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T Kozawa

Publications and source records attributed to T Kozawa.

30 records · Page 2Linked to original sources
PubMed1988

Conditioned suppression of motility: possibility for evaluation of learning and memory in mice.

Mice showed a marked suppression of motility when placed in the same environment where they had been given electric shocks (ES) 24 h before. This conditioned suppression of motility (CS) was attenuated by the administration of cycloheximide (CXM, 25-150 mg/kg) immediately after ES treatment in a dose-dependent manner. CXM (50 mg/kg) administered 1 h after ES failed to attenuate the CS. These effects seem to be caused by retrograde amnesia. Furthermore, the amnesic action of CXM was antagonized by naloxone (10 mg/kg), which did not affect CS. Physostigmine (0.2 mg/kg), propranolol (1 mg/kg) and cyproheptadine (2 mg/kg) did not antagonize CXM-induced amnesia significantly. In the same way, the amnesia-inducing actions of phencyclidine and scopolamine were detected. The CS method seems to be useful to examine learning and memory performances in animals and has the advantage that evaluation is extremely easy.

Animals↗
PubMed1986

Phencyclidine-induced retrograde amnesia in mice.

The amnesic action of phencyclidine (PCP) was investigated in mice using a passive avoidance- and escape-learning method. PCP (10-30 mg/kg) administered immediately after the training test dose-dependently shortened and prolonged the step-down latency and escape latency, respectively in the retention test. There was a significant inverse relationship between the step-down and escape latencies, indicating that PCP had induced amnesia. The amnesic actions of PCP were retrograde, being observed when mice were given PCP within 10 min but not more than 30 min after the training test. The amnesic effects of PCP on both variables were antagonized significantly by physostigmine and naloxone, whereas cyproheptadine and haloperidol had no effect. None of these drugs by themselves affected passive avoidance- or escape-learning performance. These results suggest that the retrograde amnesic actions of PCP were produced via either the cholinergic or the opioidergic systems or both, but not through the serotonergic and the dopaminergic systems.

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↗
PubMed1986

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

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.

Amnesia↗
PubMed1984

Bell's palsy. Nonrecurrent v recurrent and unilateral v bilateral.

Bell's palsy was classified into five categories--unilateral nonrecurrent , unilateral recurrent, simultaneous bilateral, alternating bilateral, and recurrent bilateral type--based on the clinical statistical study of two large series of patients with Bell's palsy treated at different locations in Japan. One series consisted of 1,217 patients and the other of 1,197 for a total of 2,414 patients in this study. The incidence of each type and the age and sex distributions were similar in the two groups. Clinical features of each type are described. The results imply that more specific causative factors trigger the recurrences and the simultaneous bilateral attacks.

Adolescent↗
PubMed1983

Solitary plasmacytoma of the submandibular lymph node with stromal amyloid deposits.

This report concerns a case of solitary extramedullary plasmacytoma of the left submandibular lymph node in a 56-year-old man. The tumor showed monoclonal proliferation of abnormal plasma cells which revealed highly positive stainings of both methylgreen pyronin and kappa light chain using the immunoperoxidase technique in the cytoplasms, and further revealed massive amyloid deposits in the stroma, which suggested the possibility of sequential amyloid formation upon the secretion of paraprotein by tumor cells.

Amyloid↗