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A reorganized GABAergic circuit in a model of epilepsy: evidence from optogenetic labeling and stimulation of somatostatin interneurons.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Peng, Zechun Zhang, Nianhui Wei, Weizheng Huang, Christine S.-H. Cetina, Yliana Otis, Thomas S. Houser, Carolyn R. |
| Copyright Year | 2013 |
| Abstract | Axonal sprouting of excitatory neurons is frequently observed in temporal lobe epilepsy, but the extent to which inhibitory interneurons undergo similar axonal reorganization remains unclear. The goal of this study was to determine whether somatostatin (SOM)-expressing neurons in stratum (s.) oriens of the hippocampus exhibit axonal sprouting beyond their normal territory and innervate granule cells of the dentate gyrus in a pilocarpine model of epilepsy. To obtain selective labeling of SOM-expressing neurons in s. oriens, a Cre recombinase-dependent construct for channelrhodopsin2 fused to enhanced yellow fluorescent protein (ChR2-eYFP) was virally delivered to this region in SOM-Cre mice. In control mice, labeled axons were restricted primarily to s. lacunosum-moleculare. However, in pilocarpine-treated animals, a rich plexus of ChR2-eYFP-labeled fibers and boutons extended into the dentate molecular layer. Electron microscopy with immunogold labeling demonstrated labeled axon terminals that formed symmetric synapses on dendritic profiles in this region, consistent with innervation of granule cells. Patterned illumination of ChR2-labeled fibers in s. lacunosum-moleculare of CA1 and the dentate molecular layer elicited GABAergic inhibitory responses in dentate granule cells in pilocarpine-treated mice but not in controls. Similar optical stimulation in the dentate hilus evoked no significant responses in granule cells of either group of mice. These findings indicate that under pathological conditions, SOM/GABAergic neurons can undergo substantial axonal reorganization beyond their normal territory and establish aberrant synaptic connections. Such reorganized circuitry could contribute to functional deficits in inhibition in epilepsy, despite the presence of numerous GABAergic terminals in the region. |
| Starting Page | ii |
| Ending Page | iii |
| Page Count | 2 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://www.jneurosci.org/content/jneuro/33/36/14392.full.pdf |
| Alternate Webpage(s) | https://www.aesnet.org/sites/default/files/file_attach/ProfessionalEducation/Currents/2014/epcu-14-4-213%20Basic%20Commentary%20Smith.pdf |
| PubMed reference number | 24005292v1 |
| Alternate Webpage(s) | https://doi.org/10.1523/JNEUROSCI.2045-13.2013 |
| DOI | 10.1523/jneurosci.2045-13.2013 |
| Journal | The Journal of neuroscience : the official journal of the Society for Neuroscience |
| Volume Number | 33 |
| Issue Number | 36 |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Acetoxolone Aluminum Salt Axon CA1 field Cognition Disorders Dopaminergic Neurons Epilepsy Epilepsy, Temporal Lobe Interneurons Monilonema lacunosa Optogenetics Pilocarpine Plexus Presynaptic Terminals Somatostatin Structure of dentate gyrus Synapses Tissue fiber Tracer nerve supply recombinase |
| Content Type | Text |
| Resource Type | Article |
