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PubMedDate not supplied

[The role of GABA-A and GABA-B receptors in the development of amnesia].

The paper deals with analysis of the influence of blockade of separate components of benzodiazepine-GABA-ionophore complex on the recovery of memory trace amnesia under GABA-A and GABA-B receptors activation in the experiments with conditioned reaction of passive avoidance of mice. Activation of GABA-A receptors did not change the behavioural amnesia manifestation at all terms of testing. Activation of GABA-B receptors before learning and amnestic influence caused spontaneous recovery of avoidance reaction. Blockade of chloride channel by picrotoxin and of benzodiazepine receptor by flumazepil restored the reproduction of the memory trace disturbed against the background of GABA-B receptors activation. Systemic flumazepil administration contributed to the memory trace reproduction against the background of GABA-A receptors activation by muscimol in the dose of 0.5 mg/kg. In conditions of amnesia development against the background of muscimol in the dose of 1 mg/kg the blockade of any component of benzodiazepine-GABA-ionophore complex was not effective. The obtained data testify that activation of GABA-A and GABA-B receptors changes the amnesia development and correction of amnesia memory trace by the blockade of separate components of benzodiazepine-GABA-ionophore complex.

Amnesia↗
PubMed2001

Voxel-based mapping of brain hypometabolism in permanent amnesia with PET.

In this study, we used voxel-based mapping methods to compare the resting cerebral metabolic rate of glucose (CMRglc) measured with PET in five patients with permanent amnesia (three with chronic Wernicke-Korsakoff and two with postanoxia syndrome) to that of nine healthy age-matched subjects. We assessed (i) a group pattern of relative hypometabolism; and (ii) the consistency of this group pattern, if any, in individual subjects, according to etiology. The results from the group analysis documented that permanent amnesia is associated with hypometabolism in the thalamus, posterior cingulate cortex, and mesial prefrontal cortex (near the anterior cingulate gyrus), bilaterally, as well as in the left supramarginal and middle temporal gyri. The individual analysis showed that this group pattern was found in essentially each patient, regardless of the cause of amnesia. Thus, permanent amnesia is subtended by dysfunction in structures belonging to Papez/limbic circuits as well as in left-hemisphere areas typically concerned with verbal functions, probably through a mechanism of thalamo-cortical disconnection and possibly involved in retrograde amnesia. The use of a voxel-based method allowed us to map a common network of synaptic dysfunction in a neuropsychological syndrome regardless of etiology. Our results indicate that this should be a powerful method in functional neuropsychology.

Adult↗
PubMed2001

The ameliorating effect of the water layer of Fructus Schisandrae on cycloheximide-induced amnesia in rats: interaction with drugs acting at neurotransmitter receptors.

Our previous study indicated that the water layer present in Fructus Schisandra(FS(w)) at 10 and 25 mg kg(-1)significantly counteracted cycloheximide (CXM)-induced amnesia. Therefore, the mechanism of action of the ameliorating effect of FS(w)on CXM-induced amnesia in the passive avoidance task was investigated in rats. The ameliorating effect of FS(w)on CXM-induced amnesia was depressed by scopolamine. The serotonin releaser, p -chloroamphetamine significantly antagonized the ameliorating effect of FS(w)on CXM-induced amnesia. Furthermore, the ameliorating effect was also inhibited by the 5-HT(1A)receptor agonist 8-OH-DPAT, but potentiated by the 5-HT(2)receptor antagonist ritanserin. Finally, the GABA(A)receptor antagonist bicuculline blocked the ameliorating effect of FS(w). These results suggest that the beneficial effect of FS(w)on CXM-induced amnesia is amplified by treatment with serotonergic 5-HT(2)receptor antagonists, but reduced by serotonergic 5-HT(1A)receptor agonists as well as GABA(A)and cholinergic receptor antagonists.

Administration, Oral↗
PubMed1990

Effects of DM-9384 in a model of amnesia based on animals with GABAergic neuronal dysfunctions.

