No abstract available.
Animals ; Brain* ; Hippocampus* ; Kainic Acid* ; Rats*

The excitotoxic effect of kainic acid on dendrites and neuronal cell bodies of hippocampus and dentate gyrus was studied with time (1, 4, 8, 16 hours, 2, 7, 14 days) light and electron microscopically by intraperitonial injection into rat. The results obtained were as follows. 1) The acute dendrotoxic effect was observed as laminar pattern of swelling along pyramidal cell body layer and dendritic fields and was most prominently at 2-4 hours after kainic acid injection. In ultractructural study, the acute change occurred in dendrites of pyramidal cells in hipocampus because the synapses between nerve terminals and swollen components were not destroyed and remained intact and, identified the swollen structures as dendrites. So, it was obvious from the results that the acute change by kainic acid was osmolysis and was continued till initial 4 hours but was finally faded out. 2) The distribution of kainic acid receptor within hippocampus was different because the prominent dendritic swelling occurred in proximal basilar dendritic field of CA 3 and 4 and the proximal and distal basilar dendritic fields of CA 1 and 2, and no change was observable in dentate granule cell. The sensitivity of hippocampal dendritic fields to kainic acid could be put in decreasing order as CA3, CA4, CA1, CA2 and dentate granule cell 3) With the elapse of time, the acute change disappeared and pyramidal cells began to degenerate by the chronic reaction about 7 days after kainic acid injury, and the pyramidal cell density in CA regions greatly decreased. Almost all pyramidal cells degenerated the dentate granule cells were not affected to kainic acid throughout the time. In conclusions, hippocampal neurons were postulated to be very sensitive to kainic acid, and in contrast to the gradual disappearance of acute change within several hours, the degeneration of pyramidal neurons by chronic change was developed within several days regardless of acute change.
Animals ; Brain* ; Dendrites ; Dentate Gyrus ; Hippocampus ; Kainic Acid* ; Neurons* ; Pyramidal Cells ; Rats* ; Receptors, Kainic Acid ; Synapses

Santonin-kainic acid complex was evaluated as a chemotherapeutic of the mass treatment of the Ascaris lumbricoides infection in Korea. The results could be summarized as follows: The negative conversion rate was 82.9% in average in 4 treated groups. Some variations of negative conversion rate among the treated groups were noticed. The egg reduciton rate was 97.7% in average and the results were rather uniform among the three evaluated groups. By the analysis of egg reduction, it seems that the lightly infected cases whose E.P.G. were under 5,000 were resistant to treatment with the less reduced egg output. After the treatment with this complex, the number of egg discharged cases were reduced to 1.84% and the average number of discharge eggs per incompletely treated or untreated cases were reduced to 12.5% compared with the level of before-treatment egg output. The successive observations of the pattern of worm expulsion after drug intake was made. The worms were mostly expelled in the stool within 3 days, and 58.9% of total expelled worms were collected within 24-hour stool. The minimum length of the immature worms expelled was 7.6cm. Among the 659 Ascaris collected in the first-day stool from 91 rural people, 8.5% were in the range of 7.6-12.2 cm-long, immature worms. The sex ratio, male: female= 0.69: 1.
parasitology-helminth-nematoda ; Ascaris lumbricoides ; chemotherapy ; Santonin ; kainic acid

PURPOSE: Excitotoxic injury of the dendrites of inhibitory interneurons could lead to decrease in their synaptic activation, and explain subsequent local circuit hyperexcitability and epilepsy. A hallmark of dendrotoxicity at least in principal neurons of the hippocampus and cortex are focal or varicose swellings of dendritic abors. This research was designed to study morphologic changes of interneuron dendrite in kainate-treated hippocampal slice culture overtime. METHODS: Cultures aged 15-16 Equivalent Postnatal Days (EPD) were exposed to 10 microM kainic acid (KA), and analyzed at 0, 8, 24, 48, 72 hours after transient (1 hour) KA exposure. Neuronal injury was determined by morphologic changes of interneuron dendrites in area CA1 of DiI stained sections. RESULTS: 1) Transient (1 hour) exposure of hippocampal explant cultures to KA produced marked focal swellings of the dendrites of DiI stained interneurons in a highly reproducible manner. 2) The presence of focal swellings was reversible with kainate washout. The dendrites of KA treated explants were no longer beaded at 8, 24, 48, 72 hours after KA exposure. 3) There was no significant difference in the thickness of dendrites in DiI stained interneuron among 8hr, 24hr, 48hr and 72hr recovery group, compared with control group. CONCLUSION: The presence of focal swellings was reversible with kainate washout, and was not accompanied by interneuronal cell death.
Cell Death ; Dendrites* ; Epilepsy ; Hippocampus ; Interneurons* ; Kainic Acid ; Neurons

