Generation of a synthetic memory trace

We investigated the effect of activating a competing, artificially generated, neural representation on encoding of contextual fear memory in mice. We used a c-fos-based transgenic approach to introduce the hM(3)D(q) DREADD receptor (designer receptor exclusively activated by designer drug) into neurons naturally activated by sensory experience. Neural activity could then be specifically and inducibly increased in the hM(3)D(q)-expressing neurons by an exogenous ligand. When an ensemble of neurons for one context (ctxA) was artificially activated during conditioning in a distinct second context (ctxB), mice formed a hybrid memory representation. Reactivation of the artificially stimulated network within the conditioning context was required for retrieval of the memory, and the memory was specific for the spatial pattern of neurons artificially activated during learning. Similar stimulation impaired recall when not part of the initial conditioning.     

Synaptic protein degradation underlies destabilization of retrieved fear memory

Reactivated memory undergoes a rebuilding process that depends on de novo protein synthesis. This suggests that retrieval is dynamic and serves to incorporate new information into preexisting memories. However, little is known about whether or not protein degradation is involved in the reorganization of retrieved memory. We found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after retrieval of contextual fear memory. Moreover, the infusion of proteasome inhibitor into the CA1 region immediately after retrieval prevented anisomycin-induced memory impairment, as well as the extinction of fear memory. This suggests that ubiquitin- and proteasome-dependent protein degradation underlies destabilization processes after fear memory retrieval. It also provides strong evidence for the existence of reorganization processes whereby preexisting memory is disrupted by protein degradation, and updated memory is reconsolidated by protein synthesis.     

Amygdalar and hippocampal theta rhythm synchronization during fear memory retrieval

The amygdalohippocampal circuit plays a pivotal role in Pavlovian fear memory. We simultaneously recorded electrical activity in the lateral amygdala (LA) and the CA1 area of the hippocampus in freely behaving fear-conditioned mice. Patterns of activity were related to fear behavior evoked by conditioned and indifferent sensory stimuli and contexts. Rhythmically synchronized activity at theta frequencies increased between the LA and the CA1 after fear conditioning and became significant during confrontation with conditioned fear stimuli and expression of freezing behavior. Synchronization of theta activities in the amygdalohippocampal network represents a neuronal correlate of conditioned fear, apt to improve neuronal communication during memory retrieval.     

正确认识年龄损害记忆——动物学研究

年龄相关性学习记忆能力减退是从人到啮齿类动物的常见现象.但因受到支持的记忆系统不同,各种类型的记忆形式受到年龄影响各不相同.并非所有形式的记忆都受损.受损的记忆消失也并非同时出现,且受损程度不同,以空间性记忆受损最早最重.衰老过程中,不同形式的记忆可能此消彼长,有些形式的记忆甚至可能增强.因此,在研究年龄相关性学习记忆能力减退时最好使用多个任务进行记忆评估.     

Fear erasure in mice requires synergy between antidepressant drugs and extinction training

Antidepressant drugs and psychotherapy combined are more effective in treating mood disorders than either treatment alone, but the neurobiological basis of this interaction is unknown. To investigate how antidepressants influence the response of mood-related systems to behavioral experience, we used a fear-conditioning and extinction paradigm in mice. Combining extinction training with chronic fluoxetine, but neither treatment alone, induced an enduring loss of conditioned fear memory in adult animals. Fluoxetine treatment increased synaptic plasticity, converted the fear memory circuitry to a more immature state, and acted through local brain-derived neurotrophic factor. Fluoxetine-induced plasticity may allow fear erasure by extinction-guided remodeling of the memory circuitry. Thus, the pharmacological effects of antidepressants need to be combined with psychological rehabilitation to reorganize networks rendered more plastic by the drug treatment.     

Calcium-permeable AMPA receptor dynamics mediate fear memory erasure

Traumatic fear memories can be inhibited by behavioral therapy for humans, or by extinction training in rodent models, but are prone to recur. Under some conditions, however, these treatments generate a permanent effect on behavior, which suggests that emotional memory erasure has occurred. The neural basis for such disparate outcomes is unknown. We found that a central component of extinction-induced erasure is the synaptic removal of calcium-permeable α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs) in the lateral amygdala. A transient up-regulation of this form of plasticity, which involves phosphorylation of the glutamate receptor 1 subunit of the AMPA receptor, defines a temporal window in which fear memory can be degraded by behavioral experience. These results reveal a molecular mechanism for fear erasure and the relative instability of recent memory.     

