Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMNESIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMedDate not supplied

Changes in brain monoamine metabolism and carbon dioxide induced amnesia in the rat.

The effect of treatment with carbon dioxide (CO2) on the performance of rats 24 hr after receiving a foot shock in a passive avoidance task was studied. Foot shock induced avoidance. Carbon dioxide produced retrograde amnesia for the foot shock induced avoidance response. Changes in brain monoamine metabolism were studied in groups of rats which had been treated with CO2, foot shock or foot shock +CO2. The rats were killed 24 hr after treatment. Changes mainly occurred in the brain stem and hippocampus. In the rats which had received foot shock alone, brain stem and hippocampal serotonin concentration were raised. This rise was not observed when the foot shock was followed by CO2 treatment. Furthermore, it was found that there was an increased release of noradrenaline in those rats subjected to foot shock alone but a decreased release of this amine in the group which received foot shock followed by CO2. It is suggested that the amnesic effect of CO2 parallels changes in brain serotonin and noradrenaline metabolism.

Amnesia↗
PubMed1979

Distribution, survival and biological effects in mice of a behaviorally active, enzymatically stable peptide: pharmacokinetics of cyclo(Leu-Gly) and puromycin-induced amnesia.

Cyclo(Leu-Gly), the enzymatically resistant diketopiperazine formally derived from the C-terminal dipeptide sequence of oxytocin, exhibits activity in several behavioral systems. The distribution of cyclo(Leu-14C(U)Gly) in brain, and the time course of the disappearance of this labeled peptide from brain and plasma after subcutaneous injection into mice have been studied. The intact peptide was distributed equally in the five cerebral areas studied, for up to 96 hours after injection. Two exponential components were determined for peptide disappearance rates in plasma and brain; peptide half-lives in plasma up to 10 hr and from 24--96 hr after injection were, respectively, 0.8 and 33 hr; in brain, 1.0 and 42 hr. The peptide was found to accumulate in brain intracellular space to some degree. The time course of distribution of labeled cyclo(Leu-Gly) in subcellular fractions of mouse brain was also examined, and the concentration of peptide in the synaptosomal fraction was significantly correlated with the degree of protection against puromycin-induced amnesia of a maze-learning test. The results obtained not only confirm that cyclo(Leu-Gly) penetrates brain tissue intact and remains intact after peripheral administration in order to exert its behavioral effects, but, moreover, suggest an intriguing dynamic relationship between peptide concentration in the synaptosomal fraction and behavioral activity.

Amnesia↗
PubMed1986

The antagonistic effects of naloxone on cycloheximide and anisomycin-induced amnesia.

The amnesia induced by cycloheximide (CXM) injected SC and by CXM or anisomycin injected ICV immediately after the training test was antagonized in combination with an opiate antagonist, naloxone (NLX). This antagonism occurred on both the passive avoidance- and escape-learning responses in a dose-dependent manner in mice. NLX alone (0.3-10.0 mg/kg) did not alter the performances of these tasks. Furthermore, the decrease in retention performance on shuttle avoidance in rats induced by CXM was also antagonized by NLX. Treatment with CXM and/or NLX did not affect spontaneous locomotor activity. The interaction of these drugs on the performance of the passive avoidance- and escape-learning and the shuttle avoidance tasks may be related to neurochemical memory processes. These results suggest that an opioid system may participate in the amnesic actions induced by protein synthesis inhibitors in these models.

Amnesia↗
PubMed1989

Amnesia of a passive avoidance task due to the beta 2-adrenoceptor antagonist ICI 118,551.

The selective beta 2-adrenoceptor antagonist ICI 118,551 induces amnesia in the domestic chick when given systemically, 10 min after a one-trial PAL task. Young chicks will spontaneously peck at a small bright bead. If the bead has been coated with a distasteful substance, the chicks will learn in a single trial not to peck at a similar bead on subsequent presentation. Administration of ICI 118,551 prevented retention of this task. Vehicle-injected chicks which learnt the task, avoided a similar bead to the training bead in the retention test, but did not avoid a bead of a different colour. The effect of ICI 118,551 is unlikely to be a direct effect on performance since amnesic chicks pecked both beads freely and equally in the test.

Adrenergic beta-Antagonists↗
PubMed1994

The 5-HT2 receptor antagonist ketanserine prevents electroconvulsive shock- and clonidine-induced amnesia.

