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PubMed2004

Stress generates emotional memories and retrograde amnesia by inducing an endogenous form of hippocampal LTP.

Models of the neurobiology of memory have been based on the idea that information is stored as distributed patterns of altered synaptic weights in neuronal networks. Accordingly, studies have shown that post-training treatments that alter synaptic weights, such as the induction of long-term potentiation (LTP), can interfere with retrieval. In these studies, LTP induction has been relegated to the status of a methodological procedure that serves the sole purpose of disturbing synaptic activity in order to impair memory. This perspective has been expressed, for example, by Martin and Morris (2002: Hippocampus 12:609-636), who noted that post-training LTP impairs memory by adding "behaviorally meaningless" noise to hippocampal neural networks. However, if LTP truly is a memory storage mechanism, its induction should represent more than just a means with which to disrupt memory. Since LTP induction produces retrograde amnesia, the formation of a new memory should also produce retrograde amnesia. In the present report, we suggest that one type of learning experience, the storage of fear-related (i.e., stressful) memories, is consistent with this prediction. Studies have shown that stress produces potent effects on hippocampal physiology, generates long-lasting memories, and induces retrograde amnesia, all through mechanisms in common with LTP. Based on these findings, we have developed the hypothesis that a stressful experience generates an endogenous form of hippocampal LTP that substitutes a new memory representation for preexisting representations. In summary, our hypothesis implicates the induction of endogenous synaptic plasticity by stress in the formation of emotional memories and in retrograde amnesia.

Amnesia, Retrograde↗
PubMed1993

Nonverbal amnesia and asymmetric cerebral lesions following encephalitis.

Global amnesia after herpes simplex encephalitis has been typically associated with lesions of anterior and medial temporal lobe, inferior and medial frontal lobe, and insula. The neuropathologic correlates of this disease are usually considered to be bilateral and similar across cases. We describe a 27-year-old woman whose chronic amnesia and cerebral lesions after viral encephalitis indicate a different pattern. Two features distinguish her presentation: (1) markedly asymmetric lesions extensively involving the right temporal lobe but sparing almost all of the same structures on the left and (2) severe compromise of nonverbal learning and a nonverbal retrograde amnesia in contrast to disproportionately small impairments of verbal learning and retention. The findings suggest that encephalitis patients cannot be treated as a homogeneous group and that detailed analysis of variability in their anatomic lesions may be an important explanatory factor in neural accounts of these severe human amnesias.

Adolescent↗
PubMed1996

Long-term perceptual priming in transient global amnesia.

This paper addresses the question as to whether long-term perceptual priming can occur during transient global amnesia. A patient who displayed the classical features of transient global amnesia was assessed during the episode and again 7 days later. During the episode, she was administered a task that required the perceptual identification of fragmented pictures over a number of learning trials. Seven days later, after recovery from the episode, she was required to identify the same fragmented pictures together with a new set of pictures that she had never seen before. She was significantly better at identifying the old pictures than the new pictures, in spite of having amnesia for the period of the attack. Matched control subjects who had never seen either set of pictures before, were also tested and performed at a similar level on the old and the new pictures. Our findings extend the clinical domain of implicit memory phenomena and parallel similar observations in chronic amnesia (Cave & Squire, 1992). We provide the first demonstration of a residual capacity for long-term perceptual priming during an acute episode of apparent total loss of memory.

Amnesia↗
PubMed1988

Antagonism by exifone, a new cognitive enhancing agent, of the amnesias induced by four benzodiazepines in mice.

Exifone is a novel compound proposed for treating cognitive decline associated with age and shows corrective effects in animal models of memory dysfunction. The present experiments examined the antagonism by exifone of the amnesias induced in mice in a passive avoidance test by four benzodiazepines: bromazepam, diazepam, lorazepam and triazolam. Subsequent experiments investigated the specificity of exifone's antagonism of benzodiazepine-induced amnesia by examining its interaction with the effects of the benzodiazepines in the staircase test (anxiolytic/sedative activity) and the electroshock test (anticonvulsant activity). The results indicated that exifone clearly antagonised the amnesias induced by the four benzodiazepines, but was without intrinsic effects in the staircase or electroshock test and did not antagonise the effects of the benzodiazepines in these two tests. These results suggest that exifone might be useful for decreasing the amnesias induced by commonly used benzodiazepines without affecting their anxiolytic or anticonvulsant activity.

