Zaburzenia snu i rytmu dobowego w modelach zwierzęcych padaczki płata skroniowego
Sleep and circadian rhythm disruptions in animal models of temporal lobe epilepsy
W skrócie
Padaczka płata skroniowego często powoduje problemy ze snem i zaburzenia wewnętrznego zegara biologicznego organizmu. Naukowcy badali te problemy na myszach i szczurach, używając trzech różnych modeli choroby, aby zrozumieć jak epilepsja i sen są ze sobą powiązane. Badania pokazały, że u zwierząt z padaczką sen jest spętniony, a geny kontrolujące rytm dobowy pracują nieprawidłowo, chociaż szczegóły różnią się w zależności od modelu i etapu choroby.
Oryginalny abstract (angielski)
Temporal lobe epilepsy (TLE) is frequently accompanied by disruptions to sleep and circadian rhythms, which substantially contribute to disease burden. Human studies are often confounded by antiseizure medications, limiting insight into underlying mechanisms. Animal models therefore provide critical opportunities to examine causal interactions, yet their translational validity has not been systematically evaluated. In this review, we first outline the relevance of rodent models for studying epilepsy- and sleep-related processes. We then examine current evidence for sleep and circadian disturbances across three commonly used TLE models: the pilocarpine (PILO) model, the kainic acid (KA) model, and the traumatic brain injury (TBI) model. We summarize circadian patterns of seizure occurrence, alterations in sleep-wake architecture, and changes in core circadian clock gene expression, as well as alterations in subcortical brain regions involved in sleep-wake regulation. Across models, sleep is consistently fragmented, and circadian molecular machinery is profoundly disrupted, although the direction and magnitude of changes vary by species, protocol, and epilepsy stage. By comparing findings across animal models and patient studies, this review highlights convergences, discrepancies, and key research gaps. Despite variability, animal models remain indispensable for probing the bidirectional links between epilepsy and sleep-circadian regulation.