Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

Fleming, Sheila M.; Ekhator, Osunde R.; Ghisays, Valentins

doi:10.3791/50303

Cited by 131 publications

(123 citation statements)

References 29 publications

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“…Rats were placed in an upright translucent acrylic cylinder, measuring 30 cm high and 20 cm in diameter, to encourage rearing and vertical exploration with the forepaws (similar to [56,57]). Forelimb-use asymmetry was calculated as ipsilateral limb wall contacts, plus 1/2 the number of “both” contacts, divided by the total number of contacts (limited to 20 per session) [21,58,59].…”

Section: Methodsmentioning

confidence: 99%

Vocal training, levodopa, and environment effects on ultrasonic vocalizations in a rat neurotoxin model of Parkinson disease

Kelm‐Nelson

Bräuer

Ciucci

2016

Behavioural Brain Research

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Levodopa does not improve dysarthria in patients with Parkinson Disease (PD), although vocal exercise therapy, such as “LSVT/LOUD®”, does improve vocal communication. Most patients receive vocal exercise therapy while concurrently being treated with levodopa, although the interaction between levodopa and vocal exercise therapy on communication in PD is relatively unknown. Further, carryover of vocal exercise therapy to novel situations is critical for successful outcomes, but the influence of novel situations on rehabilitated vocal communication is not well understood. To address the influence of exercise, medications, and environment on vocal communication with precise experimental control, we employed the widely used 6-OHDA rat neurotoxin model of PD (infusion to the medial forebrain bundle), and assessed ultrasonic vocalizations after: vocal exercise, vocal exercise with levodopa, levodopa alone, and control conditions. We tested USVs in the familiar training environment of the home cage and a novel cage. We hypothesized that parkinsonian rats that undergo vocal exercise would demonstrate significant improvement of ultrasonic vocalization (USV) acoustic parameters as compared to the control exercise and levodopa-only treatment groups. We further hypothesized that vocal exercise in combination with levodopa administration, similar to what is common in humans, would lead to improvement in USV outcomes, particularly when tested in a familiar versus a novel environment. We found that the combination of exercise and levodopa lead to some improvement in USV acoustic parameters and these effects were stronger in a familiar vs. a novel environment. Our results suggest that although treatment can improve aspects of communication, environment can influence the benefits of these effects.

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Section: Methodsmentioning

confidence: 99%

Vocal training, levodopa, and environment effects on ultrasonic vocalizations in a rat neurotoxin model of Parkinson disease

Kelm‐Nelson

Bräuer

Ciucci

2016

Behavioural Brain Research

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“…The hind limb beam walking test was used to assess agility and coordination [21]. Twelve mice from each of the two age groups were weighed, and each mouse was then individually placed on a 50-mm beam suspended between two containers and encouraged to walk a length of 1 m across the beam from one end to the other.…”

Section: Methodsmentioning

confidence: 99%

Loss of Maspardin Attenuates the Growth and Maturation of Mouse Cortical Neurons

Davenport

Bivona²,

Latson³

et al. 2016

Neurodegener Dis

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Background: Mast syndrome, an autosomal recessive, progressive form of hereditary spastic paraplegia, is associated with mutations in SPG21 loci that encode maspardin protein. Although SPG21^-/- mice exhibit lower limb dysfunction, the role of maspardin loss in mast syndrome is unclear. Objective: To test the hypothesis that loss of maspardin attenuates the growth and maturation of cortical neurons in SPG21^-/- mice. Methods and Results: In a randomized experimental design SPG21^-/- mice demonstrated significantly less agility and coordination compared to wild-type mice in beam walk, ledge, and hind limb clasp tests for assessing neuronal dysfunction (p ≤ 0.05). The SPG21^-/- mice exhibited symptoms of mast syndrome at 6 months which worsened in 12-month-old cohort, suggesting progressive dysfunction of motor neurons. Ex vivo, wild-type cortical neurons formed synapses, ganglia and aggregates at 96 h, whereas SPG21^-/- neurons exhibited attenuated growth with markedly less axonal branches. Additionally, epidermal growth factor markedly promoted the growth and maturation of SPG21^+/+ cortical neurons but not SPG21^-/- neurons. Consequently, quantitative RT-PCR identified a significant reduction in the expression of a subset of EGF-EGFR signaling targets. Conclusions: Our current study uncovered a direct role for maspardin in normal and EGF-induced growth and maturation of primary cortical neurons. The loss of maspardin resulted in attenuated growth, axonal branching, and attenuation of EGF signaling. Reinstating the functions of maspardin may reverse hind limb impairment associated with neuronal dysfunction in mast syndrome patients.

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“…In balance beam, mice were tested for their ability to traverse a 100 cm-long in a 20-mm wide wooden dowel elevated 30 cm from the floor. In this test, latency to cross a flat beam and number of slips were recorded [30,31]. The videos was scored ipsilateral and contralateral foot slips, and time required to reach the end of the beam.…”

Section: Behavioral Testingmentioning

confidence: 99%

“…The grip was kept in a 60 0 -inclined position. The mouse was allowed to climb this grid and errors in walking/climbing or falling down time is recorded [30,34].…”

Section: Behavioral Testingmentioning

confidence: 99%

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

Bhowmick

D’Mello

Ponery

et al. 2017

Preprint

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Abstract:Traumatic brain injury (TBI) can result in persistent sensorimotor and cognitive deficits, which occur through a cascade of deleterious pathophysiological events over time. In this study, we investigated the hypothesis that neurodegeneration caused by TBI leads to impairments in sensorimotor function. TBI induces the activation of the caspase-3 enzyme, which triggers cell apoptosis in an in vivo model of fluid percussion injury (FPI).We analyzed caspase-3 mediated apoptosis by TUNEL staining and PARP and annexin V western blotting. We correlated the neurodegeneration with sensorimotor deficits by conducting the animal behavioral tests including grid walk, balance beam, inverted screen test, and climb test. Our study demonstrated that the excess cell death or neurodegeneration correlated with the neuronal dysfunction and sensorimotor impairments associated with TBI.

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Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

Cited by 131 publications

References 29 publications

Vocal training, levodopa, and environment effects on ultrasonic vocalizations in a rat neurotoxin model of Parkinson disease

Vocal training, levodopa, and environment effects on ultrasonic vocalizations in a rat neurotoxin model of Parkinson disease

Loss of Maspardin Attenuates the Growth and Maturation of Mouse Cortical Neurons

Neurodegeneration and Sensorimotor Deficits in the Mouse Model of Traumatic Brain Injury

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