Quantitative evaluation of central-type benzodiazepine receptors with [125I] Iomazenil in experimental epileptogenesis
Autor: | Hiroshi Tamagami, Kiyoshi Morimoto, Miki Kakumoto, Akihiro Tanaka, Takashi Ninomiya, Toru Hirao, Takemi Watanabe |
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Rok vydání: | 2004 |
Předmět: |
medicine.medical_specialty
Iomazenil Hippocampal sclerosis Chemistry Dentate gyrus Kainate receptor Status epilepticus Hippocampal formation medicine.disease Epileptogenesis Temporal lobe Endocrinology nervous system Neurology Internal medicine medicine Neurology (clinical) medicine.symptom Neuroscience |
Zdroj: | Epilepsy Research. 61:105-112 |
ISSN: | 0920-1211 |
DOI: | 10.1016/j.eplepsyres.2004.07.011 |
Popis: | This study aimed at quantitatively evaluating hippocampal central-type benzodiazepine receptors (BZRs) in the kainate model of temporal lobe epilepsy (TLE) by in vitro autoradiography (ARG) using [(125)I] Iomazenil (IMZ) specific ligand for central-type BZRs. Kainate (1 microg/0.5 microl) was injected into the left amygdala to induce limbic status epilepticus. One, three, or six months after injection, in vitro ARG with [(125)I] IMZ and cell counts were performed in the hippocampal CA1-4 regions and dentate gyrus ipsilateral to the kainate injection site, and were compared with the vehicle-injected control group. In all kainate-treated rats, clear pyramidal neuron loss was observed in left hippocampal areas CA1-4. Compared with the control group, progressive reduction of [(125)I] IMZ binding was also observed. This resulted in a marked binding decrease paralleling pyramidal neuron loss in hippocampal areas CA1 (down to 83% of control), CA2 (76%), CA3 (75%), and CA4 (90%) at 6 months after kainate administration. Conversely, [(125)I] IMZ binding significantly increased in the dentate gyrus (up to 106% of control) at 1 month, but returned to nearly normal at 3-6 months. These results suggest that central-type BZR neuroimaging is useful in detecting hippocampal sclerosis in the mesial TLE, though central BZR alterations differ depending on hippocampal subfields and post-seizure time-courses. |
Databáze: | OpenAIRE |
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