PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Amnesia, Retrograde”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 127 records · Page 7Linked to original sources
PubMed1985

The roles of information reactivation and nonassociative arousal in recovery from ECS-induced retrograde amnesia.

Restoration of memory by pretest reminder treatments following ECS-induced amnesia in principle could be mediated by nonassociative arousal and/or reactivation of information by the reminder stimuli. In the present research, arousal value of the reminder treatment was largely a function of the novelty of the context in which the reminder cues occurred. After producing ECS-induced amnesia in rats for a signaled passive avoidance task, presentation of the signal outside of the training and test context proved to be an effective reminder cue. However, prereminder familiarization with the reminder location, which was sufficient to reduce exploratory behavior suggestive of a decrease in the arousal value of the context, did not influence recovery from amnesia. These data indicate that reminder treatments are capable of reversing experimental amnesia by initiating further processing of previously acquired information even when the treatment does not produce appreciable arousal.

Amnesia↗
PubMed1976

DDC-induced retrograde amnesias prevented by injections of dl-DOPS.

Injection of a dopamine beta-hydroxylate inhibitor, diethyldithiocarbamate (DDC) in rats 30 min prior to training of a step-down passive avoidance task impaired performance of the task 24 hr later. Similarly, injection of DDC 30 min prior to testing blocked retrieval of a passive avoidance habit trained in normal rats the previous day. Injection of a direct norepinephrine (NE) precursor, dl-thero 3,4-dihydroxyphenylserine (DOPS) 60 min before DDC prevented both amnesias. These data support the hypothesis that reduced levels of NE are responsible for DDC-induced amnesias.

Amnesia, Retrograde↗
PubMed1977

Effect of lysine vasopressin on pentylenetetrazol-induced retrograde amnesia in rats.

Lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial facilitated passive avoidance retention. Amnesia was produced when a single 50 mg/kg (IP) injection of pentylenetetrazol was given immediately following the passive avoidance acquisition trial. A single injection of lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial antagonized the amnesia.

Amnesia↗
PubMed1986

Retrograde amnesia induced by post-trial injection of atropine into the caudate-putamen. Protective effect of the negative reinforcer.

A series of experiments was performed to test the reliability of previous reports which indicated that cholinergic blockade of the caudate-putamen produces memory deficits of passive avoidance, and to determine whether overtraining of this task protects against such deficits. In the first experiment the effects of different doses of atropine injected into the caudate-putamen of rats shortly after training were assessed, and a dose-dependent retention deficit was found. In two additional experiments it was observed that by increasing the magnitude of the negative reinforcer used in training, a protection against such retention deficit was produced. These results support the hypotheses that (a) cholinergic activity of the caudate-putamen is critically involved in memory processes that mediate passive avoidance behavior, and (b) after overtraining the control of this behavior is transferred from the striatal cholinergic system to other neurochemical systems within, or outside, the striatum.

Amnesia↗
PubMed1989

Retrograde amnesia induced by lidocaine injection into the striatum: protective effect of the negative reinforcer.

A variety of manipulations which interfere with the activity of the striatum, including cholinergic blockade and spreading depression, produce amnesia. However, it has been demonstrated that with overtraining, striatal spreading depression and injections of anticholinergic drugs do not produce memory deficits in positively-rewarded tasks. In the present experiment 2% lidocaine was injected into the striatum shortly after training of passive avoidance, using three levels of footshock (0.2, 0.3, and 0.4 mA). Highly significant retention deficits were produced when the lower intensities were studied; in contrast, the animals trained with 0.4 mA showed near-perfect performance. The data show that the enhanced learning experience, which may be equivalent to overtraining, also protects against memory deficits in negatively-rewarded behaviors, and suggest that it induces a transfer of mnemonic functions from the striatum to other neural structures.

Amnesia↗
PubMed2006

AM251, a selective antagonist of the CB1 receptor, inhibits the induction of long-term potentiation and induces retrograde amnesia in rats.

Long-term potentiation (LTP) has a long history as putative mechanism of memory formation, specially in the hippocampus, a structure essential for memory formation. Endocannabinoids are one of the endogenous systems that modulate this plasticity event: the activation of hippocampal CB1 receptors may inhibit local GABA release. Here, we have studied both (1) the role of the selective CB1 antagonist AM251 upon LTP induction in a hippocampal slice preparation, and (2) the effect of its intrahippocampal administration in the step-down inhibitory avoidance (IA) and the open field habituation tasks (OF). Standard extracellular electrophysiology techniques were used to record field excitatory postsynaptic potentials from the dendritic region of CA1 neurons in response to a high frequency stimulation of Schaffer's collaterals; a micropipette ejected 0.2 microM of AM251 (in DMSO/PBS) 2 min before the stimulus: LTP was induced and lasted more than 30 min in the control, but not in the AM251-treated group. Immediately after training, either in IA (footshock, 0.5 mA) or OF, animals received a bilateral infusion of 0.55 or 5.5 ng/side of AM251 or its vehicle in the CA1 region, and test was performed 24 h later. AM251 has caused a significative decrease in the test step-down latency when compared to the control group, but no differences were detected in the OF task, including the number of crossings, i.e., there were no motor effects. The LTP supression could be caused by AM251 acting over GABAergic interneurons that modulate the LTP-bearing glutamatergic neurons. Endocanabinoids would then be the natural dis-inhibitors of local plasticity in the dorsal hippocampus, and the amnestic action of AM251 would be due to a disruption of this endogenous modulatory system.

Amnesia, Retrograde↗
PubMed2003

Blockade of striatal 5-HT2 receptors produces retrograde amnesia in rats.

We have recently reported that intrastriatal administration of the serotonin (5-HT) releasing drug p-chloroamphetamine, and of 5-HT itself, produces a significant retention deficit of inhibitory avoidance. It is not known which of the 5-HT receptors are involved in the amnesic effect of serotonin. The present experiment was aimed at determining whether 5-HT2 receptors within the striatum are involved in memory consolidation. Ketanserine (0.5, 1.0, 2.0, or 4.0 ng) was infused bilaterally into the striatum of Wistar rats immediately after training of inhibitory avoidance, and retention of the task was measured 24 h later. A dose-dependent retention deficit was found. Together with the results from appropriate control groups, the results strongly suggest that striatal 5-HT2 receptors participate in memory consolidation of this aversive task.

Amnesia, Retrograde↗
PubMed1999

Retrograde amnesia in patients with diencephalic, temporal lobe or frontal lesions.

Patients with focal diencephalic, temporal lobe, or frontal lobe lesions were examined on various measures of remote memory. Korsakoff patients showed a severe impairment with a characteristic 'temporal gradient', whereas two patients with focal diencephalic damage (and anterograde amnesia) were virtually unimpaired on remote memory measures. Patients with frontal lobe pathology were severely impaired in the recall of autobiographical incidents and famous news events. Patients with temporal lobe pathology showed severe impairment but a relatively 'flat' temporal gradient, largely attributable to herpes encephalitis patients. From recognition and cued recall tasks, it is argued that there is an important retrieval component to the remote memory deficit across all the lesion groups. In general, the pattern of performance by the frontal lobe and temporal lobe groups was closely similar, and there was no evidence of any major access/storage difference between them. However, laterality comparisons across these groups indicated that the right temporal and frontal lobe regions may make a greater contribution to the retrieval of past episodic (incident and event) memories, whereas the left temporal region is more closely involved in the lexical-semantic labelling of remote memories.

Adolescent↗