Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: KEGG:D03244 (Kaolin)
 239 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The behavior of rats with progressive hydrocephalus was examined to detect early neurological deterioration. Kaolin solution was injected into the cisterna magna of 10 of 17 anesthetized 8-week-old male rats (day 0), and saline in the other 7 rats (control group). Reaction time (RT, sec) and error ratio (ER, %) of unanesthetized rats escaping from electrical stimuli toward a nonstimulated sheet within a box were recorded daily from day 4 until autopsy after 4 weeks. Three rats in the kaolin group died in acute stage. Rats were assigned to either severe (S) (n = 4) or moderate (M) (n = 4) group according to the degree of ventricular dilatation at autopsy. The RTs prolonged and ERs increased in the kaolin group and they reached their minimum values. Values after the minimum RT value on day 12 in the M-group and 22 in the S-group during the chronic stage were compared with those in the controls, which decreased throughout the experiments (P < 0.03). In all animals in the S-group RT was prolonged each day with a linear regression (P < 0.005), although ER was decreased (0.69 > P > 0.23). In 3 rats and in another rat in the M-group RT was prolonged (P < 0.04 and P = 0.19) and ER was decreased in 3 rats (two: P = 0.41; one: P = 0.01) and increased in one (P = 0.55). In conclusion, deteriorated motor function is more important for early diagnosis in progressive hydrocephalus than behavioral symptoms.
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PMID:Progression of kaolin-induced hydrocephalus and changes in performance of operant tasks by rats. 813 9

We investigated the relationship between the degree of spatial memory impairment in an 8-arm radial maze and the changes in the contents of acetylcholine (ACh) and noradrenaline (NA) in the dorsal and ventral hippocampus and the frontal cortex, along with histological changes in kaolin-induced hydrocephalic rats. Kaolin-induced hydrocephalic rats were divided into three groups (non-impaired, impaired and severely impaired) according to the degree of impairment in a radial maze. Thirty percent of the hydrocephalic rats could not solve a radial maze (severely impaired group), while the remaining hydrocephalic rats could (non-impaired rats in the standard task). Forty percent of the non-impaired rats in the standard task failed to solve the delayed-response task (impaired group), whereas the remaining rats were able to solve it (non-impaired group). A positive correlation was observed between the impairment of spatial memory and ventricular dilatation. The ACh content in the dorsal and ventral hippocampus, and the NA content in the ventral hippocampus were decreased in the severely impaired group. Moreover, the NA content in the ventral hippocampus was decreased in the impaired group. These results suggest that the impairment of spatial memory in kaolin-induced hydrocephalic rats is associated with dysfunction of the hippocampal cholinergic and noradrenergic systems.
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PMID:Impairment of spatial memory in kaolin-induced hydrocephalic rats is associated with changes in the hippocampal cholinergic and noradrenergic contents. 1180 92

PKN (protein kinase N; also called protein kinase C-related kinase (PRK-1)), is a serine/threonine protein kinase that is ubiquitously expressed in several organs, including the brain. PKN has a molecular mass of 120 kDa and has two domains, a regulatory and a catalytic domain, in its amino-terminals and carboxyl-terminus, respectively. Although the role of PKN has not been fully elucidated, previous studies have revealed that PKN is cleaved to a constitutively active catalytic fragment of 55 kDa in response to apoptotic signals. Hydrocephalus is a pathological condition caused by insufficient cerebrospinal fluid (CSF) circulation and subsequent excess of CSF in the brain. In this study, in order to elucidate the role of PKN in the pathophysiology of hydrocephalus, we examined PKN fragmentation in hydrocephalic model rats. Hydrocephalus was induced in rats by injecting kaolin into the cisterna magna. Kaolin-induced rats (n=60) were divided into three groups according to the observation period after treatment (group 1: 3-6 weeks, group 2: 7-12 weeks, and group 3: 13-18 weeks). Sham-treated control rats, injected with sterile saline (n=20), were similarly divided into three groups. Spatial learning ability was estimated by a modified water maze test. Thereafter, brains were cut into slices and ventricular dilatation was estimated. Fragmentation of PKN was observed by Western blotting in samples collected from the parietal cortex, striatum, septal nucleus, hippocampus, and periaqueductal gray matter. All kaolin-induced rats showed ventricular dilatation. Most of them showed less spatial learning ability than those of sham-treated controls. In most regions, fragmentation of PKN had occurred in a biphasic manner more frequently than that in controls. The appearance of PKN fragmentation in periaqueductal gray matter was correlated with the extent of ventricular dilation and spatial learning disability. These results revealed that PKN fragmentation was observed in rats with kaolin-induced hydrocephalus, models for chronically-damaged brain dysfunction, suggesting that persistent brain insult, such as apoptosis, had occurred in these models. PKN fragmentation could be a hallmark for evaluating morphological and functional damage of the hydrocephalus.
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PMID:Fragmentation of protein kinase N (PKN) in the hydrocephalic rat brain. 1789 75