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.     

Deficits in passive avoidance and fear conditioning in mice with septal lesions

By means of a simple activity measure, mice with lesions of the septal forebrain were tested for passive avoidance (response inhibition) and fear conditioning. In two separate experiments animals with septal lesions showed little or no conditioning, as evidenced by lack of suppression of activity during and following activitycontingent foot shock. Results support and extend thehypothesis that these deficits in passive avoidance derive from the removal of normal inhibitory influences mediated by the septal area.     

Recovery from retrograde amnesia: a learning process

Retrograde amnesia was produced in rats by electroconvulsive shock. Memory recovered if the animals were given repeated test trials. Memory did not recover if steps were taken to reduce the conditioning properties of the test trials; the manipulations included eliminating the response, altering the apparatus cues, or extinguishing conditioned "fear" by confining animals to the apparatus during the first test trial.     

Retrograde amnesia: production of skseletal but not cardiac response gradient by electroconvulsive shock

Rats given a single electroconvulsive shock immediately after but not 60 seconds after an aversive conditioning trial exhibited behavioral retention deficits 24 hours later in a one-trial passive avoidance task. In contrast to these differential performance deficits, similar heart-rate changes, indicative of fear retention, were seen in punished animals irrespective of the time of delivery of the shock. These data suggest retention of a generalized fear to the training experience that was not revealed by the behavioral measure. The potential usefulness of concomitant behavioral and physiological response assessment in consolidation research is discussed.     

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.     

The role of social groups in the persistence of learned fear

Classical fear conditioning investigates how animals learn to associate environmental stimuli with an aversive event. We examined how the mechanisms of fear conditioning apply when humans learn to associate social ingroup and outgroup members with a fearful event, with the goal of advancing our understanding of basic learning theory and social group interaction. Primates more readily associate stimuli from certain fear-relevant natural categories, such as snakes, with a negative outcome relative to stimuli from fear-irrelevant categories, such as birds. We assessed whether this bias in fear conditioning extends to social groups defined by race. Our results indicate that individuals from a racial group other than one's own are more readily associated with an aversive stimulus than individuals of one's own race, among both white and black Americans. This prepared fear response might be reduced by close, positive interracial contact.     

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.     

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.     

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.     

Epinephrine enables Pavlovian fear conditioning under anesthesia

Rats under Pavlovian defensive conditioning (noise paired with shock) while under general anesthesia. Peripheral administration of epinephrine (0.01 to 1.0 milligram per kilogram of body weight) during training resulted in the acquisition of conditioned fear, as shown 10 days later by conditioned suppression of water drinking. Analysis of heart rate and measurement of reflexes during training indicated that epinephrine did not lighten the state of anesthesia. These results indicate that epinephrine enables the learning of conditioned fear in the anesthetized brain.     

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.     

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.     

Classical conditioning of pain-elicited aggression

Unconditioned aggression between paired animals in response to electric shock has been previously demonstrated. In this study, with the use of classical Pavlovian conditioning procedures, aggression was produced between paired rats as a response to a tone stimulus.     

Crossmodal interactions between olfactory and visual learning in Drosophila

Different modalities of sensation interact in a synergistic or antagonistic manner during sensory perception, but whether there is also interaction during memory acquisition is largely unknown. In Drosophila reinforcement learning, we found that conditioning with concurrent visual and olfactory cues reduced the threshold for unimodal memory retrieval. Furthermore, bimodal preconditioning followed by unimodal conditioning with either a visual or olfactory cue led to crossmodal memory transfer. Crossmodal memory acquisition in Drosophila may contribute significantly to learning in a natural environment.     

Infant handling: effects on avoidance learning, brain weight, and cholinesterase activity

Infant rats were "handled" by removing them periodically from their home cages. "Non-handled" rats were left undisturbed. Half of the animals were killed at weaning, and weights and cholinesterase activity were determined on four different sections of the brain. The remaining animals were conditioned to avoid an administered shock. Handling increased ventral-cortex and subcortical weights and decreased subcortical cholinesterase. No differences in avoidance conditioning were observed.     

Amnesia: a function of the temporal relation of footshock to electroconvulsive shock

When rats received a brief footshock upon stepping off an elevated platform, and an electroconvulsive shock 30 seconds or 6 hours afterward, amnesia was not observed 24 hours later. If a second footshock (noncontingent) was delivered 0.5 second before the electroconvulsive shock, amnesia was observed. The amnesia was temporary if conditioning was strong and permanent if conditioning was weak.     

利用RAP-PCR检测高盐刺激下Shewanella piezotolerans WP3的基因差异表达

选取高盐刺激为条件，利用实验室模拟极端环境培养条件下的菌体提取RNA，采用差异显示方法RAP—PCR扫描盐刺激下基因的差异表达。结果表明，在高盐刺激下，WP3下调表达的基因是SSl：hypotheticalproteins SS2：ferroxidase。上调的基因是SS3：gamme-butyrobetaineantiporter；SS4：hypothetical protein。     

Puromycin and retention in the goldfish

A first experiment compared the behavior of goldfish injected with puromycin immediately after each of a weekly series of brief discriminative training sessions in the shuttlebox to that of appropriate controls. Discrimination was not prevented, nor was escape from shock impaired, but probability of response to the conditioned stimuli, both positive and negative, was reduced substantially. These results suggest that puromycin interferes with the consolidation of conditioned fear. The null outcome of a second experiment, in which all training was given in a single long session instead of a series of short sessions, suggests (contrary to recent indications) that consolidation begins in the training session. The conditioned-fear hypothesis is supported by the results of a third experiment in which the animals were shocked upon entering a goalbox to which they had previously learned to swim for food; animals injected with puromycin, immediately after the shock, entered the goalbox more readily 1 week later than did appropriate controls.     

Glucocorticoids can induce PTSD-like memory impairments in mice

Posttraumatic stress disorder (PTSD) is characterized by a hypermnesia of the trauma and by a memory impairment that decreases the ability to restrict fear to the appropriate context. Infusion of glucocorticoids in the hippocampus after fear conditioning induces PTSD-like memory impairments and an altered pattern of neural activation in the hippocampal-amygdalar circuit. Mice become unable to identify the context as the correct predictor of the threat and show fear responses to a discrete cue not predicting the threat in normal conditions. These data demonstrate PTSD-like memory impairments in rodents and identify a potential pathophysiological mechanism of this condition.     

Benzodiazepines: anxiety-reducing activity by reduction of serotonin turnover in the brain

The anxiety-reducing effects of minor tranquilizers in the rat conflict test were mimicked by serotonin antagonists and by p-chlorophenylalanine, an inhibitor of serotonin synthesis; the depressant effects of the minor tranquilizers were mimicked by norepinephrine antagonists. Intraventricular injections of serotonin led to a suppression of behavior, and also antagonized the anxiety-reducing action of benzodiazeprines. Intraventricular injections of norepinephrine led to a release of punished behavior from suppression, and also antagonized the depressant action of benzodiazepines. The anxiety-reducing activity, and the decrease in serotonin turnover induced by benzodiazepines, were maintained over repeated doses, whereas depressant activity, and the decrease induced in norepinephrine turnover, both rapidly underwent tolerance. Tranquilizers may exert their anxiety-reducing effects by a reduction of serotonin activity in a behaviorally suppressive punishment system, and they may exert their depressant effects by a reduction of norepinephrine activity in a behaviorally facilitatory reward system.