The 5-HT2-selective antagonist ketanserine was examined for its ability to prevent electroconvulsive shock (ECS)- or clonidine-induced performance deficit in the passive avoidance situation (step-down) in rats. The posttrain intraperitoneal injection of ketanserine at doses of 3 and 10 mg/kg prevented the ECS- or clonidine-provoked amnesia upon retention tests given 3 h, 24 h, and 7 days after training. The present data favor the view that the selective modification of 5-HT2 receptors after training can prevent the performance deficit in step-down-trained rats and suggest a role of the 5-HTergic neurotransmitter system in memory. The results of this study further suggest that 5-HTergic receptor antagonists might be useful in treatment of cognitive disorders.

Amnesia↗
PubMed1983

The effects of interaction between propranolol and somatostatin on the active avoidance behavior, open-field activity and electroconvulsive shock-induced amnesia of rats.

In the present study the role of beta-receptors in the behavioral action of somatostatin was investigated. Somatostatin inhibited extinction of the active avoidance behavior. Propranolol alone had no action on this behavior but significantly inhibited the peptide-induced effect. In the open-field test somatostatin induced locomotor activation; propranolol did not influence this effect of the peptide. Somatostatin inhibited electroconvulsive shock-induced amnesia. Propranolol alone had no action in this test, but significantly decreased the antiamnesic effect of the peptide. These results suggest that the central beta-receptors play an important role in the behavioral action of somatostatin.

Amnesia↗
PubMed1994

Effects of vasoactive intestinal peptide (VIP) on scopolamine-induced amnesia in the rat.

The effects of vasoactive intestinal peptide (VIP) on spatial cognitive deficits induced in the rat by injections of scopolamine were examined in a radial arm maze. A single intraperitoneal (i.p.), subcutaneous (s.c.) or intracerebroventricular (i.c.v.) injection of VIP inhibited the reduction in the number of initial correct responses in rats with scopolamine-induced amnesia. The inhibition was associated with a bell-shaped dose-response curve. Thus, VIP appears to have an ameliorating effect on spatial cognitive deficits induced by scopolamine in the rat.

Amnesia↗
PubMed1993

Bicuculline administered into the amygdala blocks benzodiazepine-induced amnesia.

This experiment investigated the effect of intra-amygdala administration of the GABAergic antagonist bicuculline methiodide on benzodiazepine-induced amnesia. Male Sprague-Dawley rats were implanted bilaterally with cannulae aimed at the amygdala and allowed to recover for 1 week. Ten minutes before training in a continuous multiple trial inhibitory avoidance task a buffer solution or bicuculline methiodide (56 pmol/0.5 microliters) was injected bilaterally into the amygdala and this injection was immediately followed by a systemic injection of saline or midazolam (1.0 mg/kg). In comparison with saline controls, midazolam-treated animals required more trials to reach the acquisition criterion of remaining in the starting chamber for 100 s. The midazolam effect on acquisition was not attenuated by intra-amygdala infusion of bicuculline methiodide, suggesting that the midazolam-induced changes in acquisition behavior do not involve the amygdaloid GABAergic system. On a 48-h retention test the performance of the midazolam-treated animals was significantly poorer than that of the controls. However, the retention performance of animals given intra-amygdala injections of bicuculline methiodide prior to the systemic injection of midazolam was comparable to that of the saline controls. These results suggest that the amygdaloid GABAergic system mediates the impairing effects of midazolam on retention of inhibitory avoidance training.

Amnesia↗
PubMedDate not supplied

A critical evaluation of monkey models of amnesia and dementia.

In this review we consider various models of amnesia and dementia in monkeys and examine the validity of such models. In Section 2 we describe the various types of memory tests (tasks) available for use with monkeys and discuss the extent to which these tasks assess different facets of memory according to present theories of human memory. We argue that the rules which govern correct task performance are best regarded as a form of semantic rather than procedural memory, and that when information about stimulus attributes or reward associations is stored long-term then that knowledge is semantic. The demonstration of episodic memory in monkeys is problematic and the term recognition memory has been used too loosely. In particular, it is difficult to dissociate episodic memory for stimulus events from the use of semantic memory for the rule of the task, since dysfunction of either can produce impairment on performance of the same task. Tasks can also be divided into those which assess memory for stimulus-reward associations (evaluative memory) and those which tax stimulus-response associations including spatial and conditional responding (non-evaluative memory). This dissociation cuts across the distinction between semantic and episodic memory. In Section 3 we examine the usefulness of the classification of tasks described in Section 2 in clarifying our understanding of the contribution of the temporal lobes and the cholinergic system to memory. We conclude that evaluative and non-evaluative memory are mediated by separate parallel systems involving the amygdala and hippocampus, respectively.

