ReviewCorticosteroids enhance convulsion susceptibility via central mineralocorticoid receptors
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Hippocampal glucocorticoid receptors modulate status epilepticus severity
2023, Neurobiology of DiseaseThe glucocorticoid receptor specific modulator CORT108297 reduces brain pathology following status epilepticus
2021, Experimental NeurologyPrenatal stress and elevated seizure susceptibility: Molecular inheritable changes
2019, Epilepsy and BehaviorSeizure-induced disinhibition of the HPA axis increases seizure susceptibility
2014, Epilepsy ResearchCitation Excerpt :Further, restoration of the chloride gradient with bumetanide and blocking the seizure-induced activation of the HPA axis decreases future seizure susceptibility. Patients with epilepsy have increased cortisol levels, which has been implicated in numerous pathological consequences, including increased seizure susceptibility (for review see Joels, 2009; Sawyer and Escayg, 2010; Roberts and Keith, 1995) as well as the comorbidity of depression in epilepsy (Pineda et al., 2010; Sankar and Mazarati, 2013). However, the underlying mechanisms leading to elevated levels of cortisol in patients with epilepsy are unknown.
Functional characterization of the hypothalamic-pituitary-adrenal axis of the Wistar Audiogenic Rat (WAR) strain
2011, Brain ResearchCitation Excerpt :This higher response to exogenous ACTH in WARs could be ascribed to their increased adrenal gland weight. It will be interesting to test whether this adrenal weight increase in WARs might be a phenomenon compatible with the known pro-convulsant effect of glucocorticoids (Roberts and Keith, 1995). It is well known that glucocorticoids exert neuronal excitatory effects, which are mediated through binding to central mineralocorticoid receptor (MR) in the hippocampus.
Stress within the postseizure time window inhibits seizure recurrence
2010, Epilepsy and BehaviorCitation Excerpt :In general, activation of MRs increases neuroexcitability [10], and activation of GRs suppresses neuroexcitability, particularly when MRs are activated [8,11]. This view is supported by the observation that MR antagonists have anticonvulsive effects [12,13]. In contrast, the influence of GRs on seizures is reported to be inconsistent [13,14].