PubMed HealthSearch

PubMed · 3747545

Step-down-type passive avoidance- and escape-learning method. Suitability for experimental amnesia models.

Abstract

A method for evaluating passive avoidance- and escape-learning responses simultaneously has been developed for the study of learning and memory in mice. Prolongation of the step-down latency and shortening of the escape latency in the retention test depended on the strength of the voltage of the electric shocks delivered during the training test. Therefore, the step-down latency and escape latency may be good parameters of learning and memory performance. By cycloheximide treatment immediately after training, the step-down latency and escape latency were shortened and prolonged, respectively, in a dose-related manner, and the relationship between the step-down latency and escape latency was significant. Treatment with cycloheximide within 30 min after training caused significant amnesia, but not after more than 60 min. Furthermore, amnesic action of cycloheximide developed 24 hr after the treatment, but not within 4 hr. On the other hand, the step-down latency and/or the escape latency in the training test were changed by pretreatment with diethyldithiocarbamate and scopolamine. Therefore, the amnesic action of these drugs administered before the training should be investigated in detail. The present method, simultaneously estimating passive avoidance- and escape-learning responses, may be useful for the development of experimental amnesia models.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T Kameyama, T Nabeshima, T Kozawa. 1986. Step-down-type passive avoidance- and escape-learning method. Suitability for experimental amnesia models.. https://doi.org/10.1016/0160-5402(86)90027-6

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Implicit knowledge: new perspectives on unconscious processes.

Recent evidence from cognitive science and neuroscience indicates that brain-damaged patients and normal subjects can exhibit nonconscious or implicit knowledge of stimuli that they fail to recollect consciously or perceive explicitly. Dissociations between implicit and explicit knowledge, which have been observed across a variety of domains, tasks, and materials, raise fundamental questions about the nature of perception, memory, and consciousness. This article provides a selective review of relevant evidence and considers such phenomena as priming and implicit memory in amnesic patients and normal subjects, perception without awareness and "blindsight" in patients with damage to visual cortex, and nonconscious recognition of familiar faces in patients with facial-recognition deficits (prosopagnosia). A variety of theoretical approaches to implicit/explicit dissociations are considered. One view is that all of the various dissociations can be attributed to disruption or disconnection of a common mechanism underlying conscious experience; an alternative possibility is that each dissociation requires a separate explanation in terms of domain-specific processes and systems. More generally, it is concluded that rather than reflecting the operation of affectively charged unconscious processes of the kind invoked by psychodynamic or Freudian theorists, dissociations between implicit and explicit knowledge are a natural consequence of the ordinary computations of the brain.

Amnesia

D-cycloserine, a modulator of the N-methyl-D-aspartate receptor, improves spatial learning in rats treated with muscarinic antagonist.

The results of the present study indicate that D-cycloserine, a partial agonist at the glycine binding site, which is a positive modulation site of the N-methyl-D-aspartate receptor, could improve dose dependently the acquisition of a water maze task in rats treated with scopolamine, a muscarinic antagonist. The low to moderate doses of D-cycloserine which improved learning did not affect swimming speed in scopolamine-treated rats. The higher dose did not improve learning, but it increased swimming speed in scopolamine-treated rats. These results show a dissociation between impaired acquisition and abnormal behavioral activity in scopolamine-treated rats in the water maze task. Furthermore, the present results suggest that D-cycloserine can act as a cognitive enhancer at the appropriate doses.

Amnesia

The selective protein kinase C inhibitor, NPC 15437, induces specific deficits in memory retention in mice.

We studied the effects of a selective inhibitor of protein kinase C (PKC), 2,6-diamino-N-[(1-(1-oxotridecyl)-2-piperidinyl]methyl)hexamide (NPC 15437), on acquisition and memory retention of a Y-maze avoidance task in mice. Post-training administration of NPC 15437 (0.1-10 mg/kg i.p.) induced a dose-dependent deficit in retention of the temporal but not the spatial component of the task. This selective amnesia does not reflect state dependence and NPC 15437 (1 mg/kg) had no effect on acquisition and memory retrieval. Our results suggest that this new PKC inhibitor interferes with mechanisms underlying memory consolidation. This is in agreement with recent findings suggesting that PKC is involved in memory processes.

Amnesia