Lindseyrowland3996

Intra-LC DAMGO altered the LFP power spectrum selectively in male but not female rats, resulting in a time-dependent increase in the power in delta and alpha frequency bands. LC microinfusion of ACSF had no effect on either sex. Together, the results are consistent with previous evidence for decreased MOR function in the female rat LC and demonstrate that this translates to a diminished effect on cortical activity that can account for sex differences in cognitive consequences. Decreased LC-MOR function in females could contribute to greater stress-induced activation of the LC and increased vulnerability of females to hyperarousal symptoms of stress-related neuropsychiatric pathologies.During puberty, sexual hormones induce crucial changes in neural circuit organization, leading to significant sexual dimorphism in adult behaviours. The ventrolateral division of the ventromedial nucleus of the hypothalamus (VMHvl) is the major neural site controlling the receptive component of female sexual behaviour, which is dependent on ovarian hormones. The inputs to the VMHvl, originating from the medial nucleus of the amygdala (MeA), transmit essential information to trigger such behaviour. In this study, we investigated the projection pattern of the MeA to the VMHvl in ovariectomized rats at early puberty. Six-week-old Sprague-Dawley rats were ovariectomized (OVX) and, upon reaching 90 days of age, were subjected to iontophoretic injections of the neuronal anterograde tracer Phaseolus vulgaris leucoagglutinin into the MeA. Projections from the MeA to the VMHvl and to other structures included in the neural circuit responsible for female sexual behaviour were analysed in the Control and OVX groups. The results of the semi-quantitative analysis showed that peripubertal ovariectomy reduced the density of intra-amygdalar fibres. The stereological estimates, however, failed to find changes in the organization of the terminal fields of nerve fibres from the MeA to the VMHvl in the adult. The present data show that ovariectomized rats during the peripubertal phase did not undergo significant changes in MeA fibres reaching the VMHvl; however, they suggest a possible effect of ovariectomy on MeA connectivity under amygdalar subnuclei.Previous studies have reported that real-time functional magnetic resonance imaging (fMRI) neurofeedback using motor imagery can modulate the activity of several motor-related areas. However, the differences in these modulatory effects on distinct motor-related target regions using the same experimental protocol remain unelucidated. This study aimed to compare neurofeedback effects on the primary motor area (M1) and the ventral premotor cortex (PMv). Of the included participants, 15 received blood oxygenation level-dependent (BOLD) signals from their left M1, and the other 15 received signals from their left PMv. Both groups were instructed to try to increase the neurofeedback score (NF-Score), which reflected the averaged activation level of the target region, by executing or imagining a right-hand clenching movement. The result revealed that during imagery condition, the left M1 was deactivated in the PMv-group but not in the M1-group, whereas the left PMv was activated in the PMv-group but not in the M1-group. Our finding indicates that neurofeedback from distinct motor-related regions has different effects on brain activity regulation.Methamphetamine (METH) may cause long‒lasting neurotoxic effects and cognitive impairment. On the other hand, the ovarian hormones estrogen and progesterone have neuroprotective effects. In the current study, we aimed to examine the effects of estrogen and progesterone on anxiety‒like behavior and neuronal damage in METH‒exposed ovariectomized (OVX) rats. Three weeks after ovariectomy, the animals received estrogen (1 mg/kg, i.p.), or progesterone (8 mg/kg, i.p.), or estrogen plus progesterone (with the same doses), or vehicle during 7 consecutive days (days 22-28). On day 28, OVX rats were exposed to a single‒day METH regimen (6 mg/kg, four s.c. Injections, with 2 h interval) 30 min after the hormone treatment. The next day (on day 29), the animals were assessed for anxiety‒related behaviors using the open field and elevated plus‒maze tasks. The animals were then sacrificed and brain water content, cell apoptosis and expression of IL-1β were evaluated. The findings showed that treatment with estrogen or progesterone alone in METH‒exposed rats significantly improved hyperthermia, anxiety‒like behavior, neuronal damage, and inflammation in the CA1 area. Also, treatment with estrogen plus progesterone improved hyperthermia and brain edema. Taken together, the findings suggest that treatment with ovarian hormones can partially prevent hyperthermia and anxiety‒related behaviors induced by METH in OVX rats, which could be accompanied by their neuroprotective effects in the hippocampus.Neurodegenerative diseases lead to a progressive demise of neuronal functions that ultimately results in neuronal death. Besides a large variety of molecular pathways that have been linked to the degeneration of neurons, dysfunctions of the microtubule cytoskeleton are common features of many human neurodegenerative disorders. Yet, it is unclear whether microtubule dysfunctions are causative, or mere bystanders in the disease progression. A so-far little explored regulatory mechanism of the microtubule cytoskeleton, the posttranslational modifications of tubulin, emerge as candidate mechanisms involved in neuronal dysfunction, and thus, degeneration. Here we review the role of tubulin polyglutamylation, a prominent modification of neuronal microtubules. We discuss the current understanding of how polyglutamylation controls microtubule functions in healthy neurons, and how deregulation of this modification leads to neurodegeneration in mice and humans.Pain is a common and devastating symptom among cancer patients. It can be caused by the cancer itself or by certain therapies like surgery, radiation or chemotherapy. Opioids are the first line of treatment for moderate to severe cancer-related pain. Opioids alone or in combination with non-opioid analgesics and adjuvant medications are important components for pain management during the perioperative period for cancer patients. Opioids act on the μ-opioid receptor (MOR), which is expressed in cancer cells and non-malignant cells of the tumor microenvironment. read more Retrospective studies suggest an association between the expression of MOR in cancers and shorter survival. In addition, recent evidence suggests that opium use and prescription opioids can influence clinical oncological outcomes. In this review, we will summarize the clinical evidence regarding the effect of opioid administration and survival in patients with cancer as well as the current evidence involving MOR expression and cancer progression.