Y-maze Test. Conclusion Kunming mice used in our assays might possess resistance to cognitive impairment induced by 3-NP, which is consistent with previous findings in Swiss EPM-M1 mice.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 81%

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No spatial memory deficit exists in Kunming mice that recently recovered from motor defects following 3-nitropropionic acid intoxication

Zhu

et al. 2009

Neurosci. Bull.

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“…TUDCA (EMD Chemicals, Gibbstown, NJ) is a taurine conjugate of UDCA that crosses the blood-brain barrier (15,30), where it demonstrates antioxidant properties (31) and affords neuroprotection across several murine models of CNS injury (15,30,32). In vitro, TUDCA prevents the production of reactive oxygen species (12,16) and limits neuronal apoptosis (30), UCB-induced mitochondrial permeabilization, and cytochrome c release (33).…”

Section: Pharmacologic Interventionsmentioning

confidence: 99%

“…The sodium salt of TUDCA (200 mg/kg s.c.) or vehicle (0.15 mol/l NaHCO 3 ) was administered as a single dose 15 min before administration of sulfa. This regimen was based on preliminary studies showing effective lipid peroxidation inhibition at 200 mg/kg in sulfa-dosed j/j pups, reports of TUDCA neuroprotection in other murine CNS injury models at doses ranging from 50 to 500 mg/kg (15,30,32), and pilot studies showing toxicity (death) in both N/j and nonsulfa-dosed j/j pups at doses ≥400 mg/ kg. Administration of TUDCA (200 mg/kg) alone in j/j pups was not associated with any neurobehavioral abnormalities, change in total serum bilirubin, and/or brain bilirubin content as compared with saline treatment in j/j counterparts.…”

Section: Pharmacologic Interventionsmentioning

confidence: 99%

Lipid peroxidation is not the primary mechanism of bilirubin-induced neurologic dysfunction in jaundiced Gunn rat pups

2012

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Acute effects of pulsed microwaves and 3‐nitropropionic acid on neuronal ultrastructure in the rat caudate‐putamen

Seaman

Phelix

2005

Bioelectromagnetics

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Ultrastructure of the medium sized "spiny" neuron in rat dorsal-lateral caudate-putamen was assessed after administration of 3-nitropropionic acid (3-NP) and exposure to pulsed microwaves. Sprague-Dawley male rats were given two daily intraperitoneal doses of 0 or 10 mg/kg 3-NP and 1.5 h after each dose were exposed to microwave radiation at a whole body averaged specific absorption rate (SAR) of 0 (sham exposure), 0.6, or 6 W/kg for 30 min. Microwave exposure consisted of 1.25 GHz radiation delivered as 5.9 micros pulses with repetition frequency 10 Hz. Tissue samples taken 2-3 h after the second sham or microwave exposure showed no injury with light microscope methods. Blinded qualitative assessment of ultrastructure of randomly selected neurons from the same samples did reveal differences. Subsequent detailed, quantitative measurements showed that, when followed by sham exposure, administration of 3-NP significantly increased endoplasmic reticulum (ER) intracisternal width, ER area density, and nuclear envelope thickness. Microwave exposure at 6 W/kg alone also significantly increased these measures. Exposure of 3-NP treated animals at 6 W/kg significantly increased effects of 3-NP on ultrastructure. Although exposure at 0.6 W/kg alone did not affect ultrastructure measures, exposure of 3-NP treated animals at 0.6 W/kg reduced the effects of 3-NP. We concluded that 3-NP changed neuronal ultrastructure and that the microwave exposures used here changed neuronal ultrastructure in ways that depended on microwave SAR and neuron metabolic status. The apparent cancellation of 3-NP induced changes by exposure to pulsed microwaves at 0.6 W/kg indicated the possibility that such exposure can protect against the effects of mitochondrial toxins on the nervous system.

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A Bile Acid Protects against Motor and Cognitive Deficits and Reduces Striatal Degeneration in the 3-Nitropropionic Acid Model of Huntington's Disease

Cited by 114 publications

References 62 publications

No spatial memory deficit exists in Kunming mice that recently recovered from motor defects following 3-nitropropionic acid intoxication

No spatial memory deficit exists in Kunming mice that recently recovered from motor defects following 3-nitropropionic acid intoxication

Lipid peroxidation is not the primary mechanism of bilirubin-induced neurologic dysfunction in jaundiced Gunn rat pups

Acute effects of pulsed microwaves and 3‐nitropropionic acid on neuronal ultrastructure in the rat caudate‐putamen

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