Ebrahim Rahmani Moghadam, Saied Karbalay-Doust, Mehrnaz Ghalavandi, Mahboobeh Erfanizadeh, Mohammad Reza Namavar,
Volume 26, Issue 2 (6-2024)
Abstract
Background: Sleep deprivation, a common problem in modern life, can induce oxidative stress and inflammatory responses, exerting adverse effects on cognitive functions. These injuries may be the result of cellular and molecular changes in some areas of the brain, such as the frontal nucleus of the thalamus and mammary bodies, which have received assiduous attention. These nuclei participate in learning, memory, and emotional (and recently sleep) functions. The present study aimed to assess the effect of chronic sleep deprivation on structural changes in these areas.
Materials and Methods: A total of 21 adult male rats were randomly assigned to three groups: control, control-grid, and sleep deprivation, and examined for 21 days. Brains were removed and fixed with buffered formalin. Brains were serially and systematically cut and stained with Giemsa. The total volume of nuclei and their total number of neurons and non-neurons were unbiasedly estimated by stereological methods.
Results: The findings of this study demonstrated that chronic sleep deprivation reduced the total volume of all nuclei (anterior nuclei of the thalamus and mammillary bodies of the hypothalamus) when compared with control groups (P<0. 05). Moreover, the total number of neurons and non-neurons in these structures significantly decreased in sleep-deprived animals when compared with control groups.
Conclusion: Chronic sleep deprivation has detrimental effects on the central nervous system and limbic system, as well as on the anterior nucleus of the thalamus, which, until recently, was believed to be not involved in sleep. These effects could be partly due to a decrease in cell (neuron and non-neuron) number, resulting in functional loss of this system.
Maryam Mohammadian, Aminollah Bahaoddini, Mohammadreza Namavar,
Volume 27, Issue 1 (12-2025)
Abstract
Background: Abnormalities of electrocardiogram and cardiac arrhythmias after stroke are very common. This study investigated the effect of IC87201, a molecule affecting the NMDA receptor intracellular signaling pathway, on reducing QT interval prolongation, as the most common electrocardiogram change after cerebral ischemia, in male rats.
Materials and Methods: In this study, 15 male adult rats were randomly divided into three groups: MCAO, MCAO+DXM (dextromethorphan hydrobromide monohydrate, NMDA receptor antagonist), and MCAO+IC87201 (n=5 each). Two hours after ischemia, solvent, DXM, and IC87201 were injected intraperitoneally into these three groups, respectively. Pre-ischemia, four hours, and forty-eight hours post-ischemia neurological-behavioral scores were assessed using the neurological deficit score test. Statistical differences were measured using repeated measures analysis of variance (P<0.05).
Results: QT interval significantly prolonged after ischemia. Administration of IC87201 significantly reduced this interval, whereas DXM did not have such an effect. The LF/HF ratio, as an index of autonomic nervous system balance on cardiac performance, significantly increased forty-eight hours after ischemia. This imbalance improved forty-eight hours after the injection of both IC87201 and DXM.
Conclusion: The results of this study indicated that cerebral ischemia could lead to an increase in sympathetic activity, which in turn causes prolonged QT interval. The administration of IC87201 may be effective in improving this condition by reducing the QT interval. Therefore, IC87201 may potentially be considered a suitable option for reducing cardiac complications following stroke.