Localization of a stable neural correlate of associative memory

Do learning and retrieval of a memory activate the same neurons? Does the number of reactivated neurons correlate with memory strength? We developed a transgenic mouse that enables the long-lasting genetic tagging of c-fos-active neurons. We found neurons in the basolateral amygdala that are activated during Pavlovian fear conditioning and are reactivated during memory retrieval. The number of reactivated neurons correlated positively with the behavioral expression of the fear memory, indicating a stable neural correlate of associative memory. The ability to manipulate these neurons genetically should allow a more precise dissection of the molecular mechanisms of memory encoding within a distributed neuronal network.     

Monkeys reared in isolation with pictures as visual input: evidence for an innate releasing mechanism

Monkeys reared in isolation from birth to 9 months received varied visual input solely from colored slides of monkeys in various activities and from nonmonkey pictures. Exploration, play, vocalization, and disturbance occurred most frequently with pictures of monkeys threatening and pictures of infants.From 2.5 to 4 months threat pictures yielded a high frequency of disturbance.Lever-touching to turn threat pictures on was very low during this period. Pictures of infants and of threat thus appear to have prepotent general activating properties, while pictures of threat appear to release a developmentally determined, inborn fear response.     

The involvement of the anterior cingulate cortex in remote contextual fear memory

Although the molecular, cellular, and systems mechanisms required for initial memory processing have been intensively investigated, those underlying permanent memory storage remain elusive. We present neuroanatomical, pharmacological, and genetic results demonstrating that the anterior cingulate cortex plays a critical role in remote memory for contextual fear conditioning. Imaging of activity-dependent genes shows that the anterior cingulate is activated by remote memory and that this activation is impaired by a null alpha-CaMKII mutation that blocks remote memory. Accordingly, reversible inactivation of this structure in normal mice disrupts remote memory without affecting recent memory.     

Electroconvulsive shock effects on a reactivated memory trace: further examination

Rats showed amnesia for conditioned fear training if given an electroconvulsive shock immediately after training. Retention was unimpaired, however, when the electroconvulsive shock treatment was given 1 day after training immediately after the presentation of the stimulus used in the fear conditioning training. These results support the view that electroconvulsive shock disrupts memory trace consolidation but does not disrupt a recently reactivated memory trace.     

基于SPR技术的农产品物流安全管理的研究

随着农产品质量安全事件频繁爆发、国际农产品贸易屡屡受阻,不仅影响到我国的国际声誉、政府形象,对农产品行业在国际贸易中的竞争力构成威胁,直接损害农产品供给主体的经济利益,而且威胁到消费者的身体健康和生命安全,并造成公众的消费的心理恐慌。将SPR技术应用于农产品物流安全管理中,设计出一种光学SPR生物分析仪,对农产品中残留的农、兽药进行检测,最后通过对实验数据的分析,展望了SPR技术在进行农产品物流安全管理中的应用前景。     

Electrical synapses control hippocampal contributions to fear learning and memory

The role of electrical synapses in synchronizing neuronal assemblies in the adult mammalian brain is well documented. However, their role in learning and memory processes remains unclear. By combining Pavlovian fear conditioning, activity-dependent immediate early gene expression, and in vivo electrophysiology, we discovered that blocking neuronal gap junctions within the dorsal hippocampus impaired context-dependent fear learning, memory, and extinction. Theta rhythms in freely moving rats were also disrupted. Our results show that gap junction-mediated neuronal transmission is a prominent feature underlying emotional memories.     

