Activity rhythms were recorded from hamsters in three conditions: during timed feedings of an attractive diet with free access to regular food, during restriction to 70% of normal food consumption, and during moderate food deprivation with limited temporal access to an attractive diet. An attractive diet given to intact animals did not induce anticipatory activity or entrainment, but damage to the suprachiasmatic nuclei (SCN) led to the development of anticipatory activity. Food restriction to 70% of normal intake led to anticipatory components in some intact animals, without entraining the dominant circadian pacemaker. The combination of a palatable diet and food restriction led to anticipatory activity before the daily feeding times and entrainment of a previously free-running circadian rhythm in some animals. Ablation of the SCN did not eliminate anticipatory activity in experimental animals, but did eliminate the free-running component of the rhythms. These results indicate that hamsters have a mechanism separate from the SCN that can anticipate daily feeding times, as rats do, and that they may show entrainment of the SCN-based pacemaker to such feeding schedules.

Pituitary adenylate cyclase activating polypeptide (PACAP) is found in two forms of 27 and 38 amino acids (PACAP-27 and PACAP-38 respectively) in the mammalian central nervous system. Using antibodies to these two forms of PACAP, we examined the distribution of PACAP immunoreactivity in the rat hypothalamus and a number of extrahypothalamic areas. The patterns of immunostaining for PACAP-27 and PACAP-38 were similar: prominent terminal labelling was present in the retrochiasmatic area, median eminence, and posterior periventricular nucleus of the hypothalamus as well as the bed nucleus of the stria terminalis and amygdaloid complex. After colchicine treatment, immunopositive cell bodies were found in the preoptic region of the periventricular zone of the hypothalamus, the suprachiasmatic and paraventricular hypothalamic nuclei, neural structures adjacent to the median eminence (including the retrochiasmatic area, arcuate nucleus, ventromedial hypothalamus, and tuber cinereum), and the lateral mammillary and supramammillary nuclei. In all these areas, immunolabelling appeared specific since it was abolished by preabsorption of primary antisera with the appropriate PACAP peptide. However, the number of immunopositive cells in the suprachiasmatic nucleus was also reduced by preabsorption of PACAP-27/38 antisera with vasoactive intestinal polypeptide, suggesting that a subpopulation of cells in the suprachiasmatic nucleus express a peptide which has significant sequence homology with both PACAP-27/38 and vasoactive intestinal polypeptide. The distribution of PACAP immunoreactivity throughout the hypothalamus, bed nucleus of the stria terminalis, and amygdala suggests the involvement of PACAP in a number of processes including limbic, autonomic, and neuroendocrine functions as well as regulation of the circadian pacemaker.

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Parkinson's disease (PD) is a neurodegenerative disorder that is typified by motor signs and symptoms but can also lead to significant cognitive impairment and dementia Parkinson's Disease Dementia (PDD). While dementia is considered a nonmotor feature of PD that typically occurs later, individuals with PD may experience mild cognitive impairment (PD-MCI) earlier in the disease course. Olfactory deficit (OD) is considered another nonmotor symptom of PD and often presents even before the motor signs and diagnosis of PD. We examined potential links among cognitive impairment, olfactory functioning, and white matter integrity of olfactory brain regions in persons with early-stage PD. Cognitive tests were used to established groups with PD-MCI and with normal cognition (PD-NC). Olfactory functioning was examined using the University of Pennsylvania Smell Identification Test (UPSIT) while the white matter integrity of the anterior olfactory structures (AOS) was examined using magnetic resonance imaging (MRI) diffusion tensor imaging (DTI) analysis. Those with PD-MCI demonstrated poorer olfactory functioning and abnormalities based on all DTI parameters in the AOS, relative to PD-NC individuals. OD and microstructural changes in the AOS of individuals with PD may serve as additional biological markers of PD-MCI.

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