RESUMO
Ankle sprain is the most commonly diagnosed injury experienced by ballet dancers with few studies investigating preventive support measures such as Kinesio taping. The need exists to examine the mechanical support characteristics of Kinesio taping and effect of application on ankle motion and performance. This may be important to understanding the mechanical mechanisms attributed to Kinesio ankle taping and justify its use in the prevention and treatment of jump landing injuries in ballet dancers. This study compared Kinesio taping with and without tension and no tape (control) on active and passive measures of ankle complex motion in healthy ballet dancers. A secondary objective was to examine the effect of Kinesio taping on balance using time to stabilization. Participants performed three ballet jumps with single-leg landings on a force plate across three ankle support conditions consisting of Kinesio taping, sham-Kinesio taping, and no tape. Sagittal and frontal plane motion and load-displacement of the ankle complex for each support condition were obtained using an ankle arthrometer. Kinesio taping with tension significantly restricted inversion-eversion rotation and increased inversion stiffness of the ankle complex (p < 0.05). No significant differences were found among the three ankle support conditions for jump landing time to stabilization (p > 0.05). Arthrometric results indicate Kinesio taping significantly restricted ankle complex motion in the frontal plane that is associated with lateral ankle sprain. Objective information on the nature of Kinesio taping support can assist sports medicine practitioners when recommending ankle support to athletes.
RESUMO
Maintenance of a low intracellular Cl- concentration ([Cl-]i) is critical for enabling inhibitory neuronal responses to GABAA receptor-mediated signaling. Cl- transporters, including KCC2, and extracellular impermeant anions ([A]o) of the extracellular matrix are both proposed to be important regulators of [Cl-]i Neurons of the reticular thalamic (RT) nucleus express reduced levels of KCC2, indicating that GABAergic signaling may produce excitation in RT neurons. However, by performing perforated patch recordings and calcium imaging experiments in rats (male and female), we find that [Cl-]i remains relatively low in RT neurons. Although we identify a small contribution of [A]o to a low [Cl-]i in RT neurons, our results also demonstrate that reduced levels of KCC2 remain sufficient to maintain low levels of Cl- Reduced KCC2 levels, however, restrict the capacity of RT neurons to rapidly extrude Cl- following periods of elevated GABAergic signaling. In a computational model of a local RT network featuring slow Cl- extrusion kinetics, similar to those we found experimentally, model RT neurons are predisposed to an activity-dependent switch from GABA-mediated inhibition to excitation. By decreasing the activity threshold required to produce excitatory GABAergic signaling, weaker stimuli are able to propagate activity within the model RT nucleus. Our results indicate the importance of even diminished levels of KCC2 in maintaining inhibitory signaling within the RT nucleus and suggest how this important activity choke point may be easily overcome in disorders such as epilepsy.SIGNIFICANCE STATEMENT Precise regulation of intracellular Cl- levels ([Cl-]i) preserves appropriate, often inhibitory, GABAergic signaling within the brain. However, there is disagreement over the relative contribution of various mechanisms that maintain low [Cl-]i We found that the Cl- transporter KCC2 is an important Cl- extruder in the reticular thalamic (RT) nucleus, despite this nucleus having remarkably low KCC2 immunoreactivity relative to other regions of the adult brain. We also identified a smaller contribution of fixed, impermeant anions ([A]o) to lowering [Cl-]i in RT neurons. Inhibitory signaling among RT neurons is important for preventing excessive activation of RT neurons, which can be responsible for generating seizures. Our work suggests that KCC2 critically restricts the spread of activity within the RT nucleus.
