Neuronal activity in the subcortically denervated hippocampus: A chronic model for epilepsy
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Cited by (102)
Chronic Loss of CA2 Transmission Leads to Hippocampal Hyperexcitability
2017, NeuronCitation Excerpt :Moreover, inhibition of CA3 PC transmission leads to changes in both rate and temporal coding in CA1 (Middleton and McHugh, 2016), a decrease in the intrinsic frequency of CA1 ripples (Nakashiba et al., 2009), and a resistance to KA seizure induction (Yu et al., 2016). Here we find that CA2-PC silencing leads to a largely opposing set of phenotypes, a pathophysiology similar to that seen in pre-epileptic models (Buzsáki et al., 1989; Wadman et al., 1983), an increase in the frequency and magnitude of fast-oscillations during rest, and an increase in susceptibility to excitotoxic challenge (Figures 7C and 7D). Understanding which EC inputs to CA2 engage this circuit and under what circumstances this occurs will be crucial to further clarifying the role of CA2-CA3 mutual inhibition in normal hippocampal function.
Interictal spike frequency varies with ovarian cycle stage in a rat model of epilepsy
2015, Experimental NeurologyTransient impact of spike on theta rhythm in temporal lobe epilepsy
2013, Experimental NeurologyCitation Excerpt :Interictal-like activity (ILA) during epileptogenesis is an electrophysiological signature of the reverberating neural circuits (Alarcon et al., 1997; Buzsaki et al., 1989, 1991; Cossart et al., 2001; Demont-Guignard et al., 2009; El-Hassar et al., 2007), with the spike discharges being its most common form.
Hippocampal excitability is increased in aged mice
2013, Experimental NeurologyCitation Excerpt :Such CA3-to-CA3 recurrent circuitry is crucial for the generation of physiological EEG activities as well as epileptiform field potentials (Beenhakker and Huguenard, 2009; Chrobak et al., 2000; Miles and Wong, 1986; Miles and Wong, 1987). It has been postulated that in intact animal brains the hippocampus may be under inhibitory control by sub-cortical afferent inputs, as the surgically deafferented hippocampus can allow large-amplitude population activities to occur in vivo (Buzsáki et al., 1989). In line with this view, it is conceivable that in the absence of extra-hippocampal inhibitory inputs, the hippocampal slices are able to generate longer population events (such as SFPs) if the recurrent axonal connections of the CA3 pyramidal neurons are sufficiently preserved in vitro.
Epilepsy as a dynamic disease of neuronal networks
2012, Handbook of Clinical NeurologyCitation Excerpt :In addition, we may speculate that enhanced activity in this re-entrant circuit may constitute the anatomical and physiological substrate for reverberation to occur, i.e., persistent activity in these loops in the absence of external input. Indeed, it has been suggested that in the subcortically denervated hippocampus of the freely moving rat, removal of tonic inhibitory influences allows reverberation of information in the entorhinal–hippocampal–entorhinal cortex circuitry (Buzsáki et al., 1989). It has not yet been established experimentally, however, whether this kind of reverberation is an important mechanism making these rats more susceptible to the occurrence of epileptic seizures.
Different phases of afterdischarge during rapid kindling procedure in mice
2009, Epilepsy Research