亚磁环境孵化对雏鸡厌恶性条件化记忆的影响及相关的树突棘密度变化

地磁场是地球上生命活动环境的基本要素之一,而外太空中磁场强度接近于零,以往研究显示,地磁场消除（即亚磁场）对生物体结构和功能有多方面的负面影响,但对其作用机制了解仍然很少,本文使用厌恶性条件化学习任务,研究亚磁环境孵化对日龄雏鸡长时记忆的影响,分析雏鸡中枢记忆相关核团IMM和MSt中树突棘密度的变化,探讨亚磁场生物效应的神经基础,实验结果显示,在自然地磁环境中孵化的雏鸡,训练后4h保持显著的厌恶性条件化记忆,其后记忆随时间逐渐消退;而在亚磁环境中孵化的雏鸡,训练后4h已不具有对厌恶性刺激的记忆,对于正常雏鸡,厌恶性刺激导致两侧脑IMM和MSt中树突棘密度均显著升高,在保持记忆的样本中,树突棘密度升高幅度更大,并呈现左侧优势,对于亚磁雏鸡,树突棘密度升高幅度仅与不具有长时记忆的地磁雏鸡大致相当或略低,由此可见,中枢记忆相关核团中树突棘大幅增生是长时记忆的必要前提,地磁场消除可能抑制由厌恶性刺激引发的树突棘增生,从而造成雏鸡记忆功能受损。     

学习记忆相关基因研究进展

学习记忆是脑的重要功能之一,与学习记忆相关的基因很多,它们通过影响突触功能、信号转导、转录和翻译控制、能量代谢等途径进行学习记忆行为的调控。研究相关基因可为阐明学习记忆的分子机制和遗传机制奠定基础。     

雏鸡听觉印记学习

雏鸡听觉印记学习是研究新生个体在早期发育阶段学习与记忆形成的神经机制的良好实验模型.听觉刺激对印记学习有很好的强化作用,作用效果依赖于频率、强度和持续时间等声音特征.从声音的选择、听觉刺激所引起的分子水平和组织水平改变等方面综述雏鸡听觉印记学习的研究进展.     

apamin 对日龄雏鸡长时记忆的影响

日龄雏鸡的一次性被动回避学习任务模型被广泛应用于记忆机制研究, 具
有多方面的优势和便利性. apamin 是SK 通道(钙离子激活的小电导钾离子通道)的一
种选择性阻断剂, 以往研究显示其可能增进记忆. 但人们对其作用机制的了解不是很
充分. 使用颅内微量注射方法, 在雏鸡中枢记忆相关核团IMM 施加apamin, 研究其
对记忆形成和保持的影响. 实验结果显示, 雏鸡在弱刺激条件下的被动回避任务中本
不能形成稳定的长时记忆, 但在训练前短时间内或训练后立即注射适量apamin, 可
以易化长时记忆的形成. 然而, apamin 对记忆随时间衰退的过程几乎没有影响, 即对
记忆保持没有增进作用. 此外, 在左、右脑IMM 单侧注射apamin 都可促进记忆形成,
但所需剂量高于双侧注射时, 且在左侧产生效应的时间早于右侧, 这体现了两侧
IMM 在记忆加工中作用的不对称性. 这些结果提示, apamin 可能通过阻断中枢记忆
相关核团内的SK 通道, 影响由训练诱发的、与记忆形成有关的某些分子或细胞事件,
在一定程度上起到改善记忆的作用.     

组蛋白磷酸化参与学习记忆调控的分子机制

组蛋白磷酸化是组蛋白翻译后修饰诸多方式中的一种,属于表观遗传学的范畴,在DNA损伤修复、细胞分裂等过程中发挥作用.近年来研究表明,组蛋白磷酸化在学习记忆等认知功能中也发挥重要的调节作用.本文主要就组蛋白磷酸化在学习记忆中的作用,及其上游信号通路、下游转录调控机制做一综述,旨在为认知功能障碍相关疾病提供新的理论基础和治疗靶点.     

综述: 学习和记忆的跨代遗传：果蝇能告诉我们真相吗？

学习记忆是一个获取、储存和再巩固新知识的过程,并以行为作为输出信号.学习记忆是高等生物适应动态环境不可或缺的。学习和记忆能力缺陷会导致精神类疾病,如精神分裂症、抑郁症和阿尔兹海默病等.近年来,有研究发现这些精神类疾病能够遗传给后代,所以以动物模型来研究学习和记忆的跨代遗传机制已经开始.在这篇综述里,首先简要概括了目前有关学习和记忆的分子机制、神经环路和跨代遗传的可能机制;然后,讨论了利用果蝇模型来研究学习和记忆跨代遗传的可能性.最后,我们提供了可能的策略用以揭示果蝇学习和记忆跨代遗传的表观遗传机制.     