Amnesia↗
PubMed1990

Animal models of human amnesia and dementia: hippocampal and amygdala ablation compared with serotonergic and cholinergic blockade in the rat.

The behavioral effects of combined bilateral hippocampal and amygdala ablation (previously proposed as a model of human global amnesia) were compared to those seen with central blockade of the ascending cholinergic and serotonergic projections (a possible model of human global dementia) in male hooded rats. Rats were prepared with: (a) bilateral surgical lesions of the hippocampus and amygdala; (b) pharmacological blockade of central cholinergic and serotonergic function by systemic injections of scopolamine and p-chlorophenylalanine; and (c) neurotoxic lesions of the rostrally projecting serotonergic nuclei in the brainstem using intracerebral injections of 5,7-dihydroxytryptamine, later combined with scopolamine. The behavioral tests used were: an open field test, a swim-to-platform test, and a Lashley III maze. In all 3 tests, rats with either the neurotoxin lesions plus scopolamine or p-chlorophenylalanine plus scopolamine treatment showed greater impairments in comparison with controls than did the combined lesion group. These results indicate that simultaneous blockade of central serotonergic and cholinergic transmission has a greater effect on some aspects of the organization of behavior than large surgical lesions of the hippocampus and amygdala.

Amnesia↗
PubMed1996

Retrograde amnesia in rats with dorsomedial thalamic damage.

The present research addresses the effects of dorsomedial thalamic lesions on remembering a delayed alternation problem learned before damage. Male rats were trained on a delayed alternation task. Successful performance of the test first required learning of the general principle that Go and No Go trials alternate with each other and, second, in every trial, recalling the specific consequences of the responses in the previous trial after a relatively short or long interval. The animals which had reached the learning criteria were paired by the learning level shown during the training and assigned semi-randomly to one unoperated control and one dorsomedial thalamic lesioned group. Lesions of the dorsomedial nucleus of thalamus produced a moderate and transient impairment of remembering of the delayed alternation learned before the damage for delays ranging from 0 to 40 s, and a severe impairment of the postoperative performance when delays were increased to 80 s. Detailed analysis of the animals' performance throughout the postoperative retraining confirms the role of the dorsomedial nucleus of the thalamus in memory and suggests that this thalamic region plays a role in recalling specific response-related events. Further research concerning the extension of retrograde amnesia associated with thalamic damage and the nature of the memory loss is proposed as necessary.

Amnesia, Retrograde↗
PubMed1994

Reduction of visual P300 during transient global amnesia.

Transient global amnesia (TGA) is a syndrome of selective loss of recent memory without other neurological deficits. Auditory and visual P300s were recorded during and after TGA to investigate the contribution of the short-term memory system to P300 generation. The auditory P300 during TGA was comparable to that recorded 1 week and 9 months after TGA. In contrast to the auditory modality, the visual target P300 was reduced in amplitude during TGA and at 1 week after the attack. The P300 to novel visual stimuli was also reduced during TGA. Both target and novelty visual P300 recovered by 9 months after TGA. The results support the notion that the neuronal networks responsible for P300 generation are modality dependent and that brain structures perfused by the posterior circulation are involved in visual P300 generation.

Amnesia↗
PubMed1982

Temporal order judgments with amnesia.

The hypothesis that patients with anterograde amnesia fail to recognize the temporal relations among recognizable past events was evaluated. Experiment 1 showed that order recognition for words in a list was at chance levels even though event recognition was significantly above chance. The same pattern did not obtain for intact adults. Experiment 2 examined event and order recognition for news events. Amnesics' event recognition for news events was quite accurate and comparable to controls, yet their order recognition was significantly below that of controls, again at chance levels. It is argued that the failure to encode the temporal relations among events has broad consequences for memory performance in general.

Adult↗
PubMed1988

Frontal amnesia and the dysexecutive syndrome.