The effects of N-(2,6-dimethyl-phenyl)-2-(2-oxo-1-pyrrolidinyl)acetamide (DM-9384), a cyclic derivative of GABA, were investigated and compared with those of aniracetam in an animal model of amnesia, using a passive avoidance task with animals that have GABAergic neuronal dysfunctions. Pre- and post-training administration of DM-9384 and aniracetam ameliorated bicuculline-induced amnesia, as indicated by parameters such as % retention and step-down latency. DM-9384 ameliorated picrotoxin-induced amnesia when administered pre-training, but not when administered post-training. Aniracetam failed to improve the picrotoxin-induced amnesia. DM-9384 displaced [3H]muscimol binding to GABAA receptors (-log IC50 = 8.07 M; Hill value = 0.23 +/- 0.04), but failed to displace about 20% of the specific muscimol binding, whereas aniracetam showed only a weak effect (-log IC50 = 3.63 M; Hill value = 0.37 +/- 0.06). From these results, it appears that DM-9384 ameliorated the GABA antagonist-induced amnesia by interacting with some GABAA receptors directly and/or indirectly.

Amnesia↗
PubMed1992

Involvement of the cholinergic system in the effects of nefiracetam (DM-9384) on carbon monoxide (CO)-induced acute and delayed amnesia.

The effects of N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl)-acetamide (DM-9384, nefiracetam), a cyclic derivative of GABA, were investigated in the carbon monoxide (CO)-induced amnesia model in mice using the passive avoidance task. Memory deficiency occurred when mice were exposed to CO before memory was completely consolidated after training (acute amnesia), at 7 days before training and 7 days after training (delayed amnesia). DM-9384 prolonged the step-down latency in mice with CO-induced amnesia. Scopolamine blocked the anti-amnesic effect of DM-9384 on delayed amnesia that had been induced by pre- or post-training exposure to CO. Bicuculline had a tendency to antagonize the anti-amnesic effect of DM-9384, but this tendency was not significant. Under these conditions, no significant change in the activity of choline acetyltransferase and glutamic acid decarboxylase was observed in the frontal cortex, striatum and hippocampus. These results suggest that DM-9384 potentiates cholinergic neuronal function and that it may modify acquisition and/or consolidation of memory.

Amnesia↗
PubMed1994

The great escape: a neuropsychological study of psychogenic amnesia.

This paper describes the neuropsychological test performance of a patient who experienced a "fugue" episode (functional retrograde amnesia) lasting 7 days, but who continued to complain of a virtually complete loss of autobiographical memory for well over a year. Subsequent evidence revealed that she had been at least partially simulating her amnesia during this prolonged period. Neuropsychological testing took place soon after admission to hospital, at intervals thereafter, and after an Amytal abreaction, which produced a substantial recovery of her memories. On various anterograde tests, designed to detect simulation, the patient's performance was unimpaired, including recognition memory tasks, word-stem completion priming for "neutral" word-lists and for post-onset autobiographical material, and some aspects of semantic memory. However, her pattern of performance on an autobiographical and a remote News Event test differentiated her from patients with organic amnesia, because she showed a grossly disproportionate autobiographical memory loss and an extreme recency effect. In addition, a rating scale, on which she showed impaired feelings-of-knowing for items from her autobiographical memory, suggested simulation. On a word-completion task for pre-onset autobiographical material, she showed absent "priming" relative to "baseline" material. However, following the Amytal abreaction, there was a substantial improvement on this task, relative to recognition and cued recall performance. This finding has been interpreted within an hierarchical model of awareness in memory, derived from studies of normal memory and organic amnesia; and it is suggested that patients with "psychogenic amnesia" may manifest different levels of awareness for differing memories.

Adult↗
PubMed1977

Reversal of cycloheximide-induced amnesia by adrenergic receptor stimulation.