OBJECTIVES: Both electroconvulsive shock(ECS) and kainic acid-induced seizures activate mitogenactivated protein kinases(MAPKs)in rat hippocampus. They can also induce the expression of MAPK phosphatase-1(MKP-1)in rat hippocampus. MKP-1 is known as a specific MAPK deactivator. This study aimed to elucidate the role of MKP-1 in the deactivation of MAPKs in rat hippocampus. METHODS: In order to induce MKP-1 in the hippocampus, ECS was given to the rats. At the time points when MKP-1 was sufficiently induced, the second ECS was given to them and the subsequent phosphorylation or activation of MAPKs were measured in the hippocampus. A second group of rats were injected with kainic acid and the relationship between MKP-1 expression and MAPK phosphorylation was examined in their hippocampi. RESULTS: The expression of MKP-1 did not influence the phosphorylation or activation of MAPKs following ECS in rat hippocampus. Kainic acid-induced expression of MKP-1 did not significantly reduce the phosphorylation of MAPKs. CONCLUSION: MKP-1 did not play a significant role in the deactivation of MAPKs which were activated by ECS or kainic acid in rat hippocampus.
Animals ; Electroshock ; Hippocampus* ; Kainic Acid ; Phosphorylation ; Rats* ; Seizures

PURPOSE: Excitotoxic injury of the dendrites of inhibitory interneurons could lead to decrease in their synaptic activation, and explain subsequent local circuit hyperexcitability and epilepsy. A hallmark of dendrotoxicity at least in principal neurons of the hippocampus and cortex are focal or varicose swellings of dendritic abors. This research was designed to study morphologic changes of interneuron dendrite in kainate-treated hippocampal slice culture overtime. METHODS: Cultures aged to 15-16 Equivalent Postnatal Day (EPD) were exposed to 10microM kainic acid (KA), and were analyzed at 0, 8, 24, 48, 72 hours after transient (1 hour) KA exposure. Neuronal injury was determined by morphologic changes of parvalbumin (PV) positive interneuron dendrites in area CA1 of PV-immunohistochemically stained sections. RESULTS: 1) Transient (1 hour) exposure of hippocampal explant cultures to KA produced marked focal swellings of the dendrites of PV-immunoreactive interneurons in a highly reproducible manner. 2) The presence of focal swellings was reversible with kainate washout. The dendrites of KA treated explants were no longer beaded at 8, 24, 48, 72hours after KA exposure.3) The number of cells in PV-immunoreactive interneuron was decreased at 0, 8, 24 hours after exposure. But there was no significant difference among 48hr and 72hr recovery group compare with control group.4) The total length of dendrites was decreased between 0 and 8hours after exposure. But there was no significant difference among 24, 48, and 72hr recovery group compare with control group.5) The branches of dendrites were decreased just after exposure. But there was no significant difference among 8hr, 24hr, 48hr, and 72hr recovery group compare with control group. CONCLUSION: The presence of focal swellings was reversible with kainate washout, and was not accompanied by interneuronal cell death.
Cell Death ; Dendrites* ; Epilepsy ; Hippocampus ; Interneurons* ; Kainic Acid ; Neurons

Objective To investigate the role of OpenBCI module in the electroencephalographic (EEG) detection of epileptic discharge.Methods C57BL/6J mice aged 8-12 weeks were divided into two groups:the sham-operated group and kainic acid-induced epileptic group. Spontaneous seizures were monitored continuously for 3 weeks either by EEG or by OpenBCI.Results Up to 8 mice could be simultaneously monitored by OpenBCI. Meanwhile,the module accurately recorded the resting discharge,EEG spikes,and seizures.Conclusion Compared with the conventional brain function monitoring system,the OpenBCI module has lower cost and data occupancy and thus may be applied in clinical settings.
Animals ; Electroencephalography ; Epilepsy ; Kainic Acid ; Mice ; Mice, Inbred C57BL ; Seizures

