Biomedical subjects

R M Benca

Publications and source records attributed to R M Benca.

29 records · Page 2Linked to original sources

PubMed1996

Analysis of the retinohypothalamic tract in congenic albino and pigmented rats.

To determine whether differences in the retinohypothalamic tract (RHT) were related specifically to albinism, we analyzed the distribution and trajectory of this pathway in congenic F344-c/+ albino and pigmented rats using the inactive subunit of cholera toxin conjugated to horseradish peroxidase as an anterograde tracer. We found that the overall volume of the tract in the albino rats was greater than in the pigmented rats (P < 0.05). We also noted shape differences.

Albinism↗

PubMed1996

Increased basal REM sleep but no difference in dark induction or light suppression of REM sleep in flinders rats with cholinergic supersensitivity.

Increased cholinergic sensitivity in the central nervous system has been postulated to account for some of the neuroendocrine abnormalities and sleep disturbances seen in human depressives. The Flinders Sensitive Line (FSL) rats, which exhibit increased sensitivity to cholinergic agents, have been shown to have REM sleep patterns similar to those seen in depressives, including shorter REM sleep latency and increased daily percentage of REM sleep. We studied the response of FSL and control rats to brief dark pulses administered during the normal light period (which are known to stimulate REM sleep in albino rats) and to brief light pulses during the normal dark period (which suppress REM sleep in albino rats) to determine whether these responses are affected by central cholinergic hypersensitivity. FSL rats showed REM sleep patterns indistinguishable from controls during light or dark pulses, which does not support the primary involvement of cholinergic systems in this mechanism of REM sleep regulation. We also examined REM and non-REM (NREM) sleep patterns in FSL rats and their controls to determine whether they show sleep continuity disturbances or decreased sleep intensity as seen in depression. In agreement with an earlier study, we found that FSL rats had more daily REM sleep and accumulated less NREM sleep between REM bouts than controls. Duration of NREM sleep bouts, total daily NREM sleep time, and EEG amplitude of NREM sleep did not differ between FSL and control rats, suggesting that the cholinergic abnormalities in FSL rats do not produce substantial NREM sleep changes.

Animals↗

PubMed1996

Sleep in psychiatric disorders.

Psychiatric disorders are some of the most common causes of sleep-related complaints, particularly insomnia. Sleep abnormalities may be caused by CNS abnormalities associated with psychiatric illnesses as well as by accompanying behavioral disturbances. Although sleep patterns are not necessarily diagnostic of particular psychiatric disorders, there are relationships between certain sleep abnormalities and categories of psychiatric disorders. Sleep disturbances associated with psychiatric disorders and general approaches to treatment are reviewed.

Anxiety Disorders↗

PubMed1996

Effects of drugs on sleep.

Many commonly prescribed medications and substances of abuse can have significant effects on sleep and wakefulness. Chronic use or abuse of certain drugs may lead to the development of substance-related sleep disorders. Primary sleep disorders, such as apnea, periodic movement disorders, and parasomnias, may be exacerbated by various drugs. This article summarizes the effects of widely used medications and recreational drugs on sleep.

Anticonvulsants↗

PubMed1993

Failure to induce rapid eye movement sleep by dark pulses in pigmented inbred rat strains.

Studies of albino Lewis rats, pigmented Brown Norway rats, and their F2 backcross progeny have demonstrated that the ability to trigger rapid eye movement (REM) sleep by turning off cage lights (dark pulses) is associated with albinism in these rat strains. Other studies have shown that pigmented inbred rats show REM sleep induction in the dark portion of short light:dark cycles or skin temperature changes. In the present study, these same pigmented breeds, Dark Agouti and hooded Long-Evans rats, were subjected to 5-min dark pulses and failed to show any evidence of REM sleep triggering. In fact, they showed trends towards REM sleep suppression during dark pulses. These results extend the finding that dark pulse triggering of REM sleep, readily evoked in albino rats, does not appear in pigmented rat strains.

Animals↗

PubMed1993

Differences in the retinohypothalamic tract in albino Lewis versus brown Norway rat strains.

Differences in sleep-wake patterns in response to light-dark stimulation have been observed between albino Lewis and pigmented Brown Norway strains of rats, which may be associated with albinism. Since several anatomical differences have been demonstrated in the visual pathways of albino and pigmented mammals, the present study was undertaken to determine whether additional differences in visual pathways of these rat strains exist that might account for their behavioral differences. Using anterograde tracing techniques and image analysis, we have investigated the retinal projections of Lewis and Brown Norway rats. Our results demonstrate that the distribution of retinal terminals in the hypothalamic suprachiasmatic nucleus extends over a greater area in Lewis compared to Brown Norway rats. This zone of termination corresponds to a cytoarchitectonically definable ventrolateral subdivision of the suprachiasmatic nucleus (SCN), which is also greater in Lewis than in Brown Norway rats. These results may have implications for behaviors related to the SCN.