Amnesia for a multiple trial appetitive spatial dicrimination habit induced by the protein synthesis inhibitor cycloheximide (CXM) was reversed by peripheral injections of both alpha (clonidine) and beta (isoproterenol) norepinephrine receptor stimulators. Stimulation of dopamine receptors with piribedil and acetylcholine receptors with pilocarpine was ineffective in reversing amnesia. The clonidine-induced recovery was blocked by phentolamine and the isoproterenol recovery by propranolol. Examination of the temporal parameters of clonidine-induced recovery indicated that the amnesia was prevented if the agonist was injected either before training and CXM treatment, up to 1 hr after training and up to 3 hr prior to testing. Clonidine also alleviated amnesia induced by another protein synthesis inhibitor anisomycin, for a shock motivated brightness discrimination habit. These data suggest that the transient amnesia induced by CXM may be a consequence of disruption of adrenergic mechanisms and more specifically that norepinephrine may play an important role in memory retrieval.

Amnesia↗
PubMed1983

Temporal and pharmacological parameters of puromycin-induced amnesia.

Mice were trained in step-down passive avoidance behavior. Bitemporal injections of puromycin (PM) were given either immediately or delayed until 24 hrs after training. PM produced a marked amnesia in both cases during retention testing 3 days later. The amnesia persisted during a second retention test 6 days after training. Of all the antibiotics, only PM is effective as an amnestic agent when injections are delayed 24 or more hours after training. cycloheximide (CXM) was also injected bitemporally immediately after training. However, CXM produced a weaker amnestic effect even though it produced a much greater inhibition of cerebral protein synthesis, more rapidly, and of longer duration. In an effort to attenuate the amnesia produced by PM, in separate experiments, the mice were injected with combined injections of PM and and CXM (bitemporally): mice were also given combined injections of PM (bitemporally) and amphetamine (subcutaneously). The amnesia produced by immediate injections of PM wa not attenuated by either CXM or amphetamine. However, the amnesia produced by delayed injections of PM was attenuated by both CXM and amphetamine. These results suggest that delayed injections of PM (25 hours after training) block the expression or retrieval of memory. This study also supports the contention that puromycin has two separate effects on memory with different temporal parameters depending on when the drug is injected relative to initial training.

Amnesia↗
PubMed1989

Persistence of retrieval enhancement by amphetamine following scopolamine-induced amnesia.

Little information is available on the permanence of pharmacologically-induced retrieval enhancement following amnesia. This was studied by comparing the rate of forgetting of a memory reactivated by d-amphetamine after amnesia with spontaneous forgetting of undisturbed fear conditioning. Mice were treated with either saline or scopolamine before conditioning and retention was tested three days later. Scopolamine-treated mice received either saline or amphetamine before testing while the saline controls received a second saline injection. The scopolamine-saline group exhibited robust amnesia, whereas both saline-saline and scopolamine-amphetamine groups showed good retention. To test the persistence of these effects mice in the three groups were subdivided and given a second retention test either 1 day, 1 week or 1 month after the first test. Amphetamine was not administered before the second test. The scopolamine-saline mice continued to exhibit amnesia for up to 1 month while the scopolamine-amphetamine and saline-saline groups continued to show strong memory with only a modest decrement in performance by 1 month after the first test. These results show that amphetamine results in a permanent recovery from scopolamine amnesia.

Amnesia↗
PubMedDate not supplied

Effects of glutaurine treatment on electroshock-induced amnesia. Antiamnesic action of glutaurine.

The effects of oral glutaurine (gamma-L-glutamyl-taurine, LitoralonR Chinoin, Budapest) treatment on electroconvulsive shock-induced amnesia were studied. Oral treatment with glutaurine in a dose of 1-20 micrograms was ineffective on electroshock-induced amnesia if the treatment was applied before the electroconvulsive shock. Fifty micrograms given in the same experimental paradigm could attenuate the amnesia considerably. When the treatment with glutaurine was applied immediately after the electroconvulsive shock, even 1 and 10 micrograms doses were effective in attenuating the amnesia in both the 24h and 48h retestings. However when glutaurine was given one hour before the 24h and 48h retestings, it proved to be ineffective. The data indicate that glutaurine is able to prevent electroconvulsive shock-induced amnesia by counteracting the effect of the electroconvulsive shock on the memory consolidation phase, but it is less effective on learning or it is ineffective on retrieval processes.

Amnesia↗
PubMed2005

Amnesia, traumatic brain injury, and posttraumatic stress disorder: a methodological inquiry.

