Beam Walk (BW) test - beam height value

General Details:

Name:
Beam Walk (BW) test - beam height value
Steward:
NINDS
Definition:
Value of height of the beam (in cm), as part of Beam Walk (BW) test
Registration Status:
Qualified

Permissible Values:

Data Type:
Number
Unit of Measure:
cm
Ids:
Value Code Name Code Code System Code Description

Designations:

Designation:
Beam Walk (BW) test - beam height value
Tags:
Designation:
Beam height value
Tags:
Preferred Question Text
Designation:
Beam Walk (BW) test - beam height value
Tags:

Designations:

Definition:
Value of height of the beam (in cm), as part of Beam Walk (BW) test
Tags:
Definition:
Value of height of the beam (in cm), as part of Beam Walk (BW) test
Tags:
Short Description,Definition

Reference Documents:

ID:
Title:
Amphetamine, haloperidol, and experience interact to affect rate of recovery after motor cortex injury.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=7100929
Provider Org:
Language Code:
en-us
Document:
Rats subjected to unilateral ablation of the motor cortex and placed on a narrow beam displayed transient contralateral paresis. An immediate and enduring acceleration of recovery was produced by a single dose of d-amphetamine given 24 hours after injury. This effect was blocked by haloperidol or by restraining the animals for 8 hours beginning immediately after amphetamine administration. A single dose of haloperidol given 24 hours after injury markedly slowed recovery. This effect was also blocked by restraining the animals.
ID:
Title:
Characterization of progressive motor deficits in mice transgenic for the human Huntington's disease mutation.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=10191337
Provider Org:
Language Code:
en-us
Document:
Transgenic mice expressing exon 1 of the human Huntington's disease (HD) gene carrying a 141-157 CAG repeat (line R6/2) develop a progressive neurological phenotype with motor symptoms resembling those seen in HD. We have characterized the motor deficits in R6/2 mice using a battery of behavioral tests selected to measure motor aspects of swimming, fore- and hindlimb coordination, balance, and sensorimotor gating [swimming tank, rotarod, raised beam, fore- and hindpaw footprinting, and acoustic startle/prepulse inhibition (PPI)]. Behavioral testing was performed on female hemizygotic R6/2 transgenic mice (n = 9) and female wild-type littermates (n = 22) between 5 and 14 weeks of age. Transgenic mice did not show an overt behavioral phenotype until around 8 weeks of age. However, as early as 5-6 weeks of age they had significant difficulty swimming, traversing the narrowest square (5 mm) raised beam, and maintaining balance on the rotarod at rotation speeds of 33-44 rpm. Furthermore, they showed significant impairment in prepulse inhibition (an impairment also seen in patients with HD). Between 8 and 15 weeks, R6/2 transgenic mice showed a progressive deterioration in performance on all of the motor tests. Thus R6/2 mice show measurable deficits in motor behavior that begin subtly and increase progressively until death. Our data support the use of R6/2 mice as a model of HD and indicate that they may be useful for evaluating therapeutic strategies for HD, particularly those aimed at reducing the severity of motor symptoms or slowing the course of the disease.
ID:
Title:
A modified beam-walking apparatus for assessment of anxiety in a rodent model of blast traumatic brain injury.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=26367471
Provider Org:
Language Code:
en-us
Document:
The elevated plus maze (EPM) is used to assess anxiety in rodents. Beam-walking tasks are used to assess vestibulomotor function. Brain injury in rodents can disrupt performance on both of these tasks. Developing novel paradigms that integrate tasks like these can reduce the need for multiple tests when attempting to assess multiple behaviors in the same animal. Using adult male rats, we evaluated the use of a modified beam-walking (MBW) apparatus as a surrogate indicator for anxiety. We used a model of blast-induced traumatic brain injury (bTBI). A total of 39 rats were assessed before and at 3, 6, 24, 72, and 168h either post- bTBI (n=33) or no-injury (n=6) using both EPM and MBW. A novel anxiety index was calculated that encompassed peeks and re-emergences on MBW. The proposed MBW anxiety index was compared with the standard anxiety index calculated from exploration into different sections of EPM. Post- bTBI, rats had an increased anxiety index when measured using EPM. Similarly, they peeked or fully emerged less out of the safe box on MBW. It was found that this novel MBW anxiety index captured similar aspects of behavior when compared to the standard anxiety index obtained from EPM. Further, these effects were dissociated from the effects of bTBI on motor function simultaneously measured on MBW. Over the course of 168h post-bTBI, rats gradually recovered on both EPM and MBW. The MBW apparatus succeeded at capturing and dissociating two separate facets of rat behavior, motor function and anxiety, simultaneously.