Amnesia↗
PubMed1986

[Amnesia and responsibility following brain concussion. A study of 70 patients].

Hit- and run traffic accidents frequently occur because an intention to hide drunkenness. Later, the accused claims that he or she had amnesia due to concussion at the time of accident and what followed. In most cases, the question arises as to whether it is the truth or just a story to protect the defendant from punishment. To study this question, 70 patients (39 male, 31 female) were interrogated. They were asked about the duration of their amnesia and their ability to recall their own actions, or what they had been told. In 80% of the persons examined there was only a short period of amnesia (less than 30 min). Of 12 cases with a longer period of amnesia, 7 were also intoxicated from alcohol (one case had a concentration of 3.1%). In only one person suffering from concussion could it definitely be proved that the actions taking place long after the accident, were usually not comparable with evidence given in court.

Accidents, Traffic↗
PubMed1987

Benzodiazepine--induced event amnesia following a stressful surgical procedure.

In a randomised, double-blind, parallel groups study, 40 patients undergoing surgical removal of impacted third molar teeth received either midazolam 15 mg orally followed at 35 min by intravenous saline or oral placebo followed by intravenous diazepam 10 mg (Diazemuls). Episodic (event) memory was assessed by showing patients photographs of dental and neutral objects both before and after sedation and by testing subsequent recognition at 1 week. Recall of actual surgical events was assessed by questionnaire. Both treatments induced significant amnesia for visual stimuli and for surgical events. However, the degree of amnesia was more profound for artificial stimuli and no relationship was found between the extent of amnesia for the two types of event. Drilling of bone was found to provoke the greatest cardiovascular stress response and a significant relationship was found between the degree of cardiovascular activation and subsequent memory for drilling. It is concluded that the extent of benzodiazepine-induced event-amnesia may be modified by cognitive factors and especially by the extent to which the event is cognitively encoded and elaborated.

Adult↗
PubMed1992

Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats.

Amnesia can be induced in rats in the passive avoidance paradigm by administration of scopolamine, a central muscarinic receptor antagonist. Tacrine or galanthamine, inhibitors of acetylcholinesterase, given in conjunction with scopolamine partially reversed the scopolamine-induced deficit in passive avoidance performance. Four so-called cognitive enhancers, all widely used for the treatment of the symptoms associated with mental aging, cerebral insufficiency and senile memory disorder, were investigated in this paradigm. Piracetam, an extract of Ginkgo biloba, dihydroergocristine and a combination of raubasine with dihydroergocristine, all attenuated the amnesia induced by scopolamine. In contrast, nicergoline had no significant effect. Raubasine alone also failed to significantly attenuate scopolamine-induced amnesia, although some doses of raubasine had a non-significant tendency (P less than 0.10) to reduce the amnesia.

Amnesia↗
PubMed1995

Transient global amnesia: memory and metamemory.

Twenty patients (mean age 64 years) with a previous episode of transient global amnesia (TGA) were examined to assess the functioning of objective memory (by using the Randt Memory Test), the metamemory capacities (Sehulster Memory Scale), the residual level of retrograde amnesia (Questionnaire of Remote Events), and the level of depression (Geriatric Depression Scale). Patients with residual retrograde amnesia scored significantly lower than non-amnesic ones on indices of both short-term and long-term memory, and for one of three main metamemory components, namely self-rating of memory functioning through comparison with memory functioning of peers (Set3). Age, time interval from TGA attack and TGA duration did not prove to influence memory and metamemory scores. Retrograde amnesia and depression were rather substantially associated (1/5), and this association was found to negatively influence nearly all memory and metamemory scores. Depression level showed a positive correlation with short-term memory functioning in non-amnesics. The different pattern and strength of the relationships between metamemory components and objective memory dimensions observed in amnesics and non-amnesics indicate that metamemory evaluations are more closely related to memory functioning in amnesics than in non-amnesics.

Aged↗
PubMed1995

[Analgesia-sedation for maxillo-facial surgery with midazolam-pentazocine and miazolam-ketamine. Clinical double-blind study of anxiety, analgesia, sedation and amnesia].