Forms of memory failure

Memory may fail in a variety of ways. Patients with Korsakoff's syndrome demonstrate global memory deficits similar to those seen in patients with early progressive dementia. Korsakoff's patients, however, may recall rules and principles for organizing information and can gain access to their previously acquired knowledge (semantic memory), whereas recent memory may be grossly impaired. In contrast, dementia patients may have little access to previously acquired knowledge and therefore have great difficulty in organizing and encoding ongoing events. These contrasting forms of memory failure have implications for understanding the structure and mechanisms of memory and learning, particularly the relationship between episodic and semantic memory, as well as the development of therapeutic strategies for cognitive impairments.     

Retrograde amnesia produced by electroconvulsive shock after reactivation of a consolidated memory trace

Rats had a memory loss of a fear response when they received an electroconvulsive shock 24 hours after the fear-conditioning trial and preceded by a brief presentation of the conditioned stimulus. No such loss occurred when the conditioned stimulus was not presented. The memory loss in animals given electroconvulsive shock 24 hours after conditioning was, furthermore, as great as that displayed in animals given electroconvulsive shock immediately after conditioning. This result throws doubt on the assertion that electroconvulsive shock exerts a selective amnesic effect on recently acquired memories and thus that electroconvulsive shock produces amnesia solely through interference with memory trace consolidation.     

Stability of retrieved memory: inverse correlation with trace dominance

In memory consolidation, the memory trace stabilizes and becomes resistant to certain amnesic agents. The textbook account is that for any memorized item, consolidation starts and ends just once. However, evidence has accumulated that upon activation in retrieval, the trace may reconsolidate. Whereas some authors reported transient renewed susceptibility of retrieved memories to consolidation blockers, others could not detect it. Here, we report that in both conditioned taste aversion in the rat and fear conditioning in the medaka fish, the stability of retrieved memory is inversely correlated with the control of behavior by that memory. This result may explain some conflicting findings on reconsolidation of activated memories.     

Reversal of antipsychotic-induced working memory deficits by short-term dopamine D1 receptor stimulation

Chronic blockade of dopamine D2 receptors, a common mechanism of action for antipsychotic drugs, down-regulates D1 receptors in the prefrontal cortex and, as shown here, produces severe impairments in working memory. These deficits were reversed in monkeys by short-term coadministration of a D1 agonist, ABT 431, and this improvement was sustained for more than a year after cessation of D1 treatment. These findings indicate that pharmacological modulation of the D1 signaling pathway can produce long-lasting changes in functional circuits underlying working memory. Resetting this pathway by brief exposure to the agonist may provide a valuable strategy for therapeutic intervention in schizophrenia and other dopamine dysfunctional states.     

Postsynaptic receptor trafficking underlying a form of associative learning

To elucidate molecular, cellular, and circuit changes that occur in the brain during learning, we investigated the role of a glutamate receptor subtype in fear conditioning. In this form of learning, animals associate two stimuli, such as a tone and a shock. Here we report that fear conditioning drives AMPA-type glutamate receptors into the synapse of a large fraction of postsynaptic neurons in the lateral amygdala, a brain structure essential for this learning process. Furthermore, memory was reduced if AMPA receptor synaptic incorporation was blocked in as few as 10 to 20% of lateral amygdala neurons. Thus, the encoding of memories in the lateral amygdala is mediated by AMPA receptor trafficking, is widely distributed, and displays little redundancy.     

Neuronal competition and selection during memory formation

Competition between neurons is necessary for refining neural circuits during development and may be important for selecting the neurons that participate in encoding memories in the adult brain. To examine neuronal competition during memory formation, we conducted experiments with mice in which we manipulated the function of CREB (adenosine 3',5'-monophosphate response element-binding protein) in subsets of neurons. Changes in CREB function influenced the probability that individual lateral amygdala neurons were recruited into a fear memory trace. Our results suggest a competitive model underlying memory formation, in which eligible neurons are selected to participate in amemorytrace as a function of their relative CREB activity at the time of learning.     

提高园林专业学生树种识别能力的方法与途径

树种识别是高校园林专业学生应该掌握的基本技能之一,但是由于学生在学习过程中存在畏难情绪、缺乏系统整理等原因,导致其对树种的识别能力还有待提高。该文基于教学实践的基础之上,总结了理论与实践相结合、多种记忆方法配合使用、教材与辅导书相配套、网络资源的有效利用等提高树种识别能力的方法与途径。