The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
Disrupted Dentate Granule Cell Chloride Regulation Enhances Synaptic Excitability during Development of Temporal Lobe Epilepsy
Open accessAbstract
GABA A receptor-mediated inhibition depends on the maintenance of intracellular Cl − concentration ([Cl − ] in ) at low levels. In neurons in the developing CNS, [Cl − ] in is elevated, E GABA is depolarizing, and GABA consequently is excitatory. Depolarizing GABAergic synaptic responses may be recapitulated in various neuropathological conditions, including epilepsy. In the present study, rat hippocampal dentate granule cells were recorded using gramicidin perforated patch techniques at varying times (1–60 d) after an epileptogenic injury, pilocarpine-induced status epilepticus (STEP). In normal, non-epileptic animals, these strongly inhibited dentate granule cells act as a gate, regulating hippocampal excitation, controlling seizure initiation and/or propagation. For 2 weeks after STEP, we found that E GABA was positively shifted in granule cells. This shift in E GABA altered synaptic integration, increased granule cell excitability, and resulted in compromised “gate” function of the dentate gyrus. E GABA recovered to control values at longer latencies post-STEP (2–8 weeks), when animals had developed epilepsy. During this period of shifted E GABA , expression of the Cl − extruding K + /Cl − cotransporter, KCC2 was decreased. Application of the KCC2 blocker, furosemide, to control neurons mimicked E GABA shifts evident in granule cells post-STEP. Furthermore, post-STEP and furosemide effects interacted occlusively, both on E GABA in granule cells, and on gatekeeper function of the dentate gyrus. This suggests a shared mechanism, reduced KCC2 function. These findings demonstrate that decreased expression of KCC2 persists for weeks after an epileptogenic injury, reducing inhibitory efficacy and enhancing dentate granule cell excitability. This pathophysiological process may constitute a significant mechanism linking injury to the subsequent development of epilepsy.
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Cites
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Perturbed Chloride Homeostasis and GABAergic Signaling in Human Temporal Lobe Epilepsy
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Cited by
Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction
Goldberg, E. M., & Coulter, D. A. (2013) · Nature Reviews Neuroscience · doi:10.1038/nrn3482 · Cited by 542
Self-citationExcessive activation of mTOR in postnatally generated granule cells is sufficient to cause epilepsy
Pun, R. Y. K., Rolle, I. J., LaSarge, C. L., Hosford, B. E., Rosen, J. M., Uhl, J. D., Schmeltzer, S. N., Faulkner, C., Bronson, S. L., Murphy, B. L., et al. (2012) · Neuron · doi:10.1016/j.neuron.2012.08.002 · Cited by 266
Gatto (2010) · Frontiers in Synaptic Neuroscience · doi:10.3389/fnsyn.2010.00004 · Cited by 204
Seizure-like activity in hyaluronidase-treated dissociated hippocampal cultures
Vedunova, M., Sakharnova, T., Mitroshina, E., Perminova, M., Pimashkin, A., Zakharov, Y., Dityatev, A., & Mukhina, I. (2013) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2013.00149 · Cited by 107
Armstrong, C., Szabadics, J., Tamás, G., & Soltesz, I. (2011) · Journal of Comparative Neurology · doi:10.1002/cne.22577 · Cited by 86
Metadata
- Authors
- Pathak, H. R., Weissinger, F., Terunuma, M., Carlson, G. C., Hsu, F.-C., Moss, S. J., & Coulter, D. A.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2007-12-19
- Volume
- 27
- Issue
- 51
- Pages
- 14012-14022
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1965286805
- Cited by
- 271
- References
- 49
- FWCI
- 8.01
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Pathak, H. R., Weissinger, F., Terunuma, M., Carlson, G. C., Hsu, F.-C., Moss, S. J., & Coulter, D. A. (2007). Disrupted Dentate Granule Cell Chloride Regulation Enhances Synaptic Excitability during Development of Temporal Lobe Epilepsy. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.4390-07.2007
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