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PubMed1996

Amnesia induced in mice by centrally administered beta-amyloid peptides involves cholinergic dysfunction.

Substantial evidences suggest that the increased cerebral deposition, and neurotoxic action of the beta-amyloid peptide, the major constituent of senile plaques, may represent the underlying cause of the cognitive deficits observed in Alzheimer's disease. Herein, we attempted to verify this hypothesis by inducing a potential Alzheimer's-type amnesia after direct intracerebroventricular administration of aggregated beta 25-35-amyloid peptide in mice. In this aim, mnesic capacities were evaluated after 6-13 days, using spontaneous alternation in the Y-maze, step-down type passive avoidance and place learning in a water-maze. Pretraining administration of aggregated beta 25-35 peptide induced dose-dependent decreases in both alternation behaviour and passive avoidance, at doses of 3 and 9 nmol/mouse. A reduced but still significant impairment was observed when the peptide was not aggregated, or 'aged', by preincubation for 4 days at 37 degrees C. The beta 1-28 peptide, at 3 nmol/mouse, also induced a marked decrease in step-down latency. Posttraining, but not preretention, administration of beta 25-35 peptide also significantly impaired learning. The beneficial effects of cholinergic agents on beta 25-35-induced amnesia was examined using the cholinesterase inhibitor tacrine (THA, 1.3 and 4.3 mumol/kg i.p.) and the nicotinic receptor agonist (-)-nicotine (NIC, 0.06 and 0.2 mumol/kg i.p.). Both drugs induced a dose-dependent abrogation of the beta 25-35-induced decreases in alternation behaviour and passive avoidance. Furthermore, THA, at 1.3 mumol/kg, and NIC, at 0.2 mumol/kg, also reversed the beta 25-35-induced impairment of place learning and retention in the water-maze. Histological examination of Cresyl violet-stained brain sections indicated a moderate but significant cell loss within the frontoparietal cortex and the hippocampal formation of mice treated with aged beta 25-35 peptide (9 nmol). Examination of Congo red-stained sections in the same animals demonstrated the presence of numerous amyloid deposits throughout these brain areas. These results confirm that the deposition of beta-amyloid peptide in the brain is in some way related to impairment of learning and cholinergic degeneration and suggest that the [25-35] fragment of the beta-amyloid protein, sufficient to induce neuronal death in cultures, also induces an Alzheimer's-type amnesia in mice.

Acetylcholine↗
PubMed1993

Posthypoxic amnesia: regional cerebral glucose consumption measured by positron emission tomography.

Using positron emission tomography (PET), the regional cerebral metabolic rate of glucose consumption (rCMRGlc) was measured in 7 subjects suffering from chronic posthypoxic amnesia and in 12 controls. In 6 of the 7 patients regional decreases in rCMRGlc below normal limits were found involving the thalamus in 3 cases, the medial temporal cortex in 2 cases, and the caudate nucleus and cerebellum in one case each. No significant decrease in rCMRGlc was observed in any of the neocortical regions in any of the patients studied. Significant differences between group means of rCMRGlc were found only for the thalamus and the medial temporal cortex. These data suggest that posthypoxic amnesia stems from damage to the medial temporal cortex and its thalamic projection areas and not from neocortical dysfunction, confirming recent theories on the genesis of amnesia in man.

Adult↗
PubMed1983

Recall of remote episodic memory in amnesia.

Recall of remote episodic memory was assessed in three types of amnesic patient whose remote semantic memory had been evaluated previously. Patients with Korsakoff's syndrome, case N.A. and patients receiving electroconvulsive therapy all succeeded in recalling specific autobiographical episodes in response to single-word cues, and in many conditions performed as well as control subjects. Their pattern of performance generally paralleled that obtained in previous tests of remote semantic memory. These results argue against a view that amnesia reflects a selective deficit of episodic memory and suggest that the semantic-episodic distinction cannot illuminate the fundamental deficit in amnesia. Nor can the facts of amnesia confirm or deny the validity of this distinction in normal memory.

Adult↗
PubMed1991

Disproportionate intentional spatial-memory impairments in amnesia.