UNLABELLED: Ketamine and midazolam, applied as intravenous medication for conscious sedation in day-case maxillo-facial surgery, has been proven to be superior to pentazocine and midazolam concerning cardiovascular parameters and respiratory depression. The aim of this study was to evaluate the effects of low-dose ketamine/midazolam on anxiety, analgesia, amnesia and subjective feelings. METHODS. 140 out-patients (ASA I) were randomly divided into four groups. The double-blind study was prospective. CONTROL GROUP: Local anaesthesia (LA), articaine 4% plus epinephrine 1:200,000 (n = 35); test group P/M: LA, additional pentazocine 0.40 mg/kg bw and midazolam 0.075 mg/kg bw i.v. (n = 35); test group K25/M: LA, additionally ketamine 0.25 mg/kg bw and midazolam 0.075 mg/kg bw i.v. (n = 35), test group K50/M: LA, additionally ketamine 0.5 mg/kg bw and midazolam 0.075 mg/kg bw i.v. (n = 35). LA was injected 3 min after application of the systemic medication in the test groups or application of a placebo (saline 0.9%) in the control group. Three further minutes later, operation was started. For evaluation questionnaires, visual analogue scales (VAS) and the state-trait anxiety inventory (STAI) were used. For testing retrograde and anterograde amnesia, acoustic sensations were delivered before application of the systemic medication (a Christmas carol) and during operation (the German national anthem). RESULTS. The control group and the test groups were comparable with regard to biological data, duration of operation, applied dosage of local anaesthetics and actual anxiety before operation. The patients in all test groups rated intraoperative anxiety as mild, in contrast to the control group. Nearly no pain sensation during the operation was remembered in all test groups. Retrograde amnesia was not found in any group. Complete anterograde amnesia was observed in all test groups with respect to the intraoperative sensation, but even in the control group 50% of the patients did not remember having heard the national anthem. As subjective feelings negative criteria were mainly reported in the control group, where as in all test groups positive sensations dominated. Dreams were reported mostly after the higher dosage of ketamine, but no patient experienced any unpleasant dreams. The clinical assessment of the different regimes were excellent for test groups P/M and K50/M, modest for the control group and test group K25/M. Postoperatively, patients of test group P/M were remarkably sedated, but no clinically relevant sedation or motor weakness were observed in the other groups. Postoperative pain sensations were rated more intense in all test groups than in the control group. In test groups P/M and K25/M an increasing pain level was recorded during the postoperative period, with the consequence of a higher demand rate for analgesics. CONCLUSIONS. Dental surgery can be performed safely with low-dose ketamine/midazolam. Compared to pentazocine/midazolam, the higher dosage of ketamine (0.5 mg/kg bw) showed identical results intraoperatively, but was superior during the postoperative period (vigilance), and thus may represent a suitable dosage. The lower dosage of ketamine resulted in worse operating conditions, but a dosage higher than 0.5 mg/kg bw might lead to unconscious sedation and might increase the frequency of unpleasant dreams.

Adjuvants, Anesthesia↗
PubMed1998

[Diffusion-weighted MR imaging in a case of dissociative amnesia].

The differential diagnosis of psychogenic vs. organic amnestic syndromes may cause difficulty in certain cases. Here, we report a case of psychogenic amnesia which occurred after alcohol intoxication and mild head trauma. The initial memory deficit was very severe consisting of near-complete retrograde amnesia and anterograde amnesia covering 12 hours. The deficits resolved within a 4-week period of time. Brain CT and MRI scans revealed two circumscribed lesions of the right temporal lobe which were interpreted as old posttraumatic lesions. To ascertain the diagnosis, diffusion-weighted MR imaging (DWI) and brain perfusion SPECT were performed. The basal temporal lobes neither showed focal changes of perfusion, nor enhanced signal intensity on DWI as has been recently reported in patients with transient global amnesia. Later, the dissociative nature of the disorder could be confirmed by the exploration of recent psychological conflicts and the delayed type of recovery. We regard diffusion-weighted MRI as a powerful means to differentiate acute amnestic syndromes.

Adult↗
PubMed2006

Effects of activation of D1 dopamine receptors on extinction of a conditioned passive avoidance reflex and amnesia in aggressive and submissive mice.