ID:
Title:
Clonidine impairs recovery of beam-walking after a sensorimotor cortex lesion in the rat.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=2306622
Provider Org:
Language Code:
en-us
Document:
Beam-walking in the rat is a useful model for studying the effects of drugs on motor recovery following brain injury. In the present experiment, the effect of clonidine HCl on beam-walking recovery was investigated. Groups of rats were first trained to traverse a narrow elevated beam and then subjected to a right sensorimotor cortex suction-ablation injury. After 24 h, each rat received a single dose of clonidine HCl (20, 60, or 200 micrograms/kg, i.p., salt weight) or saline. Recovery of beam-walking ability was scored over the next 12 days. Treatment with clonidine significantly slowed the rate of recovery (Kruskal-Wallis H = 8.755, df = 3; 0.02 less than P less than 0.05). Furthermore, the impairment persisted for at least 5 days after the rats were treated (Kruskal-Wallis H = 8.47, df = 3; 0.02 less than P less than 0.05). These data are consistent with the hypothesis that norepinephrine, working through central alpha 2-adrenergic receptors, influences motor recovery after a unilateral sensorimotor cortex lesion in the rat. Since many stroke patients are treated with centrally acting antihypertensive drugs, the potential effects of specific classes of these drugs during the recovery period, should be carefully considered.
ID:
Title:
Sustained sensory/motor and cognitive deficits with neuronal apoptosis following controlled cortical impact brain injury in the mouse.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=9726259
Provider Org:
Language Code:
en-us
Document:
A mouse model of traumatic brain injury was developed using a device that produces controlled cortical impact (CCI), permitting independent manipulation of tissue deformation and impact velocity. The left parietotemporal cortex was subjected to CCI [1 mm tissue deformation and 4.5 m/s tip velocity (mild), or 6.0 m/s (moderate)] or sham surgery. Injured animals showed delayed recovery of pedal withdrawal and righting reflexes compared to sham-operated controls. Significant severity-related deficits in forepaw contraflexion and performance on a rotarod device were evident for up to 7 days. Using a beam walking task to measure fine motor coordination, pronounced deficits were apparent for at least 2 and 4 weeks following mild and moderate CCI, respectively. Cognitive function was evaluated using the water maze. Impairment of place learning, related to injury severity, was observed in mice trained 7-10 days following CCI. Similarly, working memory deficits were evident in a variation of this task when examined 21-23 days postinjury. Mild CCI caused necrosis of subcortical white matter with minimal damage to somatosensory cortex. Moderate CCI produced extensive cortical and subcortical white matter damage. Triple fluorescence labeling with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), antineuronal nuclear protein (NeuN), and Hoechst 33258 of parallel sections showed frequent apoptotic neurons. These findings demonstrate sustained and reproducible deficits in sensory/motor function and spatial learning in the CCI-injured mouse correlating with injury severity. Mechanisms of neuronal cell death after trauma as well as strategies for evaluating novel pharmacological treatment strategies may be identified using this model.
ID:
Title:
Sustained sensory/motor and cognitive deficits with neuronal apoptosis following controlled cortical impact brain injury in the mouse.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=9726259
Provider Org:
Language Code:
en-us
Document:

Properties:

Key:
Keywords
Value:
Beam_Walk;Preclinical
Key:
Guidelines/Instructions
Value:
Provide the beam height.

Identifiers:

Source:
NLM
Id:
m118OiGsV
Version:
1.0
Source:
BRICS Variable Name
Id:
BWBeamHeightVal
Version: