Long-term behavioral outcome after early-life hyperthermia-induced seizures

Lemmens, Evi; Aendekerk, Brenda; Schijns, Olaf; Blokland, Arjan; Beuls, E. A. M.; Hoogland, Govert

doi:10.1016/j.yebeh.2008.11.005

Cited by 14 publications

(12 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Adult rats that were exposed to repetitive early-life FSs exhibited deficits in long-term memory that were associated with decreased expression of cAMP response element-binding protein (CREB) and translocation of CaMKII from the postsynaptic density to the cytosol (Chang et al 2003, Xiong et al 2014). In contrast,Lemmens et al (2009) did not observe deficits in learning or locomotor activity in rat pups that were exposed to a single prolonged early-life FS and subsequently tested for behavioral impairments during adulthood. Similarly, while Notenboom et al (2010) reported enhanced CA1 long-term potentiation (LTP) and reduced long-term depression (LTD) in adult rats that were subjected to a prolonged early-life FS as pups, no alterations in spatial learning or memory were observed.…”

Section: Discussionmentioning

confidence: 57%

Early-life febrile seizures worsen adult phenotypes in Scn1a mutants

Dutton

Dutt

Papale

et al. 2017

Experimental Neurology

View full text Add to dashboard Cite

Mutations in the voltage-gated sodium channel (VGSC) gene SCN1A, encoding the Nav1.1 channel, are responsible for a number of epilepsy disorders including genetic epilepsy with febrile seizures plus (GEFS+) and Dravet syndrome (DS). Patients with SCN1A mutations often experience prolonged early-life febrile seizures (FSs), raising the possibility that these events may influence epileptogenesis and lead to more severe adult phenotypes. To test this hypothesis, we subjected 21-23-day-old mice expressing the human SCN1A GEFS+ mutation R1648H to prolonged hyperthermia, and then examined seizure and behavioral phenotypes during adulthood. We found that early-life FSs resulted in lower latencies to induced seizures, increased severity of spontaneous seizures, hyperactivity, and impairments in social behavior and recognition memory during adulthood. Biophysical analysis of brain slice preparations revealed an increase in epileptiform activity in CA3 pyramidal neurons along with increased action potential firing, providing a mechanistic basis for the observed worsening of adult phenotypes. These findings demonstrate the long-term negative impact of early-life FSs on disease outcomes. This has important implications for the clinical management of this patient population and highlights the need for therapeutic interventions that could ameliorate disease progression.

show abstract

Section: Discussionmentioning

confidence: 57%

Early-life febrile seizures worsen adult phenotypes in Scn1a mutants

Dutton

Dutt

Papale

et al. 2017

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…Following the hyperthermia, animals were moved to a cool surface to regain normal body and brain temperatures, then returned to their mothers for rehydration. The mice were injected with saline to prevent dehydration before the hyperthermia procedure (Lemmens et al, 2009) (10 ml 0.9% saline/kg body weight subcutaneously). To observe the difference of febrile seizures ethology between these groups after hyperthermia-induction, we analyzed data from the onset latency as well as the rate and duration of febrile seizures by the standard of febrile seizures, which is as follow: generalized myoclonic jerk, wild running, ataxic walking, circling, falling, or tonic-clonic seizures of limbs (Racine, 1972).…”

Section: Experimental Fs Paradigm In Mouse Pupsmentioning

confidence: 99%

TRPV1 promotes repetitive febrile seizures by pro-inflammatory cytokines in immature brain

Huang

Sánchez

et al. 2015

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

“…FS-like seizures can be induced by hyperthermia [29][30][31][32][33][34][35][36][37][38] or hyperthermia coupled with lipopolysaccharide (LPS) and kainic acid (KA) [39,40]. Seizures typically arise in all hyperthermia-sustaining animals [41] suggesting that genetic susceptibility is not necessarily required for their generation. However, seizure-temperature thresholds (a measure of excitability) vary among mouse strains with differing genetic make-up [26,42].…”

Section: Geneticsmentioning

confidence: 99%

Origins of Temporal Lobe Epilepsy: Febrile Seizures and Febrile Status Epilepticus

2014

View full text Add to dashboard Cite

Temporal lobe epilepsy (TLE) and hippocampal sclerosis (HS) commonly arise following early-life long seizures, and especially febrile status epilepticus (FSE). However, there are major gaps in our knowledge regarding the causal relationships of FSE, TLE, HS and cognitive disturbances that hamper diagnosis, biomarker development and prevention. The critical questions include: What is the true probability of developing TLE after FSE? Are there predictive markers for those at risk? A fundamental question is whether FSE is simply a marker of individuals who are destined to develop TLE, or if FSE contributes to the risk of developing TLE. If FSE does contribute to epileptogenesis, then does this happen only in the setting of a predisposed brain? These questions are addressed within this review, using information gleaned over the past two decades from clinical studies as well as animal models.

show abstract

Long-term behavioral outcome after early-life hyperthermia-induced seizures

Cited by 14 publications

References 40 publications

Early-life febrile seizures worsen adult phenotypes in Scn1a mutants

Early-life febrile seizures worsen adult phenotypes in Scn1a mutants

TRPV1 promotes repetitive febrile seizures by pro-inflammatory cytokines in immature brain

Origins of Temporal Lobe Epilepsy: Febrile Seizures and Febrile Status Epilepticus

Contact Info

Product

Resources

About