This study explored the relationship between mild traumatic brain injury (MTBI), amnesia, and posttraumatic stress disorder (PTSD). MTBI status and amnesia for the event were assessed in 307 consecutive admissions to a Level 1 Trauma Center. Amnesia did not always occur concurrently with MTBI: 18% of those with MTBI had full recall and over half had partial recall of the event. Just over 10% of participants developed PTSD by 12 months post-injury, with prevalence comparable across MTBI and non-MTBI groups. Non-significant differences in incidence of PTSD were apparent between those with full recall (9%), partial recall (14%) and no recall (7%). These data highlight the fact that PTSD may develop following trauma despite amnesia for the event, and illustrate the importance in both clinical and research settings of carefully examining the extent of amnesia.

Adolescent↗
PubMed2004

Malingering and retrograde amnesia: the historic case of the Collegno amnesic.

Assessment of feigned cognitive disorders is an important field of neuropsychology because of its applications to forensic settings. Strategies for detecting malingering in amnesia are available for anterograde amnesia. Less attention has been given to malingering in retrograde amnesia. The case of the 'Smemorato di Collegno' (The Collegno Amnesic) is probably the most famous case of malingered retrograde amnesia ever known in Italy. In 1926, a man who appeared to have lost all his autobiographical memories and identity spent nearly a year in the Collegno asylum of Turin without a name. He was later initially identified as Giulio Canella, Director of the 'Scuola Normale di Verona' who had disappeared during the war in 1916. He was suspected of later identified as being Mario Bruneri, a petty crook from Turin who played the part of an amnesic whose retrograde memory gradually returned. A lengthy investigation was required before this conclusion was reached. Several clinicians and renowned academics evaluated the case, but only Alfredo Coppola, diagnosed "malingered retrograde amnesia" using a method that was extremely innovative for the times. The aim of the present paper is to review the original cognitive evaluation and the strategies used for malingering detection in the "Collegno case". The outcome of the case is then discussed in the light of present-day forensic neuropsychology and the level of advancement of mental examination achieved in the 1920s in Europe is highlighted.

Amnesia, Retrograde↗
PubMed1999

Disproportionate retrograde amnesia in a patient with herpes simplex encephalitis.

We describe a patient who developed a severe but temporally limited retrograde amnesia coupled with a relatively mild anterograde amnesia following herpes simplex encephalitis. The patient showed a profound retrograde amnesia for autobiographical events extending for about 10 years prior to the disease onset. Her knowledge about public events and famous persons was also impaired for this period. An MRI and SPECT demonstrated bilateral medial temporal pathology. This case represents a further instance of a relatively focal retrograde amnesia following brain damage. We review other reported cases with focal retrograde amnesia and consider theoretical and neuroanatomical accounts for the present case. Two factors may account for her amnesic patterns: a partial disruption of the store for premorbid binding codes (i.e., information that multimodal feature representations occurred synchronously); along with a relative preservation of the encoding process required to develop new synchronous codes.

Acyclovir↗
PubMed2001

Dense amnesia in the monkey after transection of fornix, amygdala and anterior temporal stem.

The traditional explanation of dense amnesia after medial temporal lesions is that the amnesia is caused by damage to the hippocampus and related structures. An alternative view is that dense amnesia after medial temporal lesions is caused by the interruption of afferents to the temporal cortex from the basal forebrain. These afferents travel to the temporal cortex through three pathways, namely the anterior temporal stem, the amygdala and the fornix-fimbria, and all these three pathways are damaged in dense medial temporal amnesia. In four experiments using different memory tasks, we tested the effects on memory of sectioning some or all of these three pathways in macaque monkeys. In a test of scene-specific memory for objects, which is analogous in some ways to human episodic memory, section of fornix alone, or section of amygdala and anterior temporal stem sparing the fornix, each produced a significant but mild impairment. When fornix section was added to the section of anterior temporal stem and amygdala in this task, however, a very severe impairment resulted. In an object recognition memory task (delayed matching-to-sample) a severe impairment was seen after section of anterior temporal stem and amygdala alone, with or without the addition of fornix section; this impairment was significantly more severe than that which was seen in the same task after amygdalectomy leaving the temporal stem intact, with or without fornix section. Animals with combined section of anterior temporal stem, amygdala and fornix were also impaired in object-reward association learning. However, the retention of pre-operatively acquired object-reward associations was at a high level. These results show that the pattern of impairments after section of anterior temporal stem, amygdala and fornix in the monkey, leaving hippocampus intact, resembles human dense amnesia and is different from the effects of hippocampal lesions in the monkey.