学习和记忆的跨代遗传:果蝇能告诉我们真相吗?（英文）

学习记忆是一个获取、储存和再巩固新知识的过程,并以行为作为输出信号.学习记忆是高等生物适应动态环境不可或缺的。学习和记忆能力缺陷会导致精神类疾病,如精神分裂症、抑郁症和阿尔兹海默病等.近年来,有研究发现这些精神类疾病能够遗传给后代,所以以动物模型来研究学习和记忆的跨代遗传机制已经开始.在这篇综述里,首先简要概括了目前有关学习和记忆的分子机制、神经环路和跨代遗传的可能机制;然后,讨论了利用果蝇模型来研究学习和记忆跨代遗传的可能性.最后,我们提供了可能的策略用以揭示果蝇学习和记忆跨代遗传的表观遗传机制.     

Eph家族蛋白在学习记忆中作用的研究进展

作为大脑最基本和重要的功能之一,学习记忆始终是脑科学研究的热点领域。尽管相关研究已经取得了很大进展,但其具体机制尚不完全清楚。能产生促红细胞生成素的肝癌细胞(eryth-ropoietin-producing hepatocellular carcinoma cell,Eph)受体与其配体肝配蛋白被统称为Eph家族蛋白,其分布十分广泛且功能复杂。越来越多的研究表明,Eph家族蛋白能够调控包括突触发生及突触可塑性等多种细胞行为,在学习记忆中发挥不可或缺的作用。本文重点介绍Eph家族蛋白对学习记忆的作用并对其可能的作用机制进行概述。     

核酸(脱)甲基化与内源甲醛及认知损伤

核酸(DNA和RNA)甲基化/脱甲基是表观遗传调控的重要机制.甲醛参与DNA、RNA的甲基化/脱甲基过程,从而影响表观遗传的调节,包括学习记忆等认知功能.然而,甲醛代谢失调将影响核酸的甲基化与脱甲基,使动物的学习记忆能力下降,造成认知损伤.对北京地区604名老人(≥60岁)的调查显示,内源甲醛含量与被试受教育的年限相关,受教育程度越高,内源甲醛含量越低,反之亦然.这些结果表明,内源甲醛在人类学习记忆中扮演重要的角色,"活到老,学到老"可以延缓甲醛代谢失调引起的老年认知损伤.因此,研究内源甲醛代谢与核酸甲基化修饰之间的关系,对探索记忆储存及认知损伤等表观遗传学相关疾病的发生发展机制,具有一定的启示.     

昆虫联想学习记忆研究的几种双通道范式

昆虫的大多数行为一直被认为是生来就有的本能行为,然而,近年来的研究已经证明大多数昆虫具有高度的学习记忆能力,并表现出对环境的适应行为。这些研究主要是采取了联想学习记忆的双通道范式。这些双通道范式,在学习记忆神经机制的研究中起到了重要的作用。本文主要综述近年来关于昆虫学习记忆研究的进展,重点介绍昆虫联想学习记忆研究的几种双通道范式。这对充分理解昆虫联想学习记忆的神经机制以及进一步深入开展学习与记忆功能的研究有重要的科学意义。     

Effects of Lanthanum Chloride Administration in Prenatal Stage on One-Trial Passive Avoidance Learning in Chicks

Lanthanum cations (La 3+) are well known for their inhibitory actions on calcium channels. Prenatal lanthanum exposure may affect the development of embryo and alter the capacity for learning and memory in adults, and the one-trial passive avoidance learning paradigm with day-old chicks is an excellent model to study several mechanisms of memory formation. In the present study, we examined the effects of prenatal lanthanum chloride exposure on memory consolidation using one-trial passive avoidance learning task in day-old chicks. The data suggest that chicks injected with lanthanum chloride (2 mg/kg) daily from E9 to E16 had significantly impaired long-term memory at 120 min after training (p < 0.05) but not the chicks injected with lanthanum chloride (0.1 mg/kg) daily from E9 to E16.     

小鸡早期记忆形成的神经机制

小鸡是研究早期记忆形成机制的理想动物模型.一日龄小鸡在一次性被动回避实验（one-trial-passive-avoidance-test）后,与记忆形成相关脑区的神经元在时间和空间上发生了一系列复杂的生理生化反应.综述了小鸡记忆形成过程的最新研究进展,分析了与记忆形成相关的神经回路、细胞和分子机制.     

