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. Prior literature in this regard does not clearly explore the influence of task on apparent age-related differences in tongue pressure amplitudes. Furthermore, differences attributable to variations across individuals in strength, independent of age, have not clearly been elucidated. In this study, our goal was to clarify whether older adults have reduced tongue-palate pressures during maximum isometric, saliva swallowing, and water swallowing tasks, while controlling for individual variations in strength. Data were collected from 40 healthy younger adults (under age 40) and 38 healthy mature adults (over age 60). As a group, the mature participants had significantly lower maximum isometric pressures (MIPs). Swallowing pressures differed significantly by task, with higher pressures seen in saliva swallows than in water swallows. Age-group differences were not seen in swallowing pressures. Consideration of MIP as a covariate in the analysis of swallowing pressures revealed significant correlations between strength and swallowing pressures in the older participant group. Age-group differences were evident only when strength was considered in the model, suggesting that apparent age-related differences are, in fact, explained by differences in strength, which tends to be lower in healthy older adults. Our results show no evidence of independent differences in swallowing pressures attributable to age.
International audienceCognitive 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. Researchers examined the brains from STOP null mice to determine whether differences in task performance were associated with alterations in brain morphology. STOP null mice displayed deficits in both recognition and long-term memory. These behavioral deficits were accompanied by a massive enlargement of the cerebral ventricular system as well as by reductions in volume of cortical and diencephalic structures. In addition to deficits in recognition and long-term memory, STOP null mice displayed exaggerated neuroanatomical deficits somewhat reminiscent of those observed among individuals with schizophrenia
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 DFosB. By comparison to sham lesioned animals, bilateral destruction of the VH elevated DFosB expression throughout the caudate putamen and neocortex of animals lesioned as neonates. These increases were not observed in rats lesioned as young-adults, suggesting that DFosB induction in the cortex of neonatally lesioned rats may be related to altered cortical neurodevelopment. Accumulating evidence implicates DFosB in mediation of the long-lasting effects of altered dopaminergic neurotransmission on behavior. The present findings are consistent with this proposal and suggest that elevated expression of DFosB identifies overactive neurons that may contribute to the enhanced sensitivity to stress and dopaminergic agonists of rats that have sustained bilateral ventral hippocampal lesions as neonates.
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