This study analyzes the memory deficits shown by an amnesic patient with bilateral frontal damage and a dysexecutive syndrome. He resembles a classic amnesic patient in showing grossly impaired episodic memory for both verbal and nonverbal material, together with normal digit span, and on occasion normal recency in free recall. He differs from the classic amnesic pattern however in showing an impairment in both the speed and accuracy of performance on tests of semantic memory, and in clear evidence for impaired performance on some though not all procedural learning tasks. Finally, his autobiographical memory was poor and subject to substantial confabulation. It is suggested that the pattern of deficits is consistent with a combination of a classic amnesic syndrome with the additional problems associated with the frontal dysexecutive syndrome, rather than exhibiting a qualitatively different form of amnesia.

Adult↗
PubMed1988

Learning of a complex arithmetic skill in amnesia: evidence for a dissociation between compilation and production.

Two patients with severe amnesia following rupture of anterior communicating artery aneurysms were able to learn a complex algorithm for mentally squaring two-digit numbers. Although both patients learned the algorithm at a similar rate, one patient's improvement was accounted for by savings in the steps of the algorithm. The other patient, however, showed little improvement in the steps while performance of the whole algorithm improved dramatically. Neither patient showed savings in the Hebb Digit Span procedure. The results suggested a dissociation between amnesics in their capacity to learn the constituent "productions" or steps of a skill and their capacity to organize those productions into a single coherent act.

Adult↗
PubMed1991

Autonomic and behavioral evidence of "implicit" memory in amnesia.

A profoundly amnesic patient with a left retrosplenial-fornix lesion was tested on a recognition task that evaluated both verbal and electrodermal aspects of new learning. In addition, "implicit memory" tasks (mirror reading and perceptual identification) were given. The patient displayed strong evidence of learning on all tasks although the results of this learning were not represented in explicit recall or recognition. These findings suggest that autonomic as well as behavioral evidence can index spared memory functions in amnesia. The specific meaning of electrodermal recognition and its possible place in the distinction between implicit and explicit memory is discussed.

Adult↗
PubMed1992

Priming of face matching in amnesia.

Priming was studied in a task that required a speeded response to photographs of faces. On each trial, subjects viewed two faces and decided if the same person was shown twice or if two different people were shown. Both familiar and unfamiliar (i.e., well-known and unknown) faces were used, and some face pairs were repeated with a mean delay of about 10 min. Repetition was associated with faster reaction times in young subjects (Experiment 1) as well as in amnesic patients and age-matched control subjects (Experiment 2). The patients' reaction times were slower overall, although the magnitude of the priming effect did not differ from that in the control subjects. This preservation of a normal reaction-time facilitation in subjects with impaired recognition memory for faces occurred for both familiar and unfamiliar faces, suggesting that amnesia does not necessarily interfere with the acquisition of new information as indexed by this priming effect.

Adult↗
PubMed1993

Transient global amnesia.

Transient global amnesia (TGA) is a transient, benign neurological syndrome, characterized by global loss of memory, preserved consciousness and self-awareness, associated with some behavioral changes (in particular, repetitive questioning). It generally resolves within 24 h. Mild brain stem symptoms can often be demonstrated during the attack, but major neurological abnormalities never occur. The only sequel is a permanent amnesic gap for the duration of the episode. The episode is often preceded by typical precipitating events, such as physical activity, emotional stress, acute pain, comprising haemodynamic changes of the body. The diagnosis is easy provided one is acquainted with the syndrome. The prevalence of vascular risk factors is low and the risk for stroke is not increased. Although much evidence indicates the possibility of a causative ischaemia in the inferomedial parts of the temporal lobes, an atherothrombo-embolic TIA is not the cause of TGA, and TGA is unrelated to cerebrovascular disease in general. In the author's view, the cause of TGA is a transient ischemic attack (TIA) but a haemodynamic one of the vertebrobasilar system, producing a transient dysfunction of inferomedial parts of the temporal lobes, regions that are particularly sensitive to impaired blood supply. For a full pathogenetic explanation of TGA, clarification of the underlying mechanisms is a prerequisite. This touches on the genesis of migraine and Leao's spreading depression phenomenon. The term 'amnesic TIA' would reflect the pathogenesis more appropriately.

Amnesia↗