A role for Melanin-Concentrating Hormone in learning and memory

The neurobiological substrate of learning process and persistent memory storage involves multiple brain areas. The neocortex and hippocampal formation are known as processing and storage sites for explicit memory, whereas the striatum, amygdala, neocortex and cerebellum support implicit memory. Synaptic plasticity, long-term changes in synaptic transmission efficacy and transient recruitment of intracellular signaling pathways in these brain areas have been proposed as possible mechanisms underlying short- and long-term memory retention. In addition to the classical neurotransmitters (glutamate, GABA), experimental evidence supports a role for neuropeptides in modulating memory processes. This review focuses on the role of the Melanin-Concentrating Hormone (MCH) and receptors on memory formation in animal studies. Possible mechanisms may involve direct MCH modulation of neural circuit activity that support memory storage and cognitive functions, as well as indirect effect on arousal.     

Dynorphin(1–13) impairs memory formation for aversive and appetitive learning in chicks

The opioid peptide dynorphin(1–13) impairs memory formation in chicks (5). We examined whether this occurs for both aversively and appetitively motivated learning. Four-day-old chicks were injected with dynorphin(1–13) into the intermediate medial hyperstriatum ventrale and trained on either a peck avoidance (PA) or an appetitive discrimination (AD) task; 2-day-old chicks were trained on PA. In 2-day-old chicks, dynorphin was amnestic for PA at 0.01, 0.03, or 0.1 mM. In 4-day-old chicks, dynorphin impaired memory formation for PA at 0.1 mM, and for AD training at 0.03 mM. Thus, similar doses of dynorphin impair memory formation for both appetitive and aversive conditioning.     

Metabotropic glutamate receptors (mGluRs) are involved in early phase of memory formation: possible role of modulation of glutamate release

Metabotropic glutamate receptors (mGluRs) groups I and II are involved in the cellular processes of long-term potentiation (LTP) and learning and memory formation. I.c.v. injection of the mGluRs agonist 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) can impair memory formation in some types of learning task. The role of mGluRs in neurotransmitters release and production of second messengers has been suggested. The aim of the present study was to determine the effect of i.c.v. administration of the new potent mGluRs agonist ABHxD-I and compare its effect with that of ACPD. We studied the effect of both agonists on acquisition and memory for a one-trial passive avoidance learning task in day-old chicks and on the training related glutamate (Glu) release. ACPD or ABHxD-I (50 nmole per chick, i.c.v. injection) were administered at different times before or after training and chicks were tested at various times after training. Chicks injected with ABHxD-I 30 min before training showed amnesia when tested 30 min or 3h after training. The amnestic effect of ACPD was significant only 30 min after training. Glu release evoked by 70 mM KCl was measured in slices prepared from the IMHV of chick brain isolated from animals injected with either ACPD or ABHxD-I 30 min before training and tested 30 min after training. Glu concentration was measured using HPLC. Both ACPD and ABHxD-I significantly increased Glu release in slices isolated from untrained chicks (30 and 48% compare to control, respectively, P<0.05). Training itself increased Glu release (41% compared to control, P<0.01) and no additional effect of either ACPD or ABHxD-I was observed. These results suggest that mGluRs groups I and II are involved in the early stages of memory formation and that application of either of the studied mGluRs agonists may interfere with that process. The amnestic effect of ABHxD-I seems to be stronger and longer lasting. Although the mechanism of this effect still remains unclear, our results suggest that disregulation of Glu release by mGluR agonists may participate in this process.     

Neurospecific Proteins and Memory

The review reports on the experimental models that are used in studies of memory formation (in particular, passive avoidance training) and on brain structures, which have special relevance to this phenomenon. The advanced knowledge about the sequence of neurochemical processes that occur in the synaptic mechanisms during fixation of a memory trace is analyzed. The special role of neurospecific proteins (in particular, the cell adhesion proteins) in plastic modifications of the neuronal links relevant to memory is emphasized. Attention is drawn to the general features of the mechanisms providing the development of nerve tissue and memory formation.     