Amnesia↗
PubMed2003

Preserved ability to recognize keywords related to remote events in the absence of retrieval of relevant knowledge: a case of postencephalitic amnesia.

We describe a case of severe anterograde and retrograde amnesia resulting from herpes simplex encephalitis. Magnetic resonance imaging revealed pathological changes in the bilateral hippocampi, parahippocampal gyri, fusiform gyri, medial temporal poles, posterior part of the cingulate gyri, and insula. The patient showed severe amnesia for autobiographical episodic memory in relation to events that had occurred throughout her life, but temporally graded amnesia for autobiographical semantic memory, and severe amnesia without a temporal gradient for public events and famous people. However, using a multiple-choice method, she showed a high level of accuracy when choosing keywords related to public or personal events, although this did not prompt her recollection of the events. An important indication of these results is that, even with severe retrograde amnesia, memories of past events are not completely lost. We propose that an event may be stored in a fragmented form, consisting of many components, and that normal recall of an event may require recombination or reconstruction of these components.

Amnesia↗
PubMed2005

Retrograde amnesia for semantic information in Alzheimer's disease.

Patients with mild to moderate Alzheimer's disease and normal controls were tested on a retrograde amnesia test with semantic content (Neologism and Vocabulary Test, or NVT), consisting of neologisms to be defined. Patients showed a decrement as compared to normal controls, pointing to retrograde amnesia within semantic memory. No evidence for a gradient within this amnesia was found, although one was present on an autobiographic test of retrograde amnesia that had a wider time scale. Several explanations for these results are presented, including one that suggests that extended retrograde amnesia and semantic memory deficits are in fact one and the same deficit.

Aged↗
PubMed1995

An event-related potential investigation of posthypnotic recognition amnesia.

Forty-two individuals selected for high hypnotizability or for low hypnotizability were taught lists of words during hypnosis and assessed for recognition following hypnosis using event-related potential (ERP) procedures, both before and after the cue to reverse amnesia. A subgroup of low-hypnotizable participants were asked to simulate hypnotic behavior. All participants had larger late positive component (LPC) amplitudes to learned than to unlearned words, regardless of whether amnesia was reported. The highly hypnotizable participants who reported recognition amnesia, however, had significant changes in attention-related (P1 and N1) and recognition-related (N400 and LPC) ERP component amplitudes as a function of whether amnesia was reported. These data suggest that posthypnotic amnesia may involve alterations in the processes of attention, selection, and accessibility.

Amnesia↗
PubMed1977

Somatic and autonomic indexes of recovery from electroconvulsive shock-induced amnesia in rats.

Autonomic response indexes of experimental amnesia have recently been found to have higher electroconvulsive shock (ECS) intensity thresholds and steeper retrograde gradients than have traditional somatic indexes. The present studies examined the hypothesis that recovery from somatically indexed experimental amnesia depends upon the existence of autonomically available residual memory. In a between-subjects design, a 200-mA ECS was used to produce amnesia for a tone-footshock pairing as indicated by lick suppression, defection, and bradycardia. The next day, these amnesic animals received a reminder footshock outside of the training apparatus, which was found to restore memory on a test trial 24 hr later. The behavior of control groups indicated that this reminder effect was due to the restoration of specific memory rather than systemic consequences of treatment. With a within-subjects design, a second experiment obtained a reminder effect in animals individually shown to be "fully" amnesic by all three response indexes monitored. A third experiment varied the intensity of the reminder footshock and revealed that the different memory indexes examined do not have reminder-footshock thresholds inversely related to their initial resistance to amnesia. The results support a retrieval-failure view of experimental amnesia and suggest that the same fundamental physiological processes underlie both autonomically indexed memory and somatically indexed memory.

Acoustic Stimulation↗