Verifying Efficacy of Self-Inhalation Training for Velopharyngeal Dysfunction.

Velopharyngeal closure in healthy adults during different tasksObjective: Velopharyngeal dysfunction causes not only resonance problems (so-called "hypernasality") but also dysphagia, particularly in the elderly. In our previous study, we developed a new inhaling training method to objectively improve velopharyngeal function using the measurement of peak inspiratory flow (PIF) rate, which was effective in all patients. In this study, we clarify the degree of velopharyngeal closure to determine the efficacy of our training to improve the closure mechanism. METHODS: Three healthy volunteers performed tasks in a magnetic resonance imaging (MRI) gantry in the supine position. To confirm velopharyngeal function, volunteers were first asked to distinguish the difference in the velum position between the production of a nonnasal (sustained phonation /shi:/) and a nasal (sustained phonation /n:/) sound. They were then asked to inhale forcefully through the mouth from an empty 500-mL plastic bottle. For comparison, volunteers performed exhaling forcefully, then inhaling and exhaling softly, through a straw. Each task was performed for 30 s, and the MRI images were obtained in sagittal sections. RESULTS: Inhaling forcefully from an empty plastic bottle created the strongest velopharyngeal closure between the posterior surface of the velum (soft palate) and the posterior pharyngeal wall in all volunteers. CONCLUSION: The results of our MRI study supported our training method. Using inhalation through a PIF meter or from a plastic bottle to create resistance strengthens particularly the levator veli palatini muscle for velopharyngeal closure, which may be useful in patients with other acquired velopharyngeal dysfunctions including physiological aging. Also, anyone anywhere can train with plastic bottles.

Antisense knockdown of drebrin A, a dendritic spine protein, causes stronger preference, impaired pre-pulse inhibition, and an increased sensitivity to psychostimulant.

Drebrin located in dendritic spines regulates their morphological changes and plays a role in the synaptic plasticity via spine function. Reduced drebrin has been found in the brain of patients with Alzheimer's disease or Down's syndrome. To examine whether the down-regulation of drebrin protein levels causes deficits in higher brain function, such as memory or cognition, we performed antisense-induced knockdown of drebrin A expression in rat brain using an hemagglutinating virus of Japan (HVJ)-liposome gene transfer technique. We investigated the effects of drebrin in vivo knockdown on spatial memory in a water-maze task, sensorimotor gating in a pre-pulse-inhibition test, adaptive behaviors in an open-field test, and sensitivity to psychostimulant in an amphetamine-induced locomotor response. Rats with drebrin A in vivo knockdown displayed a stronger preference for a previous event due to perseverative behavior, impaired pre-pulse inhibition (PPI), increased locomotor activity, anxiety-like behavior, and an increased sensitivity to psychostimulant, suggesting behaviors related to schizophrenia. These findings indicated that decreased drebrin produces deficits in cognitive function but not in spatial memory, probably via hypofunction of dendritic spines.