Glutamate-induced cobalt uptake reveals that non-NMDA glutamate receptors (GluRs) are present in rat taste bud cells. Previous studies involving glutamate induced cobalt staining suggest this uptake mainly occurs via kainate type GluRs. It is not known which of the 4 types of taste bud cells express subunits of kainate GluR. Circumvallate and foliate papillae of Sprague-Dawley rats (45~60 days old) were used to search for the mRNAs of subunits of non-NMDA GluRs using RT-PCR with specific primers for GluR1-7, KA1 and KA2. We also performed RT-PCR for GluR5, KA1, PLCbeta2, and NCAM/SNAP 25 in isolated single cells from taste buds. Taste epithelium, including circumvallate or foliate papilla, express mRNAs of GluR5 and KA1. However, non-taste tongue epithelium expresses no subunits of non-NMDA GluRs. Isolated single cell RT-PCR reveals that the mRNAs of GluR5 and KA1 are preferentially expressed in Type II and Type III cells over Type I cells.
Animals ; Cobalt ; Epithelium ; Glutamic Acid ; Kainic Acid ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate ; Receptors, Kainic Acid ; RNA, Messenger ; Taste Buds ; Tongue

To investigate the mechanism of the excitatory signal transmission, the effects of N-methyl-D-aspartate(NMDA, ionotropic glutamate agonist) and kynurenic acid(glutamate antagonist) on catfish retinal neurons were explored using conventional intracellular recording techniques. Horizontal cells were depolarized by glutamate, kainate, quisqualate, and NMDA but gyperpolarized by kynurenate. Transient components of both ON-and OFF-bipolar cells were reduced either by glutamate or by NMDA. Kynurenate suppressed sustained components of the third-order neurons or OFF-bipolar cells. Furthermore, kynurenate blocked the depolarizing actions of NMDA on horizontal cells and ON-sustained cells with large ON-transient components. The results suggest that NMDA would exert a tonic depolarization in the horizontal cells and the 3rd-order neurons, and there might be a preferential suppression on the a NMDA receptors by kynurenic acid in the catfish retina.
Catfishes ; Glutamic Acid ; Kainic Acid ; Kynurenic Acid* ; N-Methylaspartate ; Neurons* ; Quisqualic Acid ; Receptors, N-Methyl-D-Aspartate ; Retina* ; Retinal Neurons

OBJECTIVETo explore the effect of up-regulation of KA1 subunit of the kainate receptor on endoplasmic reticulum stress (ERS)-induced excitotoxic neurodegeneration in mouse hippocampus.

METHODSSeventy adult male KM mice were subjected to microinjections into the hippocampus of kainic acid (KA) or 500, 1000, or 2000 µg/ml tunicamycin (TM). At 1, 2, 3, 4, 5, 8, and 12 h after the injections, the mice were assessed for Bederson scores and sacrificed for FJB staining and immunofluorescence observation of the brain slices.

RESULTSAt 3, 4, 5, and 8 h after KA injection and at 4 and 5 h after of 2000 µg/ml TM injection, the mice showed severe central nervous system dysfunction, and FJB staining revealed increased cell death in the hippocampus, where up-regulated expressions of KA1 receptor and ERS marker P-eIF2α were found by immunofluorescence staining (P<0.05).

CONCLUSIONMicroinjection of KA or TM into the hippocampus causes neuronal death and ERS with up-regulated expression of KA1. In this process of neuronal apoptosis, the membrane receptor KA1 receives the apoptosis signal and transfers it to the inside of the cells to cause cell endoplasmic reticulum dysfunction and ERS response, which ultimately leads to neuronal death.

Animals ; Apoptosis ; Endoplasmic Reticulum Stress ; Hippocampus ; pathology ; Kainic Acid ; pharmacology ; Male ; Mice ; Neurons ; pathology ; Receptors, Kainic Acid ; metabolism ; Tunicamycin ; pharmacology ; Up-Regulation