Twenty-four amnesics, including patients with Korsakoff's disease, post-encephalitic amnesia and amnesia caused by rupture of an anterior communicating artery aneurysm (ACoAA), were compared with 24 matched control subjects on a task in which words were presented in any one of four positions on a computer screen and subjects were instructed to remember both the words and their locations. The patients were tested after more learning opportunity, exposure to shorter lists, and after shorter delays than were their controls in order to match the word recognition performance of the two groups. Under these conditions, the amnesics' ability to locate recognized words was significantly worse than that of their controls. Although there was a tendency for the ACoAA patients to show more severe spatial memory deficits than Korsakoff patients, there was no clear evidence that aetiology of amnesia was a critical determinant of whether spatial memory was more impaired than word recognition. It was concluded that amnesics show a disproportionately severe memory deficit for spatial information that is intentionally encoded as well as for that which is incidentally encoded.

Adolescent↗
PubMed1996

Amnesia and recognition memory: a re-analysis of psychometric data.

The present study compared the recognition memory deficit in different groups of amnesics using scores from a standard test. The data, taken from a literature search, came from 33 studies reporting the performance of amnesic subjects on the recognition memory test (RMT) [77]. A total of 112 amnesic subjects were grouped according to their pathology. In addition, the analysis included subjects with schizophrenia, amygdala damage, or frontal lobe damage. Of these three nonamnesic groups, only the frontal lobe subjects were impaired on both RMT subtests, while the schizophrenics showed a disproportionate impairment for the recognition of faces. The amygdala subjects were also poor at face recognition. Among the amnesic groups, those subjects likely to have multiple sites of pathology (e.g. Korsakoff amnesics, post-encephalitics) were found to be the most impaired on the RMT. In contrast, those amnesics with more focal, limbic lesions in the hippocampus, fornix, or mamillary body region showed much milder deficits on the RMT task, some performing at normal levels. Despite their apparent sparing of recognition, the overall severity of amnesia in those subjects with limbic lesions appeared comparable to that in the remaining amnesics. These findings indicate that deficits on both subtests of the RMT are a frequent but not inevitable component of anterograde amnesia. They also point to a distinct subgroup of amnesias associated with selective damage in the hippocampus or its diencephalic targets, in which there is a relative sparing of recognition under certain test conditions.

Adolescent↗
PubMed1982

Protein synthesis inhibition and amnesia for saccharin aversion memory in rats after intra-cisternal administration of cycloheximide.

The series of experiments reported further investigated the time course relationship of the amnesia for saccharin aversion memory in rats and the inhibition of protein synthesis resulting from cycloheximide (CXM). The first experiment showed that intraventricular CXM injected rats which had been trained 7 hrs after injection had learned the contingency under a considerable inhibition of protein synthesis. However, 1 hr after CXM injection protein synthesis inhibition was 86% and yet there was no amnesia observed 24 hr after training. It was also apparent that there were no marked regional differences in the extent of protein synthesis inhibition after intraventricular CXM. Finally, intracisternal injection of CXM 1 hr before training resulted in amnesia 24 hrs after training although this effect was greater when the injection was performed 7 hr before training. The findings (1) are consistent with Day et al's [4] suggestion of maximal protein synthesis inhibition at 1 hr post CXM injection with an approximately linear decline thereafter, and (2) provide no support for the involvement of the brain stem nucleus solitarius in taste aversion learning.

Amnesia↗
PubMed1977

Some characteristics of amnesia induced by FLA-63 an inhibitor of dopamine beta hydroxylase.

The amnesic effects of FLA-63, a potent dopamine-beta-hydroxylase (DBH) inhibitor, were investigated in a food motivated spatial discrimination task. Groups of C57BL/6J mice were injected with either 5 mg/kg, 15 mg/kg, 25 mg/kg, 35 mg/kg or physiological saline 4 hr prior to training. Amnesia was observed 24 hr following training at all dose levels except 5 mg/kh. The performance deficit was specific to memory of the discrimination and not the result of state-dependency. Training conditions which produce an increase in habit strength prevented the amnestic effects of FLS-63. Spontaneous recovery of memory occurred 48 hr following drug administration. Recovery from amnesia was also induced by injections of a monoamine oxidase inhibitor, pargyline, administered 2 hr prior to the retention test. These data suggest that amnesia induced by norpinephrine (NE) depletion is the result of impairment of mechanisms necessary for memory retrieval.