Albinism↗

PubMed1992

Sleep and psychiatric disorders. A meta-analysis.

We reviewed the literature on sleep in psychiatric disorders and evaluated the data by meta-analysis, a statistical method designed to combine data from different studies. A total of 177 studies with data from 7151 patients and controls were reviewed. Most psychiatric groups showed significantly reduced sleep efficiency and total sleep time, accounted for by decrements in non-rapid eye movement sleep. Rapid eye movement sleep time was relatively preserved in all groups, and percentage of rapid eye movement sleep was increased in affective disorders. Reduction in rapid eye movement sleep latency was seen in affective disorders but occurred in other categories as well. Although no single sleep variable appeared to have absolute specificity for any particular psychiatric disorder, patterns of sleep disturbances associated with categories of psychiatric illnesses were observed. Overall, findings for patients with affective disorders differed most frequently and significantly from those for normal controls.

Adult↗

PubMed1992

Heritability of dark pulse triggering of paradoxical sleep in rats.

A previous study showed that albino Lewis (L) rats could be triggered into paradoxical sleep (PS) by dark pulse stimulation, i.e., turning off cage lights, whereas brown Norway (BN) rats showed no evidence of PS triggering by dark pulses (2). The transmission of the PS triggering behavior was studied in L x [L x BN]F1 hybrid backcross (BC) animals. Albino BC rats increased PS% during 5-minute dark pulses to three times the average PS% for the preceding 5 minutes of lights-on. In contrast, no significant PS triggering was observed in pigmented BC rats. These data support the hypothesis that PS triggering by dark pulse stimulation is related to albinism in these rat strains. The absence of a connection between PS triggering and total daily amounts of PS suggests independent genetic transmission of these two parameters.

Albinism↗

PubMed1991

Rat strain differences in response to dark pulse triggering of paradoxical sleep.

Previous studies of inbred rats have shown that Brown Norway (BN) rats had more daily paradoxical sleep (PS) than Lewis (L) rats, while F1 progeny had intermediate amounts, suggesting codominant or polygenic transmission. Amount of PS and the induction of PS episodes may be under separate genetic control. Earlier work had shown that five-minute exposures to cage lights-off every half-hour can trigger PS in outbred albino strains. To explore the genetic controls for PS induction, PS triggering by dark pulse stimulation was examined in L and BN rats. L rats showed a five-fold increase in PS during dark pulse stimulation. Although, as in the earlier study, BN rats had more total daily PS than L rats, they exhibited no dark pulse triggering of PS. Thus L and BN rats show significant strain differences in two independent parameters of PS, and may be a useful model for studying genetic and neurologic factors which regulate PS.

Animals↗

PubMed1989

Sleep deprivation in the rat: VII. Immune function.

Immune function studies were performed on splenic lymphocytes obtained from rats subjected to total or paradoxical sleep deprivation. Spleen cell counts, in vitro lymphocyte proliferation responses to mitogens, and in vitro and in vivo plaque-forming cell responses to antigens were obtained. Sleep-deprived rats were roughly equivalent to both their yoked controls and home-cage controls in all assays. The results do not support the hypothesis that sleep deprivation results in immune suppression as measured by the above-mentioned parameters.

Animals↗

PubMed1986

Functional studies of pluripotential hemopoietic stem cells in mouse brain.

The report of pluripotential hemopoietic stem cells (PHSC) in the murine brain, as detected in the colony-forming unit (CFUs) assay (Bartlett 1982), prompted us to investigate the functional significance of these cells. Although we confirmed that the transfer of brain cells into irradiated hosts produced CFUs, they did not reconstitute erythropoietic or immune functions. Failure to reconstitute immune function was corroborated by FACS analysis. To test whether the injection of brain cells stimulates self-reconstitution, the effect of host irradiation on CFUs production was studied. CFUs frequencies resulting from the transfer of brain or irradiated brain cells were similar and significantly higher in 800 R vs. 1200 R recipients at 10 days. Our experiments do not support the existence of PHSC in the brain, and suggest that colony formation after brain cell transfer may be the result of an adjuvant effect.

Anemia↗