Eydipour Zainab, Vaezi Gholamhassan, Nasehi Mohammad, Haeri-Rouhani Seyed-Ali, Zarrindast Mohammad-Reza
Department of Biology, Damghan Branch, Islamic Azad University, Semnan, Iran.
Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
Arch Iran Med. 2017 Sep;20(9):581-588.
Serotonin receptors such as 5-HT3 plays critical role in regulation of sleep, wake cycle and cognitive process. Thus, we investigated the role of CA1 5HT3 serotonin receptors in memory acquisition deficit induced by total sleep deprivation (TSD; for 24 hour) and REM sleep deprivation (RSD; for 24 hour). Pain perception and locomotor activity were also assessed as factors that may affect the memory process.
Modified water box and multi-platform apparatus were used to induce TSD or RSD, respectively. Passive avoidance, hot plate and open field devices were used for assessment of memory acquisition, pain and locomotor activity, respectively.
Totally, 152 male Wistar rats were used in the study. Pre-training, intra-CA1 injection of 5-HT3 receptor agonist Chlorophenylbiguanide (Mchl; 0.01 and 0.001 µg/rat; P < 0.001) and antagonist Y-25130 (0.1 µg/rat; P < 0.001) reduced memory acquisition and did not alter pain response, while higher dose of both drugs increased locomotor activity in normal rats. Both TSD and RSD reduced memory acquisition (P < 0.001) and did not alter locomotor activity, while TSD (P < 0.001) but not RSD induced analgesia effect. The amnesia induced by TSD was restored by subthreshold dose of Y25130 (0.001 µg/rat; P < 0.001) but not Mchl (0.0001 µg/rat), while both drugs reversed TSD-induced analgesia effect (P < 0.01 for Mchl and P < 0.05 for Y25130), and Y25130 increased locomotor activity in TSD rats (P < 0.05). In RSD rats, subthreshold dose of both drugs did not alter memory acquisition deficit and increased locomotor activity (P < 0.001 for Mchl and P < 0.01 for Y25130), while the Y25130 (P < 0.001), but not Mchl induced analgesia in the RSD rats.
Based on the above data, CA1 5HT3 receptors seem to play a critical role in cognitive and non-cognitive behaviors induced by TSD and RSD.
血清素受体如5-HT3在睡眠、觉醒周期及认知过程的调节中起关键作用。因此，我们研究了CA1区5HT3血清素受体在完全睡眠剥夺（TSD，持续24小时）和快速眼动睡眠剥夺（RSD，持续24小时）诱导的记忆获取缺陷中的作用。疼痛感知和运动活动也作为可能影响记忆过程的因素进行了评估。
分别使用改良水盒和多平台装置诱导TSD或RSD。被动回避、热板和旷场装置分别用于评估记忆获取、疼痛和运动活动。
本研究共使用了152只雄性Wistar大鼠。训练前，向CA1区内注射5-HT3受体激动剂氯苯双胍（Mchl，0.01和0.001μg/只大鼠；P<0.001）和拮抗剂Y-25130（0.1μg/只大鼠；P<0.001）会降低记忆获取，且不改变疼痛反应，而两种药物的高剂量会增加正常大鼠的运动活动。TSD和RSD均降低了记忆获取（P<0.001），且不改变运动活动，而TSD（P<0.001）而非RSD诱导了镇痛作用。TSD诱导的失忆可通过阈下剂量的Y25130（0.001μg/只大鼠；P<0.001）而非Mchl（0.0001μg/只大鼠）恢复，而两种药物均逆转了TSD诱导的镇痛作用（Mchl为P<0.01，Y25130为P<0.05），且Y25130增加了TSD大鼠的运动活动（P<0.05）。在RSD大鼠中，两种药物的阈下剂量均未改变记忆获取缺陷，且增加了运动活动（Mchl为P<0.001，Y25130为P<0.01），而Y25130（P<0.001）而非Mchl在RSD大鼠中诱导了镇痛作用。
基于上述数据，CA1区5HT3受体似乎在TSD和RSD诱导的认知和非认知行为中起关键作用。