Amnesia↗
PubMed1977

Counteractive effects of norepinephrine and amphetamine on quabain-induced amnesia.

Ouabain, administered 5 min prior to learning induces amnesia for a single-trial passive avoidance task in day-old chickens by inhibiting memory formation during the labile sodium-pump dependent phase. Amphetamine and norepinephrine (NE) successfully counteract ouabain-induced amnesia when administered immediately after learning. The actions of these drugs on ouabain-induced amnesia parallel that of diphenylhydantoin (DPH), and within similar time constraints. It is concluded that amphetamine (through release of NE) and norepinephrine exert their effects through stimulation of Na+/K+ ATP'ase activity. This conclusion is supported by the observation that these drugs do not overcome potassium chloride (KCl) inhibition of memory formation in the short-term phase prior to formation of labile sodium-pump dependent memory, and the fact that the noradrenergic blockers, propranolol and piperoxane do not alter the couteractive influence of DPH on cycloheximide (CXM) inhibition of the protein synthesis dependent long term memory phase which follows the labile phase.

Amnesia↗
PubMed1978

Recovery as a function of the degree of amnesia due to protein synthesis inhibition.

Retrograde amnesia following inhibition of cerebral protein synthesis has generally been explained as either a failure of consolidation or impairment of a retrieval mechanism. Major evidence for the retrieval hypothesis is provided by studies which utilize a reminder (usually footshock) to attenuate the effect of the protein inhibitor. To examine this question, mice were injected subcutaneously with anisomycin (1 mg/animal, 7 mg/animal, or 1 mg/animal every 2 hr x 7) and given one training trial in a passive avoidance box. All animals received a single retention test on each of four consecutive days, starting either 1, 7, or 21 days after training. One-half of the mice in each group received a footshock reminder 1 hr after their initial test. The footshock reminder did not attenuate the inhibitor-induced amnesia, but multiple testing did produce partial recovery in animals demonstrating some memory of training (both Saline and Anisomycin animals). Animals injected with anisomycin whose testing began 1 day after training demonstrated partial recovery irrespective of drug dosage level. The extent of amnesia and recovery were dependent upon both drug dosage and training-test interval. Implications for the consolidation and retrieval hypotheses are discussed.

Amnesia↗
PubMed1980

Lysine vasopressin attenuation of diethyldithiocarbamate-induced amnesia.

The effect of lysine vasopressin on diethyldithiocarbamate-induced amnesia for a step-through passive avoidance task was studied in rats. It was determined that although the hormone attenuates the amnesia when it is administered prior to retrieval testing, it fails to do so when it is injected prior to training. These results are consistent with the reports of others which demonstrate the reversal of diethyldithiocarbamate-induced amnesia by catecholamine agonists.

Amnesia↗
PubMed1988

Role of cholinergic and GABAergic neuronal systems in cycloheximide-induced amnesia in mice.

The role of cholinergic and GABAergic neuronal systems on the cycloheximide (CXM)-induced amnesia was investigated using the step-down-type passive avoidance task in mice. CXM (7.5-120 mg/kg, SC) given just after the training caused amnesia (indicated by short latency to step down from the platform on the grid floor) in the retention test conducted 24 hr later in a dose-dependent fashion. In the CXM (60 mg/kg)-treated mice, a choline esterase inhibitor, physostigmine (PHY; 0.125 and 0.25 mg/kg, IP), or GABA agonists, muscimol (1 and 2 mg/kg, IP) and baclofen (6 and 12 mg/kg, IP), given just after training markedly prolonged step down latency (SDL), indicating reversal of amnesia. The antiamnesic action of PHY (0.125 mg/kg) was almost completely antagonized by a central acetylcholine antagonist, scopolamine (3 mg/kg, SC), but not by a peripheral acetylcholine antagonist, butylscopolamine (3 mg/kg, SC). Furthermore, the antiamnesic action of muscimol (2 mg/kg) was reversed by GABA antagonists, picrotoxin (0.5 mg/kg, SC) and bicuculline (0.5 mg/kg, SC), while the effect of baclofen (12 mg/kg) was reversed by picrotoxin (0.5 mg/kg), but not by bicuculline (0.5 mg/kg). These results suggest that the dysfunction of cholinergic and GABAergic neuronal systems play an important role in the CXM-induced memory impairment on the passive avoidance task.

