1. Sixteen rats were recorded continuously for 3 days using an automated system that detected, quantified, and stored the incidence of cortical delta waves, cortical sigma spindles, hippocampal theta rhythm, and electromyographic activity. A time series then was constructed wherein 15-s epochs were ascribed to one behavioral state: wakefulness (W), quiet sleep (QS), or active sleep (AS, a state also referred to as REM sleep). From those series, AS episodes and non-AS intervals could be determined. Episodes and intervals were defined as lasting at least two epochs and the one-epoch episodes and intervals were incorporated to the ongoing state. 2. Having established the length of each AS episode and non-AS interval, pairings were made, on the one hand between episodes and their preceding intervals, and on the other, between episodes and the intervals that followed. 3. Highly significant correlations were found between the length of AS episodes and the length of the non-AS intervals that followed. Correlations were also significant when calculated separately versus the amount of QS and of W within the following interval. Correlations improved when they were performed against the log of the interval and when only intervals with a predominance of QS were selected. 4. No significant correlation was found between the length of AS episodes and the length of the preceding non-AS intervals, except for a negative one that was present only when the statistical analysis was performed in the unsmoothed array where the one-epoch episodes and intervals were preserved. 5. These results suggest that there is a short-term homeostasis operating within the spontaneous architecture of sleep in rats. This homeostatic mechanism is not manifested by the regulation of the length of AS episodes. Instead, there is a forward regulatory mechanism that, given the duration of an AS episode, permissively controls the interval that the animal may abstain from AS, and hence the timing of the triggering of a new AS episode.

Subterranean mammals are generally considered to have reduced eyes and apparent blindness as a convergent adaptation to their lightless microhabitat. However, there are substantial interspecific differences. We have studied the prospect of vision in the Chilean subterranean rodent cururo (Spalacopus cyanus, Octodontidae) by analyzing the optical properties of the eye, the presence and distribution of rod and cone photoreceptors, and their spectral sensitivities. Cururo eye size is normal for rodents of similar body size, the cornea and lens are transparent from red to near-UV light, and the retina is well-structured. Electroretinography reveals three spectral mechanisms: a rod with peak sensitivity (lambda(max)) at about 500 nm, a cone with lambda(max) at about 505 nm (green-sensitive L-cone), and a cone with lambda(max) near 365 nm (UV-sensitive S-cone). This suggests dichromatic color vision. Immunocytochemistry with opsin-specific antibodies confirms the presence of rods, L-cones, and S-cones. Cururo rod density is much lower than that of nocturnal surface-dwelling rodents, and the cones form an unexpectedly high 10% proportion of the photoreceptors. Of these, S-cones constitute a regionally varying proportion from 2% in dorsal to 20% in ventral retina. The high cone proportion suggests adaptation to visual demands during the sporadic short phases of diurnal surface activity, rather than to the lightless subterranean environment. Our measurements on fresh cururo urine reveal a high UV reflectance, suggesting that scent marks may be visible to the UV-sensitive cones. The present results challenge the general view of convergent adaptive eye reduction and blindness in subterranean mammals.

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Abstract22q11.2 microdeletion syndrome (22qDS) was recently identified as a risk factor for development of early-onset Parkinson’s disease (PD). The classical motor manifestations of this disease are preceded by early signs and symptoms of neurodegeneration. The progression of 22qDS-associated PD is unknown. We aimed to evaluate the presence of prodromal PD in a group of adults with 22qDS using the Movement Disorders Society (MDS) Criteria for Prodromal PD. Thirty-eight persons with 22qDS and 13 age-matched controls participated in the study, and their results were compared using the Mann-Whitney U test. Persons with 22qDS had lower scores on olfaction testing (p=7.42E×10−5), higher scores on the COMPASS 31 scale for dysautonomia (p=2.28×10−3) and on the motor evaluation using Movement Disorder Society (MDS)-sponsored revision of Unified Parkinson’s Disease Rating Scale motor subscore (UPDRS-III) (p=1.84×10−4), compared with healthy controls. Home polysomnogram did not find participants with REM-sleep behavior disorder. Integrity of nigrostriatal dopaminergic system was evaluated by PET-CT imaging of presynaptic dopamine with 18F-PR04.MZ. Patients showed significantly higher specific binding ratios in the striatum, compared to controls (p=9.57×10−3 at the caudate nuclei). Two patients with 22qDS (5.2%) had decreased uptake in the posterior putamen (less than 60% of controls) and one fulfilled MDS criteria for prodromal PD. These results show that patients with 22qDS manifest some signs and symptoms of prodromal PD such as hyposmia, dysautonomia and mild movement alterations. In the majority, this was associated with elevated dopaminergic signaling, suggesting that loss of dopaminergic neurons may not be the cause. A smaller subgroup did show evidence of a decrease in nigrostriatal dopaminergic signaling, as seen in classical prodromal PD. Longitudinal studies are necessary to understand the progression to and risk of PD in persons with 22qDS.