Oral perceptual discrimination of viscosity differences for non-newtonian liquids in the nectar- and honey-thick ranges.

Thickened liquids are frequently used in the management of oropharyngeal dysphagia. Previous studies suggest that compression of a liquid bolus between the tongue and the palate in the oral phase of swallowing serves a sensory function, enabling the tuning of motor behavior to match the viscosity of the bolus. However, the field lacks information regarding healthy oral sensory discrimination ability for small differences in liquid viscosity.

Age-related differences in tongue-palate pressures for strength and swallowing tasks.

The tongue plays a key role in the generation of pressures for transporting liquids and foods through the mouth in swallowing. Recent studies suggest that there is an age-related decline in tongue strength in healthy adults. However, whether age-related changes occur in tongue pressures generated for the purpose of swallowing remains unclear.

Timing differences between cued and noncued swallows in healthy young adults.

Temporal parameters such as stage transition duration, bolus location at swallow onset, and pharyngeal transit time are often measured during videofluoroscopy, but these parameters may vary depending on assessment instructions. Specifically, "command" (cued) swallows have been observed to alter timing compared to spontaneous (noncued) situations in healthy older adults. The aim of our study was to confirm whether healthy young people show timing differences for thin liquid swallows between cued and noncued conditions.

Outcomes of tongue-pressure strength and accuracy training for dysphagia following acquired brain injury.

The purpose of this study was to measure treatment outcomes in a group of six adults with chronic dysphagia following acquired brain injury, who each completed 24 sessions of tongue-pressure resistance training, over a total of 11-12 weeks. The treatment protocol emphasized both strength and accuracy. Biofeedback was provided using the Iowa Oral Performance Instrument.

Cognitive impairments in the STOP null mouse model of schizophrenia.

Cognitive dysfunction is a primary and persisting core deficit of schizophrenia that is marginally improved by antipsychotic treatment. Adult mice that lack the stable tubule-only polypeptide (STOP) have neurochemical and behavioral abnormalities that model some features of schizophrenia. Recognition and long-term memory in the STOP null mouse were tested with the novel object recognition task and an olfactory discrimination task, respectively.

Schizophrenia: an integrative approach to modelling a complex disorder.

The discovery of candidate susceptibility genes for schizophrenia and the generation of mice lacking proteins that reproduce biochemical processes that are disrupted in this mental illness offer unprecedented opportunities for improved modelling of this complex disorder. Several lines of evidence indicate that obstetrical complications, as well as fetal or neonatal exposure to viral infection, are predisposing events for some forms of schizophrenia. These environmental events can be modelled in animals, resulting in some of the characteristic features of schizophrenia; however, animal models have yet to be developed that encompass both environmental and genetic aspects of this mental illness.

Neonatal ventral hippocampal lesions produce an elevation of DeltaFosB-like protein(s) in the rodent neocortex.

Rats that have sustained bilateral excitotoxic lesions of the ventral hippocampus (VH) as neonates develop behavioral abnormalities as adults (hyper-responsiveness to stress, diminished prepulse inhibition, and increased sensitivity to dopamine agonists), which resemble certain aspects of schizophrenia. Although this behavioral profile is thought to reflect dysregulation of the mesolimbic dopamine system, the precise neuroanatomical and neurochemical substrates that mediate the emergence of these abnormalities during brain maturation are unclear. In order to identify putative sites responsible for the development of behavioral abnormalities following neonatal lesions of the VH, we utilized the chronic neuronal activity marker DeltaFosB.