Amnesia↗
PubMed1989

Is anisomycin-induced amnesia for a passive avoidance task in chicks the result of state-dependent learning?

Many studies suggest that protein synthesis is required for formation of long-term memory. To test whether the protein synthesis inhibitor anisomycin (ANI) actually inhibits long-term memory formation or whether apparent amnesia could be attributed to state-dependency, chicks were both trained and tested under the influence of anisomycin (ANI). Two-day-old cockerels were trained in a 1-trial passive avoidance task. Intracerebral injections (10 microliters per hemisphere) of either saline (SAL) or 11.0 mM ANI were made into the medial hyperstriatum ventrale 5 min pretraining and 5 min pretest. The ANI inhibited cerebral protein synthesis by 70-80%, a level necessary to cause amnesia. Chicks that pecked a small bead dipped in methylanthranilate (MeA) and were injected with SAL both pretraining and pretest avoided pecking at test, showing memory for the bitter substance; chicks given ANI pretraining and SAL pretest pecked at the bead during test, which suggests amnesia. However, those given ANI both pretraining and pretest showed marked avoidance at test. Chicks trained to peck at a small bead dipped in water and given injections of either SAL or ANI pretraining and SAL pretest pecked readily at test. However, water-trained chicks given ANI pretest, regardless of pretraining injection, showed significantly higher avoidance at test. We conclude that peck aversion in the ANI-MeA-ANI group was not due to state-dependency but to generalized avoidance induced by pretest ANI.

Amnesia↗
PubMed1988

The implicit memory ability of a patient with amnesia due to encephalitis.

The implicit memory ability of a patient (S.S.) with severe amnesia due to encephalitis was assessed using five independent paradigms: Perceptual priming with real words and pseudowords; Word-stem completion with and without contextual cues; Word-stem completion following presentation of high- vs. low-frequency words; Biasing of the spelling of ambiguous (homophonic) words; and Conceptual priming. On the tasks in which previously acquired knowledge could potentially be activated by a prime (e.g., perceptual priming with real words), both S.S. and the Korsakoff patients performed on a normal level. However, when new learning or new associations had to be formed prior to implicit memory testing (e.g., perceptual priming of pseudowords or contextual word-stem completion), S.S.'s implicit memory performance was superior to Korsakoff amnesics. These results suggested that new learning differentially affects the priming abilities of S.S. and alcoholic Korsakoff patients. Since S.S.'s amnesia is as severe as Korsakoff patients, it was also concluded that severity of amnesia is clearly not the sole determinant of priming capacity; etiology may be equally important.

Amnesia↗
PubMed1988

Remote memory in a patient with circumscribed amnesia.

It has been suggested that extensive and severe remote memory loss is not a component of a circumscribed amnesic syndrome but may be attributable to problem solving and retrieval deficiencies associated with the frontal lobe damage which is present in some amnesic patients. In order to assess this notion, retrograde amnesia was studied in a patient, W.H., who had no apparent cortical damage revealed by radiological examination, and who evidenced no major cognitive deficiency other than amnesia. Regardless of whether remote memory was measured by recall or recognition procedures, patient W.H. exhibited impaired memory for information from the 1960s, 1970s, and 1980s, but was unimpaired in retrieving information from the 1940s and 1950s. These results demonstrate that retrograde amnesia can occur in patients who have a circumscribed memory deficit.

Amnesia↗
PubMed1988

Selective sparing of memory functioning in a patient with amnesia following herpes encephalitis.

