The molecular mechanisms of sodium taste transduction are not completely understood, especially those responsible for the portion of NaCl’s taste in rodents that is not blocked by amiloride. As a prelude to conducting genetic analyses of peripheral NaCl taste responsiveness, we performed multiunit electrophysiological recordings from the chorda tympani (CT) nerve in C57BL/6J (B6) and A/J mice. Mice were anesthetized, the CT was accessed, and taste solutions were flowed over the tongue in order to measure the integrated whole-nerve response. NaCl was delivered before and during application of 100 μM amiloride. Pre-amiloride responses were significantly larger in A/J than B6 mice for 1–8 mM NaCl. Responses to NaCl were suppressed significantly by amiloride in both strains and to similar degrees. However, the size of the amiloride-insensitive NaCl response component was significantly larger in A/J mice than in B6 mice for NaCl at 2–16 mM. These data help to explain the prior observation that the strains differ in behavioral taste thresholds for NaCl. Specifically, the results suggest that perception of sodium-specific taste by mice depends on the ratio of amiloride-sensitive and -insensitive responses in the CT, rather than on the absolute level of the whole-nerve response to NaCl or on the size of the amiloride-sensitive component alone. Because the B6 and A/J mice differed in the size of their amiloride-insensitive components, they may prove useful in future genetic work designed to characterize the underlying transduction mechanisms.
We used the C57BL/6J (B6) and PWD/PhJ (PWD) mouse strains to investigate the controls of calcium intake. Relative to the B6 strain, the PWD strain had higher preferences in two-bottle choice tests for CaCl 2 , calcium lactate (CaLa), MgCl 2 , citric acid and quinine hydrochloride, but not for sucrose, KCl or NaCl. We also measured taste-evoked chorda tympani (CT) nerve activity in response to oral application of these compounds. Electrophysiological results paralleled the preference test results, with larger responses in PWD than in B6 mice for those compounds that were more highly preferred for the former strain. The strain differences were especially large for tonic, rather than phasic, chorda tympani activity. These data establish the PWD strain as a "calcium-preferring" strain and suggest that differences between B6 and PWD mice in taste transduction or a related peripheral event contributes to the differences between the strains in preferences for calcium solutions.
Although often underdiagnosed, sleep disorders can significantly add to morbidity in neurodegenerative illnesses. Early detection and management can not only improve sleep, but also alleviate caregiver burden and assist with future prognosis. In this article, we discuss various sleep disturbances noted in neurodegenerative disorders in the aging population. Characteristics and changes in sleep architecture with normal aging are described. Various types of sleep disturbances including insomnia, hypersomnia, sleep-related movement disorders, and parasomnias associated with major neuropathological categories of synucleinopathies and tauopathies are discussed. [ Psychiatr Ann. 2018;48(6):296–302.]
Insomnia disorder in older adults is associated with dissatisfaction with quality or quantity of sleep and is also associated with difficulty falling asleep, maintaining sleep, or early morning awakening. It is frequently associated with an age-related decrease in restorative stage 3 of nonrapid eye movement sleep as well as advance phase shift leading to early morning awakening. Sleep disturbances in older adults, as in younger patients, have a bidirectional relationship with many medical and psychiatric disorders as well as polypharmacy. The health consequences of insomnia in the elderly may also include manifestation or magnification of cognitive deficits. Diagnosis of insomnia is based on history from the patient, the bed partner, self-administered questionnaire or sleep diary, comprehensive evaluation for comorbid medical/psychiatric disorders, and comprehensive medication history. Both nonpharmacological and pharmacological strategies are effective in the management of insomnia. Cognitive-behavioral therapy for insomnia (CBT-I) should be considered as an initial intervention for chronic insomnia. Pharmacological treatment with short-acting hypnotics is a valuable adjunct to CBT-I for acute insomnia for a brief period followed by a slow taper. Any treatment intervention should be in collaboration with the patient and/or family and include a discussion of the risks, benefits, and costs. [ Psychiatr Ann. 2018;48(6):279–286.]
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