Abstract
Objective : Sleep disorder or sleep deprivation (SD) is a common issue in today’s society. Numerous evidences show that sleep is essential for proper brain performance and cognitive processes; on the other hand, cognitive functions have a broad range with learning and long-term memory as the most important ones related to attention. Since many studies show that cholinergic system has a significant role in sleep, learning, and memory, this study aims to investigate the impacts of CA1 Cholinergic Nicotinic Receptors on memory acquisition deficit which is stimulated by total sleep deprivation (TSD) and REM sleep deprivation (RSD). Methodology : In this study a water box or a multi-platform apparatus was used in order to induce total sleep deprivation (TSD) or REM sleep deprivation (RSD). In order to investigate interactions of cholinergic system and hippocampus-dependent memory, nicotinic receptor agonist (nicotine) or nicotinic receptor antagonist (mecamylamine) was injected in hippocampal CA1. Results : According to the results of this study, 24 hours TSD or RSD decreased memory acquisition and injection of nicotine (0.0001 or mecamylamine (0.001 in TSD and RSD sham groups didn’t change memory acquisition. However, injection of sub-threshold dose of nicotine (0.0001 and mecamylamine (0.001 could reduce negative effects of SD in both TSD and RSD. Discussion ; According to the present study, cholinergic nicotinic receptors are effective in learning and memory improvement.
Highlights
In today’s world, prolonged wakefulness can be considered as a widespread phenomenon which probably occurs because of acute total sleep deprivation (TSD) or chronic partial sleep limitation.[1]
One-way analysis of variance (ANOVA) and post hoc Tukey test showed that intra-CA1 injection of nicotine in the normal rats at doses 0.001 and 0.1 but not 0.0001 and 0.01 μg/rat reduced memory acquisition [F (3, 24) =22.681; P < 0.05; Figure 1, panel 1A], but it did not alter pain response [F (3, 24)=4.698, P > 0.05; Figure 1, pane1 2A] while nicotine at doses 0.01 and 0.1 but not 0.0001 and 0.001 μg/rat increased response induced by loco-motor activity in normal rats [F (3, 24)=49.40, P < 0.05; Figure 1, panel 3A]
One-way ANOVA and post hoc Tukey test showed that intra-CA1 injection of mecamylamine in the normal rats at all doses reduced memory acquisition [F (3, 24) =6.252; P 0.05; Figure 1, pane1 2B] while mecamylamine at all doses increased response induced by loco-motor activity [F (3, 24)=24.69, P < 0.05; Figure 1, panel 3B]
Summary
In today’s world, prolonged wakefulness can be considered as a widespread phenomenon which probably occurs because of acute total sleep deprivation (TSD) or chronic partial sleep limitation.[1]. Studies have shown that sleep is essential to maintain energy, regulate heat, and recover tissues[4]; it is beneficial for proper cognitive functions.[5,6] On the other hand, it seems that lack of sleep or sleep disorder will have reverse effects which may cause cognitive deficiencies such as impairment in attention, decision making, learning, and various kinds of memory.[5,6] lack of sleep activates sympathetic system and leads to hypertension as well as increased cortisol,[7] while immune responses are impaired 8 and changes in mood are observed.[9]. Since many studies show that cholinergic system has a significant role in sleep, learning, and memory, this study aims to investigate the impacts of CA1 Cholinergic Nicotinic Receptors on memory acquisition deficit which is stimulated by total sleep deprivation (TSD) and REM sleep deprivation (RSD).
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