A patient with amnesia subsequent to herpes encephalitis was assessed on a series of tasks which have been shown to result in normal or near normal performance by amnesic subjects. On a pursuit rotor learning task, our patient performed normally, and continued to show evidence of memory for the skill after a period of 30 days. On a perceptual learning task, which involved the identification of line drawings, he also displayed evidence of learning and long-term retention, but his performance remained below that of control subjects. In two priming experiments, which employed a "case-control" paradigm, performance on homonym-spelling and category item-generation tasks was preceded by exposure to a selected list of words. There was no evidence of differential facilitation in respect of those words used in the initial priming task. The findings point to some degree of selectivity of preserved learning capabilities in amnesia. It is hypothesized that this selectivity may be determined by several variables, including the type of task, the etiology and site of pathology, and the severity of amnesia.

Amnesia↗
PubMed1995

Retrograde amnesia and memory consolidation: a neurobiological perspective.

The fact that information acquired before the onset of amnesia can be lost (retrograde amnesia) has fascinated psychologists, biologists, and clinicians for over 100 years. Studies of retrograde amnesia have led to the concept of memory consolidation, whereby medial temporal lobe structures direct the gradual establishment of memory representations in neocortex. Recent theoretical accounts have inspired a simple neural network model that produces behavior consistent with experimental data and makes these ideas about memory consolidation more concrete. Recent physiological and anatomical findings provide important information about how memory consolidation might actually occur.

Amnesia, Retrograde↗
PubMed2004

Histamine H3 antagonist thioperamide dose-dependently enhances memory consolidation and reverses amnesia induced by dizocilpine or scopolamine in a one-trial inhibitory avoidance task in mice.

In the literature, there is some evidence indicating that H3 histamine receptor antagonists, in particular thioperamide, can facilitate learning and memory retrieval in laboratory rodents. The present study aimed at verifying whether this also holds for memory consolidation, a phase of memory for which there is scarcity of convincing data on the effects of H3 receptor antagonists given systemically. To that end, memory consolidation was assessed in C57BL/6J mice using the one-trial step-through inhibitory avoidance task, the compounds being injected immediately after training (foot-shock) and performance measured 24 h later. More specifically, the following effects of thioperamide (1.25-20 mg/kg) were dose-dependently analysed: (1) its potential direct effects on memory consolidation; (2) its potential reversing effects on retrograde amnesia induced by the NMDA antagonist dizocilpine (MK-801, 0.5 mg/kg) and (3) its potential reversing effects on the well-known amnesia induced by the muscarinic antagonist scopolamine (0.25 mg/kg). We found that thioperamide exerted a dose-dependent facilitative effect on memory consolidation. Furthermore, the H3 receptor antagonist reversed scopolamine- and especially dizocilpine-induced amnesia. The results strongly support the view that the brain mechanisms of memory consolidation involve a functional interaction between the NMDA and the H3 sites.

Amnesia↗
PubMed2005

Amnesia for loss of consciousness in carotid sinus syndrome: implications for presentation with falls.

OBJECTIVES: The goal of this study was to compare the clinical characteristics of patients with carotid sinus syndrome who presented with falls with those who presented with syncope. BACKGROUND: Carotid sinus syndrome presents with both falls and syncope. The reasons for this differential presentation are unknown, but amnesia for loss of consciousness may be the underlying cause. METHODS: Two groups of 34 consecutive patients with carotid sinus syndrome as the sole cause of falls and syncope were recruited. Cognitive function and clinical characteristics were compared between the two groups. RESULTS: Syncopal subjects with carotid sinus syndrome were more likely to be older males (18 [53%] vs. 7 [21%] years; p = 0.006) with a longer duration of symptoms (27.9 vs. 13.3 months; p = 0.009) and more soft tissue injuries (19 [56%] vs. 9 [26%]; p = 0.03). Duration of asystole during carotid sinus massage was similar in both groups (5.1 vs. 5.4 s; p = 0.42), but witnessed amnesia for loss of consciousness was more frequent in fallers than those with syncope (21 [95%] vs. 4 [12%]; p < 0.001). Clinical characteristics and cognitive function were otherwise similar in both groups. CONCLUSIONS: Patients with carotid sinus syndrome have similar rates of witnessed loss of consciousness during laboratory testing regardless of symptoms. However, those presenting with falls are far less likely to perceive any disturbance of consciousness than those with syncope, showing for the first time the manner in which such patients manifest symptoms. Cognitive impairment does not explain the amnesia for loss of consciousness seen in fallers with carotid sinus syndrome.

Accidental Falls↗