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DC Field | Value | Language |
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dc.contributor.author | Bombardi, Cristiano | - |
dc.contributor.author | Venzi, Marcello | - |
dc.contributor.author | Crunelli, Vincenzo | - |
dc.contributor.author | Di Giovanni, Giuseppe | - |
dc.date.accessioned | 2018-04-30T08:05:21Z | - |
dc.date.available | 2018-04-30T08:05:21Z | - |
dc.date.issued | 2018 | - |
dc.identifier.citation | Bombardi, C., Venzi, M., Crunelli, V., & Di Giovanni, G. (2018). Developmental changes of GABA immunoreactivity in cortico-thalamic networks of an absence seizure model. Neuropharmacology. | en_GB |
dc.identifier.uri | https://www.um.edu.mt/library/oar//handle/123456789/29644 | - |
dc.description.abstract | 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 (S1po) 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 S1po 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 S1po suggests that functional more than structural abnormalities underlie the origin of cortical paroxysms in S1po of this AS model. | en_GB |
dc.language.iso | en | en_GB |
dc.publisher | Elsevier Ltd. | en_GB |
dc.rights | info:eu-repo/semantics/restrictedAccess | en_GB |
dc.subject | Petit mal epilepsy | en_GB |
dc.subject | Neural transmission -- Disorders | en_GB |
dc.subject | Neural transmission -- Regulation | en_GB |
dc.subject | Epilepsy | en_GB |
dc.subject | Immunohistochemistry | en_GB |
dc.subject | Interneurons | en_GB |
dc.subject | Thalamus | en_GB |
dc.subject | Thalamus -- Diseases | en_GB |
dc.title | Developmental changes of GABA immunoreactivity in cortico-thalamic networks of an absence seizure model | en_GB |
dc.type | article | en_GB |
dc.rights.holder | The copyright of this work belongs to the author(s)/publisher. The rights of this work are as defined by the appropriate Copyright Legislation or as modified by any successive legislation. Users may access this work and can make use of the information contained in accordance with the Copyright Legislation provided that the author must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the prior permission of the copyright holder. | en_GB |
dc.description.reviewed | peer-reviewed | en_GB |
dc.identifier.doi | 10.1016/j.neuropharm.2018.01.047 | - |
dc.publication.title | Neuropharmacology | en_GB |
Appears in Collections: | Scholarly Works - FacM&SPB |
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