Plasticity of intrinsic firing response gain in principal hippocampal neurons following pilocarpine-induced status epilepticus. (15th August 2017)

• Record Type: Journal Article
• Authors: Tamir, Idit; Daninos, Moshe; Yaari, Yoel
• Is Part Of: Neuroscience. Volume 357(2017)
• Page Start: 325
• Page End: 337
• Publication Date: 2017-08-15
• Subjects: aCSF artificial cerebrospinal fluid -- ANOVA analysis of variance -- AP action potential -- EEG electroencephalography -- FAHP fast after hyperpolarization -- GCs granule cells -- ISI interspike interval -- MAP mitogen-activated protein kinase -- Ns number of spikes -- PCs pyramidal cells -- PKC protein kinase C -- post-SE post status epilepticus -- RN input resistance -- sAHP slow afterhyperpolarization -- SE status epilepticus -- TLE temporal lobe epilepsy; temporal lobe epilepsy -- intrinsic neuronal plasticity -- gain -- pilocarpine -- hippocampus -- CA3; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2017.06.013
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: The firing response gain of principle hippocampal neurons is multiplied following pilocarpine-induced status epilepticus. Of the three types of principal hippocampal neurons, gain multiplication is most dramatic in CA3 pyramidal cells. Neuronal gain increase following pilocarpine-SE is due to cell-specific alterations in intrinsic physiological properties. Reduction in sAHP and increase in fraction of bursters are the main causes of gain multiplication following pilocarpine-SE. Abstract: Objective: In experimental models of temporal lobe epilepsy (TLE), brain neurons manifest multiple changes in intrinsic excitability that contribute to neuronal network hyperexcitability. We have investigated whether the intrinsic firing response gain, quantified by the slope of the function relating the number of evoked spikes (Ns) to input excitatory current intensity (I), is modified in principal rat hippocampal neurons in the pilocarpine-status epilepticus (SE) model of TLE. Methods: Intracellular recordings were made in CA3 and CA1 pyramidal cells (PCs) and dentate granule cells (GCs) in acute hippocampal slices obtained 7–36 days after pilocarpine-SE. Firing response gains were determined empirically from Ns/I relationships and compared to other measured neuronal properties. Results: The firing response gain in all three types of principal neurons, particularly in CA3 PCs, was markedly multiplied following pilocarpine-SE. Analyses of persistent changes in active and passive properties of CA3 PCs suggested that this increase is multifactorial in origin, the major factors being a reduction in amplitude of the slow afterhyperpolarization and an increase in the fraction of bursting neurons. Significance: Here we show that pilocarpine-SE causes multiplication of the firing response gain in the three principal neurons in the hippocampal trisynaptic pathway. This alteration undoubtedly would contribute to hippocampal hyperexcitability in SE-induced TLE.