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

Vol. 13, No. 6, 2004

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Original Paper

Choline Acetyltransferase, Glutamic Acid Decarboxylase and Somatostatin in the Kainic Acid Model for Chronic Temporal Lobe Epilepsy
Halina Baran^a,b, Berthold Kepplinger^c,d, Markus Draxler^a,b, Gerhard Skofitsch^e

^aInstitute of Pharmacology and Toxicology, and
^bInstitute of Physiology, Veterinary University Vienna, Vienna,
^cDepartment of Neurology, Diagnostic and Therapy Centre, Ostarrichiklinikum, Neuropsychiatric Hospital Mauer/Amstetten, Mauer/Amstetten,
^dDepartment of Neurology, Klinikum Mostviertel, General Hospital Amstetten, Amstetten, and
^eInstitute of Zoology, Karl Franzens University Graz, Graz, Austria

Address of Corresponding Author

Neurosignals 2004;13:290-297 (DOI: 10.1159/000081964)

Key Words

Kainic acid
Chronic temporal lobe epilepsy model
Glutamic acid decarboxylase
Choline acetyltransferase
Somatostatin
Cortical regions
Neuroprotection
Neurodegeneration
Epileptogenesis
Brain
Rat

Abstract

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 gamma -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.

Author Contacts

Halina Baran, PhD
Institute of Pharmacology and Toxicology
Veterinary University Vienna
AT-1210 Vienna (Austria)
Tel. +43 1 25077 4519, Fax +43 1 25077 4590, E-Mail Halina.Baran@vu-wien.ac.at

Article Information

Received: April 7, 2004
Accepted after revision: August 19, 2004
Number of Print Pages : 8
Number of Figures : 1, Number of Tables : 4, Number of References : 45

Medline Abstract (ID 15627816)

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