Quantitative expression and localization of GABA B receptor protein subunits in hippocampi from patients with refractory temporal lobe epilepsy.

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  • Additional Information
    • Source:
      Publisher: Pergamon Press Country of Publication: England NLM ID: 0236217 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7064 (Electronic) Linking ISSN: 00283908 NLM ISO Abbreviation: Neuropharmacology Subsets: MEDLINE
    • Publication Information:
      Publication: Oxford : Pergamon Press
      Original Publication: Oxford, New York, Pergamon.
    • Subject Terms:
      Drug Resistant Epilepsy/*metabolism ; Epilepsy, Temporal Lobe/*physiopathology ; Hippocampus/*metabolism ; Receptors, GABA-B/*metabolism; Adult ; Aged ; Aged, 80 and over ; Drug Resistant Epilepsy/pathology ; Drug Resistant Epilepsy/surgery ; Epilepsy, Temporal Lobe/pathology ; Epilepsy, Temporal Lobe/surgery ; Female ; Gene Expression Regulation ; Hippocampus/pathology ; Hippocampus/surgery ; Humans ; Male ; Middle Aged ; Protein Isoforms ; RNA, Messenger/metabolism ; Sclerosis/metabolism ; Sclerosis/pathology ; Sclerosis/surgery ; Young Adult
    • Abstract:
      This study investigates GABA B protein expression and mRNA levels in three types of specimens. Two types of specimens from patients with temporal lobe epilepsy (TLE), secondary to hippocampal sclerosis, sclerotic hippocampal samples (TLE-HS), and tissue from the structurally preserved non-spiking ipsilateral superior temporal gyrus (TLE-STG) removed from the same patient during epilepsy surgery; and third specimen is hippocampal tissue from individuals with no history of epilepsy (post-mortem controls, PMC). mRNA expression of GABA B subunits was quantified in TLE-HS, TLE-STG and PMC specimens by qRT-PCR. Qualitative and quantitative Western blot (WB) and immunohistochemistry techniques were employed to quantify and localize GABA B proteins subunits. qRT-PCR data demonstrated an overall decrease of both GABA B1 isoforms in TLE-HS compared to TLE-STG. These results were mirrored by the WB findings. GABA B2 mRNA and protein were significantly reduced in TLE-HS samples compared to TLE-STG; however they appeared to be upregulated in TLE-HS compared to the PMC samples. Immunohistochemistry (IHC) showed that GABA B proteins were widely distributed in PMC and TLE-HS hippocampal sections with regional differences in the intensity of the signal. The higher expression of mature GABA B protein in TLE-HS than PMC is in agreement with previous studies. However, these findings could be due to post-mortem changes in PMC specimens. The TLE-STG samples examined here represent a better 'control' tissue compared to TLE-HS samples characterised by lower than expected GABA B expression. This interpretation provides a better explanation for previous functional studies suggesting reduced inhibition in TLE-HS tissue due to attenuated GABA B currents. This article is part of the "Special Issue Dedicated to Norman G. Bowery".
      (Copyright © 2017. Published by Elsevier Ltd.)
    • Contributed Indexing:
      Keywords: GABA(B) qRT-PCR; Hippocampal sclerosis; Human temporal lobe epilepsy; Immunohistochemistry; Quantitative Western blot
    • Accession Number:
      0 (Protein Isoforms)
      0 (RNA, Messenger)
      0 (Receptors, GABA-B)
    • Publication Date:
      Date Created: 20170808 Date Completed: 20190213 Latest Revision: 20220419
    • Publication Date:
      20221213
    • Accession Number:
      10.1016/j.neuropharm.2017.08.001
    • Accession Number:
      28782512