Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats

Boyce, Richard D.; Leung, L. Stan

doi:10.1016/j.eplepsyres.2012.06.009

Cited by 5 publications

(5 citation statements)

References 44 publications

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“…Febrile convulsions also have a detrimental effect on the inhibitory circuitry, particularly at certain periods; our results showed that febrile seizures at the postnatal day of 24 (P20-P30) had long term effects, such as decrease of PPI in dentate and CA3. Other labs also found confirming results, that febrile seizures decrease inhibition in CA1 and CA3, during adulthood (Boyce, 2013). Some researchers also found decreased PPI in DG by the perforant path stimulation (Naylor, 2005).…”

Section: Loss Of Paired Pulse Inhibition In Dentate Gyrus and Ca3supporting

confidence: 59%

A Bio-Electrical Tornado in The Hippocampus: Mechanisms of Temporal Lobe Epilepsy

Sayın¹

2016

Neuroquantology

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This review summarizes the structural and electrophysiological changes in the epileptic hippocampus in various animal models of epilepsy. Tornado hypothesis of epileptic hippocampus, states that there are many progressive detrimental changes in the hippocampus of the epileptic rats. PTZ, PTZ kindling, pilocarpine, electrical kindling, kainic acid, hyperthermia and in vitro models are taken as primary animal epilepsy models in this review. Paired pulse inhibition and GABAergic transmission is decreased in dentate gyrus (DG), CA3 and CA1 regions of the epileptic hippocampus. There is interneuron loss in the hilus, DG and CA3, while excitatory input from perforant path (PP) is increased and this is fed into the CA3 area by mossy fibers (MF) which have excessive sprouting that forms novel recurrent synapses with the pyramidal cells of CA3. Gate function of DG is either impaired or lost. CA3 area of hippocampus becomes an epileptic focus and sends ictal discharges. These ictal discharges are carried into CA1 by Schaffer collaterals and then into entorhinal cortex (EC). The input from EC is amplified in the hippocampal circuitry which is fed into hippocampus from EC into DG again successively. Thus, a weak electrical input into the hippocampal formation results in an amplified signal back into EC. Since the basic ultrastructural and electrophysiological feed-back control mechanisms are impaired, this electrical tornado cannot be compensated for and an epileptic amplified ictal discharge spreads to the limbic system and other adjacent structures of the brain. Eventually the hippocampal circuitry, that has developed a vicious circle, becomes a bioelectrical amplifier which triggers an electrical tornado, under certain bio-chemical conditions.

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Section: Loss Of Paired Pulse Inhibition In Dentate Gyrus and Ca3supporting

confidence: 59%

A Bio-Electrical Tornado in The Hippocampus: Mechanisms of Temporal Lobe Epilepsy

Sayın¹

2016

Neuroquantology

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“…As we have shown, inflammatory monocytes densely infiltrate the CA1 region within hours of infection in C57BL/6J mice 6 and retraction of CA1 apical dendrites is observed shortly thereafter 8 . Apical dendrite retraction results in loss of inhibitory control of the CA3-to-CA1 circuit and is a hallmark of hyperexcitability 30 . In SJL mice infected with the Daniel’s strain of TMEV there is limited inflammatory monocyte infiltration 7 and these animals do not exhibit hippocampal injury or retraction of apical dendrites 7 and do not experience seizures 31 , further suggesting a link between inflammation and hyperexcitability in this model.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection mediated by inhibition of calpain during acute viral encephalitis

Howe

LaFrance‐Corey

Mirchia

et al. 2016

Sci Rep

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Neurologic complications associated with viral encephalitis, including seizures and cognitive impairment, are a global health issue, especially in children. We previously showed that hippocampal injury during acute picornavirus infection in mice is associated with calpain activation and is the result of neuronal death triggered by brain-infiltrating inflammatory monocytes. We therefore hypothesized that treatment with a calpain inhibitor would protect neurons from immune-mediated bystander injury. C57BL/6J mice infected with the Daniel’s strain of Theiler’s murine encephalomyelitis virus were treated with the FDA-approved drug ritonavir using a dosing regimen that resulted in plasma concentrations within the therapeutic range for calpain inhibition. Ritonavir treatment significantly reduced calpain activity in the hippocampus, protected hippocampal neurons from death, preserved cognitive performance, and suppressed seizure escalation, even when therapy was initiated 36 hours after disease onset. Calpain inhibition by ritonavir may be a powerful tool for preserving neurons and cognitive function and preventing neural circuit dysregulation in humans with neuroinflammatory disorders.

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“…41 A separate study demonstrates that early-life hyperthermic seizures lowered inhibition in the CA1 hippocampal dendrites, and suggests that the behavioral deficits are caused by a loss of CA1 apical dendritic inhibition. 42 It has also been shown that spatial memory formation by direct excitation of entorhinal to CA1 distal dendrites may be disrupted due to lowered inhibitory regulation. Repeated administration of flurothyl seizures during early development results in immature dendritic fields in pyramidal neurons within the CA1 region of the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Early-life status epilepticus induces long-term deficits in anxiety and spatial learning in mice

Smith

Ahmed

Arbuckle

et al. 2017

International Journal of Epilepsy

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Background One of the most devastating aspects of developmental epilepsy is the long-term impact on behavior. Children with epilepsy show a high co-morbidity with anxiety disorders and autism. Methods To examine whether early-life status epilepticus results in altered anxiety, repetitive behavior, social behavior, and learning and memory, we induced status epilepticus in male C57BL/6 mice on postnatal day (PD) 10. The mice received intraperitoneal injections of either kainic acid (2 mg/kg) or 0.9% normal saline. We also included a nontreated control group. Kainic acid induced status epilepticus for approximately 1.5 h. At PD60, the adult mice were then tested in a battery of behavioral tasks, including open field activity, elevated-plus maze, light-dark test, marble burying, social chamber, social partition, conditioned fear, novel object recognition, and Morris water maze. Results The early-life seizure group showed consistent increases in anxiety in the open field test (p < 0.05), elevated plus maze (p < 0.05), and light-dark task (p < 0.01). The seizure group showed significant (p < 0.01) impairment in the Morris water maze. There were no differences observed in marble burying, social partition, social chamber, novel object recognition, or delay fear conditioning tasks. Conclusions These results demonstrate that a single insult of status epilepticus during the neonatal period is sufficient to cause specific, long-term impairments in anxiety and spatial learning.

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Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats

Cited by 5 publications

References 44 publications

A Bio-Electrical Tornado in The Hippocampus: Mechanisms of Temporal Lobe Epilepsy

A Bio-Electrical Tornado in The Hippocampus: Mechanisms of Temporal Lobe Epilepsy

Neuroprotection mediated by inhibition of calpain during acute viral encephalitis

Early-life status epilepticus induces long-term deficits in anxiety and spatial learning in mice

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