The studies reported here demonstrate the relationship between the effect of activation of D1 dopamine receptors on the reproduction of a conditioned passive avoidance reflex during extinction and amnesia and the aggressive and submissive behavioral stereotypes. During extinction, the D1 receptor agonist SKF 38393 at a dose of 5 mg/kg given before acquisition of the conditioned reflex and on test day 12 suppressed the reproduction of the conditioned skill in aggressive mice and improved reproduction in submissive mice. The effects of activation of D1 receptors were also opposite relative to the stereotype in amnesia. In aggressive mice, SKF 38393 significantly decreased the resistance to amnesia characteristic of these animals; in submissive mice, SKF 38393 weakened the amnestic effects of the delay in the "dangerous" sector and restored memory traces. The possible mechanisms of the selectivity of the actions of D1 receptors in mice with alternative behavioral stereotypes in retaining memory traces related to aversive stimulation during extinction and amnesia are discussed.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1977

Dose-response relationships in attenuation of puromycin-induced amnesia by neurohypophyseal peptides.

Intracerebral injections of puromycin one day after training of mice in a Y-maze cause amnesia when the animals are tested 7 days later. This amnesia was shown to be attenuated by various neurohypophyseal hormones, analogs and fragments, administered subcutaneously immediately after training. Dose-response relationships have been obtained for the attenuation of puromycin-induced amnesia in mice by selected neurohypophyseal peptides. All of the compounds tested reduce the amnesia in a dose-related way, suggesting that these peptides may interact with specific receptors to induce their central effect. Among the peptides studied the two most potent--i.e., those that cause substantial retention of memory at the lowest doses--are the neurohypophyseal hormone arginine vasopressin and Z-prolyl-leucyl-glycinamide (Z-MIF).

Amnesia↗
PubMed1994

Behavioral evidence for a modulating role of sigma ligands in memory processes. II. Reversion of carbon monoxide-induced amnesia.

This study examined the effect of low doses of sigma ligands on amnesia induced in mice by successive carbon monoxide (CO) exposure. Mice were exposed three consecutive times to CO (10 ml/min, 30-50 s) at 38 degrees C. Spatial working memory impairment was investigated 5 days later by monitoring spontaneous alternation behavior in a Y-maze. Delayed amnesia was examined 7 days after CO exposure by using a step-down passive avoidance test. The preadministration of the sigma ligand 1,3-di-(2-tolyl)guanidine (DTG), at doses of 1 to 1000 microgram/kg, s.c., 30 min before CO exposure did not affect the resulting amnesia in either test. However, when administered 30 min before the test, i.e., 5 or 7 days after CO exposure, this agent completely reversed the CO-induced decrease in alternation performance, at doses of 10 to 100 micrograms/kg. The same effect was observed with (+)-N-allylnormetazocine ((+)-SKF 10,047), at doses of 100 to 300 micrograms/kg, but not with (-)-SKF 10,047. DTG, at the same dose range that reversed the decrease in alternation, also totally reversed the CO-induced decrease in step-down latency in the passive avoidance test. The curve for these effects was bell-shaped; the effects were not observed at the dose of 1 mg/kg. Moreover, alpha-(4-fluorophenyl-2-pyrimidinyl)-1-piperazine butanol (BMY 14802), a putative sigma antagonist (1-10 mg/kg i.p.), did not affect CO-induced amnesia, but when simultaneously administered with DTG, it completely prevented its effect in both tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Amnesia↗
PubMed1989

Effect of minaprine on cycloheximide-induced amnesia in mice.

The effects of minaprine on cycloheximide-induced amnesia were investigated in a step-down passive avoidance task in mice. Minaprine significantly improved cycloheximide-induced amnesia. This effect was inhibited by scopolamine, but was potentiated by physostigmine. The anti-amnesic effect of minaprine on the cycloheximide-induced memory impairment was also antagonized by a serotonin (5-HT) releaser, p-chloroamphetamine, and by a 5-HT precursor, 5-hydroxytryptophan, whereas a 5-HT1A-selective agonist, 8-hydroxy-2-(di-n-propylamino)tetralin, was inactive. The memory-improving effect of minaprine on cycloheximide-induced amnesia was potentiated by a selective 5-HT2 antagonist, ritanserin. These results suggest that the beneficial effect of minaprine on cycloheximide-induced amnesia may be related not only to cholinergic but also serotonergic neuronal systems (5-HT2 receptors).

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Involvement of the cholinergic neuronal system and benzodiazepine receptors in alcohol-induced amnesia.

We investigated the involvement of the GABAergic and cholinergic neuronal systems and benzodiazepine (BZP) receptors in ethanol-induced amnesia using a passive avoidance task. Pretraining administration of ethanol impaired the passive avoidance response. The BZP agonist chlordiazepoxide potentiated the amnesia, while the GABA antagonists bicuculline and picrotoxin failed to affect it. The acetylcholine esterase inhibitor physostigmine partially attenuated the ethanol-induced amnesia. These results suggest that ethanol-induced amnesia is related to BZP receptors and a dysfunction of the cholinergic neuronal system.

Amnesia↗
PubMed1991

Disproportionate incidental spatial-memory and recall deficits in amnesia.

Seventeen amnesics, including patients with Korsakoff's disease, post-encephalitic amnesia and amnesia caused by rupture of an anterior communicating artery aneurysm, were compared with 17 matched control subjects on a task in which 16 nameable shapes were placed on different squares of a 49-square grid. One version of the task tapped free recall and recognition of the shapes and a second version tapped three forms of spatial memory. The patients were tested after more learning opportunity and shorter delays than were the controls so as to match their recognition levels. Under these conditions, the amnesics performed worse than the controls on free recall, location-to-target memory, target-to-location memory and possibly on non-associative spatial memory although this was less impaired than target-to-location memory. Each of the main aetiological subgroups showed these disproportionate deficits to an apparently similar degree. The disproportionate free recall deficit was unrelated to the spatial memory deficits and overall severity of amnesia, and was associated with ageing and signs of frontal lobe dysfunction. The disproportionate spatial memory deficits were unrelated to frontal lobe dysfunction, but the target-to-location memory measure was associated with impairments of recognition and recall of target material. The results are broadly consistent with the context-memory deficit hypothesis of amnesia.

Adult↗
PubMed1993

Additive effects of forgetting and fornix transfection in the temporal gradient of retrograde amnesia.

Nine Rhesus monkeys (Macaca mulatta) learned to discriminate among 320 complex naturalistic scenes (Set A) for food reward. Six months later they learned to discriminate among a further 192 scenes (Set B). Immediately after learning Set B the animals were given a preoperative retention test of both sets, consisting of a single trial with every scene they had learned. Three monkeys were then operated upon to transect the fornix, the other six forming an unoperated control group. Two weeks after operation the scenes were presented once each in a postoperative retention test. The animals with fornix transection showed significantly poorer memory than the control animals at the postoperative retention test. Furthermore, within the fornix-transected animals' performance, postoperative amnesia for Set B was more marked than amnesia for Set A, by comparison with the animals' own preoperative retention of the two sets. However, a similar pattern of performance was also seen within the control animals' results, in that they forgot more of Set B than of Set A in the interval between the preoperative and postoperative retention tests. There was no significant difference between the groups in the gradient of forgetting, defined as the difference between forgetting of Set B and forgetting of Set A in the interval between the preoperative and postoperative retention tests. These results give no support to the idea that the severity of retrograde amnesia is graded as a function of the remoteness of the memory at the onset of amnesia, and they give some indication of possible reasons why the impression of such a gradient is frequently reported clinically.

Amnesia, Retrograde↗
PubMedDate not supplied

Time-dependent aspects of CO2 induced amnesia and hippocampal monoamine metabolism in rats.

The time course of amnesia for a one-trial passive avoidance response after treatment with carbon dioxide (CO2) was studied. Amnesia developed gradually over the first 4 hr following the amnesic treatment. Once established, amnesia remained during a 4 week test period. Previously, we reported that acquisition of the passive avoidance response was attended with a rise in the hippocampal concentration of serotonin 24 hr later and that this rise was not observed when acquisition was followed by amnesic treatment. In the present study, it was found that a rise in hippocampal serotonin parallelled the transient retention of the avoidance response 2 hr after amnesic treatment. However, 2 weeks after acquisition and amnesic treatment no changes in hippocampal monomine metabolism could be detected. Hippocampal noradrenaline did not correlate with avoidance and amnesia.

Amnesia↗