Increased prostaglandin formation in rat brain following systemic application of kainic acid

Baran, Halina; Heldt, Renate; Hertting, G.

doi:10.1016/0006-8993(87)91360-6

Cited by 60 publications

(22 citation statements)

References 25 publications

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“…The prominent productions of PGF 2␣ and PGD 2 in the initial phase (Fig. 2) agree well with a previous report (6). In addition, the lack of LT synthesis in our observation (Fig.…”

Section: Dual Phase Regulation Of Eicosanoid Productions In the Hipposupporting

confidence: 83%

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Profiling of Eicosanoid Production in the Rat Hippocampus during Kainic Acid-induced Seizure

Yoshikawa¹,

Kita²,

Kishimoto³

et al. 2006

Journal of Biological Chemistry

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“…The prominent productions of PGF 2␣ and PGD 2 in the initial phase (Fig. 2) agree well with a previous report (6). In addition, the lack of LT synthesis in our observation (Fig.…”

Section: Dual Phase Regulation Of Eicosanoid Productions In the Hipposupporting

confidence: 83%

“…Involvement of eicosanoids in the KA-induced seizure has been suggested; KA stimulates eicosanoid production in the rat brain (6), and expression levels of enzymes such as cyclooxygenase (COX)-2 (7-12) and 5-lipoxygenase (8) are affected by KA. However, the roles of eicosanoids as well as their production mechanisms are poorly understood.…”

mentioning

confidence: 99%

Profiling of Eicosanoid Production in the Rat Hippocampus during Kainic Acid-induced Seizure

Yoshikawa¹,

Kita²,

Kishimoto³

et al. 2006

Journal of Biological Chemistry

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“…KAinduced seizures cause lesions consisting in a degeneration of the nerve cells of limbic brain regions, tissue necrosis and haemorrhages involving the amygdala, piriform cortex, entorhinal cortex, hippocampus and other limbic structures [2][3][4][5][9][10][11][12][13]. Previous neurochemical investigations revealed significant changes characterised by early enhancement of the prostaglandin synthesis [14], increased turnover of mono-aminergic neurotransmitters [4,15] and a reduction of neuropeptide somatostatin [16] in the acute phase (3 h) after KA injection. Later, a selective reduction of glutamic acid decarboxylase (GAD) activity was observed in the hippocampus and the amygdala/piriform cortex as well as a reduction of choline acetyltransferase (ChAT) activity in the amygdala/piriform cortex complex 3 days after KA injection, indicating a destruction of cholinergic and Á-aminobutyric acid (GABA)ergic neurons in these brain regions [4].…”

Section: Introductionmentioning

confidence: 99%

Choline Acetyltransferase, Glutamic Acid Decarboxylase and Somatostatin in the Kainic Acid Model for Chronic Temporal Lobe Epilepsy

et al. 2004

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The aim of the study was to investigate neurochemical changes in a kainic acid (KA; 10 mg/kg, s.c.)-induced spontaneous recurrent seizure model of epilepsy, 6 months after the initial KA-induced seizures. The neuronal markers of cholinergic and γ-aminobutyric acid (GABA)ergic systems, i.e. choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) activities, and a marker for neuropeptide, i.e. level of somatostatin, have been investigated. The brain regions investigated were the hippocampus, amygdala/piriform cortex, caudate nucleus, substantia nigra and the frontal, parietal, temporal and occipital cortices. Six months after KA injection, reduced ChAT activity was observed in the amygdala/piriform cortex (47% of control; p < 0.001), increased ChAT activity in the hippocampus (119% of control; p < 0.01) and normal ChAT activity in the other brain regions. The activity of GAD was significantly increased in all analysed cortical regions (between 146 and 171% of control), in the caudate nucleus (144% of control; p < 0.01) and in the substantia nigra (126% of control; p < 0.01), whereas in the amygdala/piriform cortex, the GAD activity was moderately lowered. The somatostatin level was significantly increased in all cortical regions (between 162 and 221% of control) as well as in the hippocampus (119% of control), but reduced in the amygdala/piriform cortex (45% of control; p < 0.01). Six months after KA injection, the somatostatin:GAD ratio was lowered in the amygdala/piriform cortex (49% of control) and in the caudate nucleus (41% of control), whereas it was normal in the hippocampus and moderately increased in the cortical brain regions. A positive correlation was found between seizure severity and the reduction of both ChAT activities and somatostatin levels in the amygdala/piriform cortex. The results show a specific pattern of changes for cholinergic, GABAergic and somatostatinergic activities in the chronic KA model for epilepsy. The revealed data suggest a functional role for them in the new network that follows spontaneous repetitive seizures.

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“…An increase in prostaglandin formation in rat brain following systemic application of kainic acid has also been reported 32 . Since these mediators may interfere with the immune parameters, in the present study kainic acid lesion was avoided.…”

Section: Discussionmentioning

confidence: 83%

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2012

IJPSR

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The aim of the present study was to investigate the role of cerebellum in immunomodulation as cerebellum was thought traditionally to play an important role in voluntary motor activities. Rats weighing about 200-220 gm were subjected to bilateral electrolytic lesion of fastigial nucleus and following immune parameters were assessed-leucocyte migration inhibition test, foot pad thickness, antibody titre and estimation of cytokines -IL-2, IL-4 and IFN-γ respectively in immunized animals. Rats were divided in to three groups, namely control immunized, sham immunized and lesioned immunized groups. The sham group was strictly considered for evaluation of lesion effect as superficial structures during surgical procedure gets damaged and could also influence on immunomodulation. The significance was fixed at P<0.05. There was significant increase in migration index with concomitant decrease in foot pad thickness in bilateral lesion immunized groups. Significant alterations in cytokine levels were observed in lesion immunized groups when compared with its respective control groups.

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Increased prostaglandin formation in rat brain following systemic application of kainic acid

Cited by 60 publications

References 25 publications

Profiling of Eicosanoid Production in the Rat Hippocampus during Kainic Acid-induced Seizure

Profiling of Eicosanoid Production in the Rat Hippocampus during Kainic Acid-induced Seizure

Choline Acetyltransferase, Glutamic Acid Decarboxylase and Somatostatin in the Kainic Acid Model for Chronic Temporal Lobe Epilepsy

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