REM sleep homeostasis in the absence of REM sleep: effects of antidepressants

Most antidepressants suppress rapid eye movement (REM) sleep, which is thought to be important to brain function, yet the resulting REM sleep restriction is well tolerated. This study investigated the impact of antidepressants with different mechanisms of action, such as selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCA), on the regulation of REM sleep in rats. REM sleep was first demonstrated to be homeostatically regulated using 5, 8 and 10 hours of REM-sleep specific restriction through EEG-driven triggered arousals, with an average of 91 ± 10% of lost REM sleep recovered following a 26-29 -hour recovery period. Acute treatment with the antidepressants paroxetine, citalopram and imipramine inhibited REM sleep by 84 ± 8, 84 ± 8 and 69 ± 9% respectively relative to vehicle control. The pharmacologically-induced REM sleep deficits by citalopram and paroxetine were not fully recovered, whereas, after imipramine the REM sleep deficit was fully compensated. Given the marked difference between REM sleep recovery following the administration of paroxetine, citalopram, imipramine and REM sleep restriction, the homeostatic response was further examined by pairing REM sleep specific restriction with the three antidepressants. Surprisingly, the physiologically-induced REM sleep deficits incurred prior to suppression of REM sleep by all antidepressants was consistently recovered. The data indicate that REM sleep homeostasis remains operative following subsequent treatment with antidepressants and is unaffected by additional pharmacological inhibition of REM sleep

REM sleep homeostasis in the absence of REM sleep: effects of antidepressants

Most antidepressants suppress rapid eye movement (REM) sleep, which is thought to be important to brain function, yet the resulting REM sleep restriction is well tolerated. This study investigated the impact of antidepressants with different mechanisms of action, such as selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCA), on the regulation of REM sleep in rats. REM sleep was first demonstrated to be homeostatically regulated using 5, 8 and 10 hours of REM-sleep specific restriction through EEG-driven triggered arousals, with an average of 91 ± 10% of lost REM sleep recovered following a 26-29 -hour recovery period. Acute treatment with the antidepressants paroxetine, citalopram and imipramine inhibited REM sleep by 84 ± 8, 84 ± 8 and 69 ± 9% respectively relative to vehicle control. The pharmacologically-induced REM sleep deficits by citalopram and paroxetine were not fully recovered, whereas, after imipramine the REM sleep deficit was fully compensated. Given the marked difference between REM sleep recovery following the administration of paroxetine, citalopram, imipramine and REM sleep restriction, the homeostatic response was further examined by pairing REM sleep specific restriction with the three antidepressants. Surprisingly, the physiologically-induced REM sleep deficits incurred prior to suppression of REM sleep by all antidepressants was consistently recovered. The data indicate that REM sleep homeostasis remains operative following subsequent treatment with antidepressants and is unaffected by additional pharmacological inhibition of REM sleep

sociality and movement data

Data related to sociality test and space use

Mate Choice Data

Time spent with male Gambusia affinis in mate choice test. All times are in seconds

delta Ct values for focal genes

This file contains Delta Ct values for gene expression used in subsequent analysis. Each row represents one individual fish, "Treatment" indicates the measured concentration of bifenthrin in each treatment group. Gcliv - indicates glucocorticoid receptor (liver), ChorLliv - indicates Choriogenin L receptor (liver), VtgCliv - indicates Vitellogenin C (liver), Erabrn - indicates Estrogen receptor alpha (brain), Arabrn - indicates Androgen receptor (brain), Cyp19brn indicates Cyp19 receptor (brain), GCbrn - indicates Glucocorticoid receptor (brain), NS1brn - indicates neuroserpin 1 receptor (brain)

The importance of historical land use in the maintenance of early successional habitat for a threatened rattlesnake

Understanding how historic habitat changes have impacted species and searching the past for clues to better understand the current plight of threatened species can help inform and improve future conservation efforts. We coupled species distribution modeling with historical imagery analysis to assess how changes in land use/land cover have influenced the distribution of eastern massasauga rattlesnake (Sistrurus catenatus), a federally threatened species, and its habitat in northeastern Ohio over the past ∼75 years. We also examined land use/land cover changes throughout southern Michigan for a broader perspective on the influence of historical processes on contemporary habitat. There was a pronounced shift in northeastern Ohio land cover from 1938 to 2011 with forest cover becoming the predominant land cover type as agricultural fields were abandoned and succession occurred. Most known eastern massasauga locations in the area were at some point used for agriculture and higher habitat suitability values were associated with agricultural fields that were eventually abandoned. We observed more stable habitat conditions across southern Michigan populations indicating agricultural abandonment was not as necessary for habitat creation in this part of their range. We present a new approach for linking historical landscapes to present day habitat suitability models; permitting inferences on how prior land use/land cover states have influenced the current distribution of species and their habitats. We demonstrate how agricultural abandonment was an important source of early successional habitat for a species that requires an open canopy, a finding applicable to a broad array of species with similar habitat requirements. Keywords: Eastern massasauga, Agriculture, Aerial photography, Maxen

A Distinct Class of Antibodies May Be an Indicator of Gray Matter Autoimmunity in Early and Established Relapsing Remitting Multiple Sclerosis Patients

We have previously identified a distinct class of antibodies expressed by B cells in the cerebrospinal fluid (CSF) of early and established relapsing remitting multiple sclerosis (RRMS) patients that is not observed in healthy donors. These antibodies contain a unique pattern of mutations in six codons along V(H)4 antibody genes that we termed the antibody gene signature (AGS). In fact, patients who have such B cells in their CSF are identified as either having RRMS or developing RRMS in the future. As mutations in antibody genes increase antibody affinity for particular antigens, the goal for this study was to investigate whether AGS(+) antibodies bind to brain tissue antigens. Single B cells were isolated from the CSF of 10 patients with early or established RRMS. We chose 32 of these B cells that expressed antibodies enriched for the AGS for further study. We generated monoclonal full-length recombinant human antibodies (rhAbs) and used both immunological assays and immunohistochemistry to investigate the capacity of these AGS(+) rhAbs to bind brain tissue antigens. AGS(+) rhAbs did not recognize myelin tracts in the corpus callosum. Instead, AGS(+) rhAbs recognized neuronal nuclei and/or astrocytes, which are prevalent in the cortical gray matter. This pattern was unique to the AGS(+) antibodies from early and established RRMS patients, as AGS(+) antibodies from an early neuromyelitis optica patient did not display the same reactivity. Prevalence of CSF-derived B cells expressing AGS(+) antibodies that bind to these cell types may be an indicator of gray matter-directed autoimmunity in early and established RRMS patients