Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, 110062, India.
Exp Brain Res. 2021 Aug;239(8):2359-2374. doi: 10.1007/s00221-021-06099-4. Epub 2021 Jun 7.
Learning and memory are one of those frontier areas of neurobiology which attract us to investigate the intricacy of this process. Here, we aimed to investigate the general mechanism of "Behavioural Tagging and Capture" in long term memory (LTM) formation and to find the key factors playing role in consolidation of LTM. In this study, we've shown that not only plasticity related proteins (PRPs) but neurotransmitters and immediate early genes (IEGs) also play an important role in memory formation process. It's very well evident that memory traces can last longer if close in time novelty is introduced around memory encoding. Here our results point out that this novelty exploration acts as a modulator in memory consolidation by providing PRPs such as brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), enhancing neurotransmitters (Dopamine), IEGs (cFos) and some enzymes such as acetylcholinesterase (AChE), monoamine oxidase (MAO), sodium-potassium ATPase (NaK-ATPase). Therefore, by using a Novel Object Recognition task (NOR) in combination with novel task exposure, we evaluated the role of molecular markers in memory consolidation employing a behavioural tagging model. The purpose of the current study was first to evaluate the effect of novelty exposure around a single trail of NOR task in a critical time window on memory consolidation in rats after 24 h and second to determine the expression of BDNF, CREB, c-fos, AChE, MAO, NaK-ATPase as potential markers in the medial prefrontal cortex (mPFC) during memory formation. In the present study, to identify and validate the role of these molecular signatures in memory consolidation, infusion of the protein synthesis inhibitor Anisomycin (Ani) was done around the training session that causes a deficit in the formation of LTM when tested 24 h after weak encoding. Altogether, here we are providing the first comprehensive set of evidences indicating that BDNF, CREB, dopamine, some enzymes and c-fos role in modulating LTM by employing behavioural tagging model.
学习和记忆是神经生物学的前沿领域之一,吸引我们深入研究这一复杂过程。在这里,我们旨在研究长期记忆(LTM)形成中“行为标记和捕获”的一般机制,并找到在 LTM 巩固中起作用的关键因素。在这项研究中,我们已经表明,不仅与可塑性相关的蛋白(PRPs),而且神经递质和即刻早期基因(IEGs)也在记忆形成过程中起着重要作用。如果在记忆编码周围及时引入接近时间的新颖性,记忆痕迹可以持续更长时间,这一点非常明显。在这里,我们的结果指出,这种新颖性探索通过提供脑源性神经营养因子(BDNF)、cAMP 反应元件结合蛋白(CREB)、增强神经递质(多巴胺)、IEGs(cFos)和一些酶(如乙酰胆碱酯酶(AChE)、单胺氧化酶(MAO)、钠钾-ATP 酶(NaK-ATPase)等 PRPs,作为记忆巩固的调节剂。因此,我们使用新颖物体识别任务(NOR)结合新颖任务暴露,通过行为标记模型评估分子标记物在记忆巩固中的作用。本研究的目的首先是评估在 NOR 任务的单个试验周围的新颖性暴露在大鼠 24 小时后对记忆巩固的影响,其次是确定 BDNF、CREB、c-fos、AChE、MAO、NaK-ATPase 在记忆形成过程中作为潜在标记物在中前额叶皮层(mPFC)中的表达。在本研究中,为了鉴定和验证这些分子特征在记忆巩固中的作用,在训练过程周围给予蛋白合成抑制剂 Anisomycin(Ani),当在弱编码后 24 小时进行测试时,会导致 LTM 形成缺陷。总的来说,我们在这里提供了第一个全面的证据集合,表明 BDNF、CREB、多巴胺、一些酶和 c-fos 通过行为标记模型在调节 LTM 中发挥作用。