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Teklezghi, A. T.

Publications and source records attributed to Teklezghi, A. T..

2 recordsLinked to original sources

Effects of Long-Term Alcohol Consumption on Behavior in the P301S (Line PS19) Tauopathy Mouse Model

Alcohol consumption and misuse remain prevalent public health issues with recent reports of increased heavy consumption in older populations in the United States. Several studies have identified alcohol consumption as a risk factor for developing multiple forms of dementia. The behavioral and psychological symptoms of dementia (BPSD), such as changes in affective behavior (e.g. anxiety), precede and coincide with cognitive decline. While many studies have characterized the intersection of alcohol use and affective behaviors, little is known regarding alcohol consumption and BPSD. This study characterizes the impact of long-term alcohol consumption on various behaviors in the P301S (line PS19) tauopathy mouse model. Male and female P301S and littermate control mice underwent two-bottle choice intermittent access to alcohol for sixteen weeks starting at 12 weeks of age. There were no significant differences in total ethanol consumption between wildtype and P301S mice of the same sex; however, drinking behavior differed among genotypes, and female mice of each genotype drank significantly more ethanol than males of each genotype. Following drinking studies, mice were run through a battery of behavioral tests during a period of forced abstinence, including approach/avoidance assays, social behavior tests, and memory and cognition tests. Across these tests we observed differences between groups due to genotype, alcohol history, and interactions between alcohol exposure and genotype. These differences were not always consistent between the sexes. In total, this study reveals significant alcohol-tauopathy interactions in subsequent behavior, which may have implications for understanding how alcohol may impact BPSD in conditions associated with tauopathy like Alzheimers disease and frontotemporal dementia.

neuroscience↗

Probing different paradigms of morphine withdrawal on sleep behavior in male and female C57BL/6J mice

Opioid misuse has dramatically increased over the last few decades resulting in many people suffering from opioid use disorder (OUD). The prevalence of opioid overdose has been driven by the development of new synthetic opioids, increased availability of prescription opioids, and more recently, the COVID-19 pandemic. Coinciding with increases in exposure to opioids, the United States has also observed increases in multiple Narcan (naloxone) administrations as life-saving measures for respiratory depression, and, thus, consequently, naloxone-precipitated withdrawal. Sleep dysregulation is a main symptom of OUD and opioid withdrawal syndrome, and therefore, should be a key facet of animal models of OUD. Here we examine the effect of precipitated and spontaneous morphine withdrawal on sleep behaviors in C57BL/6J mice. We find that morphine administration and withdrawal dysregulate sleep, but not equally across morphine exposure paradigms. Furthermore, many environmental triggers promote relapse to drug-seeking/taking behavior, and the stress of disrupted sleep may fall into that category. We find that sleep deprivation dysregulates sleep in mice that had previous opioid withdrawal experience. Our data suggest that the 3-day precipitated withdrawal paradigm has the most profound effects on opioid-induced sleep dysregulation and further validates the construct of this model for opioid dependence and OUD. HighlightsO_LIMorphine withdrawal differentially dysregulates the sleep of male and female mice C_LIO_LI3-day precipitated withdrawal results in larger changes than spontaneous withdrawal C_LIO_LIOpioid withdrawal affects responses to future sleep deprivation differently between sexes C_LI

neuroscience↗