Developmental changes of GABA immunoreactivity in cortico-thalamic networks of an absence seizure model

NEUROPHARMACOLOGY

卷:136

Article

Bombardi, Cristiano¹  Venzi, Marcello²  Crunelli, Vincenzo^2,3  Di Giovanni, Giuseppe^2,3 

[1] Univ Bologna, Dept Vet Med Sci, Bologna, Italy

[2] Cardiff Univ, Sch Biosci, Neurosci Div, Museum Ave, Cardiff CF10 3AX, S Glam, Wales

[3] Univ Malta, Dept Physiol & Biochem, MSD-2080 Msida, Malta

关键词: Immunohistochemistry;    Thalamus;    Developmental GABAergic quantification;    Epilepsy;    Interneurons;   

DOI  :  10.1016/j.neuropharm.2018.01.047

来源: Elsevier

【 摘 要 】

Absence seizures (ASs) are associated with abnormalities in gamma-aminobutyric acid (GABA) neurotransmission in the thalamus and the cortex. In the present study, we used light microscopy GABA immunocytochemistry to quantify the GABA-immunoreactive (GABA-IR) neurons and neuropil in the thalamic ventral basal (VB) nucleus, the nucleus reticularis thalami (NRT), the dorsal lateral geniculate (dLGN), the primary motor cortex (M1) and perioral region of the somatosensory cortex (Slpo) of genetic absence epilepsy rats from Strasbourg (GAERS). We used both the relative non-epileptic control (NEC) and normal Wistar rats as control strains, and investigated GABA immunostaining at postnatal day 15 (P15), P25, and P90. The main findings were i) an increase in GABA-IR neuropil in the VB at P25 and P90 in GAERS but not in NEC and Wistar rats; ii) an increase in NRT GABA-IR neurons in GAERS and NEC, but not Wistar, rats at both P25 and P90; and iii) an increase in GABA-IR neuron density in Slpo of GAERS at P25 and P90 and in Wistar at P90. These results indicate that the increased GABAergic innervation in the VB at P25 most likely contributes to the enhanced tonic inhibition observed in GAERS prior to AS onset, whereas the lack of any anatomo-morphological GABAergic differences in GAERS Slpo suggests that functional more than structural abnormalities underlie the origin of cortical paroxysms in Slpo of this AS model. This article is part of the Special Issue Dedicated to Norman G. Bowery. (C) 2018 The Authors. Published by Elsevier Ltd.

【 授权许可】

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