Time-Dependent Increase in Release of Arachidonic Acid Following Passive Avoidance Training in the Day-Old Chick

Abstract: We have investigated the role of arachidonic acid, a putative retrograde messenger, in a one-trial aversive learning task in the day-old chick. The left and right intermediate medial hyperstriatum ventrale (IMHV) in the chick forebrain have previously been implicated in the formation of memory for this task. Using an ex vivo technique we have determined the concentrations of various fatty acids liberated from prisms prepared from these brain regions at different time points up to 24 h following passive avoidance training. At 30, 60, and 75 min post-training the concentration of arachidonic acid, but not of other fatty acids, in prisms prepared from the left IMHV, but not the right IMHV, was enhanced compared with that in chicks trained on a nonaversive water-coated bead. To test whether arachidonic acid liberation from the left IMHV was receptor-stimulated we showed that (a) liberation of endogenous arachidonic acid from homogenate prepared from the left and right IMHV of untrained chicks was stimulated by depolarization with KCl (50 m M ) and that (b) glutamate agonists of the NMDA and metabotropic subtypes of glutamate receptor stimulated release of preloaded [¹⁴C]arachidonic acid from prisms prepared from the left IMHV but not the right IMHV. These results indicate that arachidonic acid is liberated from the left IMHV following passive avoidance training in the day-old chick and may play a role as a retrograde messenger in this memory task.     

The role of group I metabotropic glutamate receptors in memory consolidation and reconsolidation in the passive avoidance task in 1-day-old chicks

Although reconsolidation of memory after reminder does not seem to be the simple reiteration of the sequential stages occurring during memory consolidation, both phenomena probably employ similar mechanisms including activation of glutamate receptors and protein synthesis. It is known that group I metabotropic glutamate receptors (mGluRs) are involved in memory consolidation and modulation of protein synthesis. The aim of present study was to investigate the role of mGluR5 in memory consolidation and reconsolidation and to determine whether inhibition of these receptors may affect protein synthesis in these processes. The one-trial passive avoidance task on chicks was used as the experimental model of learning. Injection of the mGluR5 antagonist MPEP into a specific chick brain region IMM resulted in amnesia, provided the injection was made either shortly before or after training, or approximately 4 h after training. This amnesia was permanent, resembling the effects of protein synthesis inhibitors. MPEP injection immediately after reminder resulted in only a transient amnesia revealed 1h later. Increased expression of Zif/268 and c-Fos proteins 2 h after initial training was abolished bilaterally in chicks injected with MPEP. Injection of MPEP immediately after reminder did not inhibit c-Fos and Zif/268 expression, on the contrary, their expression was increased, specifically in left IMM and was similar to that observed after initial training. These results show that at least in the chick model mGluR5 play an important role in both consolidation and reconsolidation of memory but the mechanisms triggered by their activation in these processes differ. It is suggested that Ca(2+) signal derived from mGluR5 stimulation is necessary for complete memory consolidation, whereas during reconsolidation other mGluR5 triggered mechanisms of protein synthesis activation and regulation may be involved.     

Prenatal testosterone improves the spatial learning and memory by protein synthesis in different lobes of the brain in the male and female rat

The high density of the steroid hormone receptors in the structures of temporal lobe involved in learning and memory, such as the hippocampus, perirhinal cortex, entorhinal cortex and amigdaloid complex, shows that there must be a direct relationship between gonadal hormones and organizational effects of steroid hormones in those structures during development of the nervous system. The present study was undertaken in order to investigate the effect of testosterone administration during the third week of gestation on the spatial memory formation of the offspring rats and the level of soluble proteins in the temporal lobe and frontal lobe of brain, as evidence of important organizational effects of androgens during prenatal development in brain sexual dimorphism. Animals have received testosterone undecanoate on days 14, 15, 16 and 19, 20, 21 of gestation. Learning and memory tests were started 100 days after the testosterone treatment. At the end of the experiments, the temporal and frontal lobes of brain were removed for assessing the level of soluble proteins. Testosterone treatment significantly improved spontaneous alternations percentage of male offspring in Y-maze task comparative with female offspring and reference memory in radial 8 arm-maze task (decreasing in number of reference memory errors in both male and female offspring groups), suggesting effects of both short and long-term memory. Also, testosterone significantly increased the brain soluble protein level of treated female rats in 14–16 prenatal days compared with the control group as well as the brain soluble protein level of treated male rats. These results suggest that steroid hormones play an important role in the spatial learning and memory formation by means of protein synthesis in different lobes of the brain.     

Fear memory and the amygdala: insights from a molecular perspective

The amygdala modulates memory consolidation and the storage of emotionally relevant information in other brain areas, and itself comprises a site of neural plasticity during aversive learning. These processes have been intensively studied in Pavlovian fear conditioning, a leading aversive learning paradigm that is dependent on the structural and functional integrity of the amygdala. The rapidness and persistence, and the relative ease, with which this conditioning paradigm can be applied to a great variety of species have made it an attractive model for neurochemical and electrophysiological investigations on memory formation. In this review we summarise recent studies which have begun to unravel cellular processes in the amygdala that are critical for the formation of long-term fear memory and have identified molecular factors and mechanisms of neural plasticity in this brain area.