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Status epilepticus in immature rats leads to behavioural and cognitive impairment and epileptogenesis
Hana Kubová1, Pavel Mares, Lucie Suchomelová
1Institute of Physiology, Academy of Sciences of the Czech Republic, Vídeòská 1083, Prague 4, CZ-142 20, Czech Republic. kubova@biomed.cas.cz
Insights
Status epilepticus (SE) in immature brains, even in early infancy, causes lasting cognitive and emotional deficits. This early-life seizure activity also leads to the development of spontaneous seizures later in life.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Epileptology
Background:
- The long-term effects of perinatal or early childhood status epilepticus (SE) on cognitive function are debated.
- Understanding the impact of early-life seizures on brain development is crucial for predicting long-term neurological outcomes.
Purpose of the Study:
- To investigate if SE induced in immature rat brains (postnatal day 12 or 25) leads to cognitive impairment and epileptogenesis.
- To compare the effects of early-life SE with SE induced in adult rats.
Main Methods:
- Induction of SE using LiCl-pilocarpine in immature (P12, P25) and adult rats.
- Assessment of cognitive function and emotional behavior using open-field and elevated plus-maze paradigms 3 months post-SE.
- Video-electroencephalography (EEG) monitoring 3 months post-SE to detect spontaneous seizures.
Main Results:
- Rats experiencing SE at P12 showed impaired memory and emotional behavior, though less severe than in older groups.
- A significant percentage of P12 (25%) and P25 (50%) rats developed spontaneous seizures.
- P12 rats exhibited nonconvulsive seizures, while P25 rats showed clonic convulsions.
Conclusions:
- SE is detrimental to the immature brain as early as postnatal day 12, mirroring potential impacts in human infancy.
- Early-life SE can cause persistent cognitive deficits and lead to the development of epilepsy.
Abstract:
It remains under dispute whether status epilepticus (SE) in the perinatal period or early childhood or the underlying neuropathology is the cause of functional impairment later in life. The present study examined whether SE induced by LiCl-pilocarpine in normal immature brain (at the age of 12 or 25 days; P12 or P25) causes cognitive decline and epileptogenesis, and the data were compared to those of rats undergoing SE as adults. Rats in the P12 group had impaired memory (repeated exposure to open-field paradigm) and emotional behaviour (lower proportion of open-arm entries and higher incidence of risk assessment period in elevated plus-maze) when assessed 3 months after SE, although not as severe as in the older age groups. Importantly, video-electroencephalography monitoring 3 months after SE demonstrated that 25% of rats in the P12 and 50% in P25 group developed spontaneous seizures. Only nonconvulsive seizures (ictal activity in hippocampus accompanied by automatisms) were recorded in the P12 group whereas rats in the P25 group exhibited clonic convulsions. The present findings indicate that SE is harmful to the immature brain as early as P12, which might be compared with early infancy in humans.
