Biomedical subjects

I Jibiki

Publications and source records attributed to I Jibiki.

75 records · Page 5Linked to original sources

PubMedDate not supplied

A new experimental model for drug studies: effects of phenobarbital and phenytoin on photosensitivity in the lateral geniculate-kindled cat.

Photosensitivity was acquired as a result of kindling in the lateral geniculate body (GL), and the GL-kindled cat pretreated with DL-allylglycine showed a stable level of photosensitivity. To test the usefulness as a model for the evaluation of anticonvulsant drugs, the effects of phenobarbital (PB) and phenytoin (PHT) on photosensitivity were studied in the GL-kindled cat under DL-allylglycine. PB (5 and 10 mg/kg intravenously, i.v.) completely suppressed photically induced seizures in most subjects at plasma concentrations of 7-16 micrograms/ml, and this anticonvulsant action persisted for at least 4 h after the injection. PHT (15 mg/kg, i.v.) at plasma concentrations of 9-15 micrograms/ml produced toxic signs, e.g., pupil dilatation, hypersalivation, and tachypnea. At this dose, PHT was inactive against photically induced myoclonus but prevented the elicitation of a generalized tonic-clonic convulsion. From these results showing that the effects of anticonvulsant drugs on photically induced seizures can be assessed in relation to plasma concentration and acute neurologic toxicity, we suggest that the GL-kindled cat is a potentially useful animal model of epilepsy for testing the efficacy of anticonvulsant drugs.

Allylglycine↗

PubMedDate not supplied

Non-Alzheimer dementia with status spongiosus and neuronal cell loss showing unusual perineuronal structures and point mutation at 129 codon of prion protein.

The subject presented with intellectual decline followed by progressive muscle weakness of the bilateral upper limbs when he was 60 years old. He had a point mutation (methionin-valine) at 129 prion protein codon. He died at the age of 63 and necropsy revealed bilateral frontal lobe atrophy. The frontal cortex showed neuronal cell loss in layers II and III with spongiform change. Reusche silver impregnation technique for beta-peptide combined with ubiquitin immunostaining revealed perineuronal structures encircling degenerated neurons and ubiquitin-immunoreactive (IR) dot-like deposits. They were distributed particularly in the temporal neocortex and entorhinal cortex. They differed from either classic senile or diffuse plaque by the absence of amyloid core in the center and of amyloid fibrils. Ubiquitin-IR materials were also found as neuronal inclusions in the hippocampal granular cells. Nigral degeneration and neuronal loss in the hypoglossal nerve nucleus and in the anterior horn of the spinal cord were also found and spinal cord motoneurons had Bunina body inclusions. The clinical features and pathological findings were consistent with non-Alzheimer dementia with status spongiosus and neuronal cell loss. The unusual perineuronal structures found in our case might be a specific cellular pathology of dementia of the frontal lobe type.

Cell Death↗

PubMedDate not supplied

Acutely administered haloperidol-induced widespread reduction of regional cerebral blood flow observed from subtraction of brain imaging with single photon emission computed tomography using technetium-99m hexamethyl-propyleneamine oxime.

Changes in brain images with single photon emission computed tomography (SPECT) using technetium-99m hexamethyl-propyleneamine oxime (99mTc HMPAO) before and after intramuscular injection of haloperidol (0.08 mg/kg) were studied in 2 unmedicated schizophrenic patients and 2 normal controls by a new technique, i.e. subtraction of brain images. The haloperidol injection reduced regional cerebral blood flow extensively in the bilateral cerebral hemispheres in one of the schizophrenics and one of the normal controls, with little or no haloperidol-induced effects in the remaining 2 subjects. The widespread cortical reduction is considered to be due to a nonspecific or indirect effect of haloperidol in view of the broad action sites inconsistent with the known anatomy of the mesocortical dopaminergic system.

Acute Disease↗