Kappa opioid receptor agonists suppress absence seizures in WAG/Rij rats
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Cited by (38)
The effect of selective opioid receptor agonists and antagonists on epileptiform activity in morphine-dependent infant mice hippocampal slices
2017, International Journal of Developmental NeuroscienceCitation Excerpt :It was found that DAMGO – a selective agonist of MOR – enhances absence epilepsy in rats, whereas the δ opioid receptor (DOR) agonist (DPDPE) showed no such effect. Interestingly, KOR agonists suppressed absence seizures in rats (Przewłocka et al., 1995). Some new facts confirm the putative anticonvulsant effects of dynorphin and other KOR agonists in self-sustaining status epilepticus in rats (Mazarati and Wasterlain, 2002) and ethanol withdrawal seizures in mice (Beadles-Bohling and Wiren, 2006).
Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development
2016, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Instead, a comparable age-related decrease in the PDYN mRNA levels was found in the frontal cortex and, to a lesser extent, in the striatum of both WAG/Rij and ACI rats (Lason et al., 1994b); this may be an independent additional factor facilitating the occurrence of SWDs, since the peptides derived from PDYN, interacting mainly with κ receptors, produce antiepileptic effects (Lason et al., 1994b; Przewlocka et al., 1995). Indeed, i.c.v. administration of U50,488H, which like PDYN-derived peptides, stimulates κ opioid receptors, decreased the number and mean duration of SWDs indicating that activation of the κ opioid receptor exerts an inhibitory effect on absence-like seizure activity in WAG/Rij rats (Przewlocka et al., 1995). κ receptor agonists not only act in a way opposite to μ receptor agonists (Lason et al., 1994a), but can also attenuate the μ agonist-induced increase of the number of SWDs; however, this receptor does not seem to be involved in the epileptogenesis process (Przewlocka et al., 1995).
The involvement of limbic structures in typical and atypical absence epilepsy
2013, Epilepsy ResearchCitation Excerpt :This increased level of α-neoendorphin represents an increase in the level of prodynorphin and this might be involved in a neurochemical mechanism that could prevent the spreading of SWDs to the limbic system. This idea is based on outcomes of neurophysiological studies indicating that prodynorphin-derived peptides exert an inhibitory influence on hippocampal neurons (Nicoll et al., 1977) and that peptides derived from prodynorphin exert antiepileptic effects in WAG/Rij rats (Przewłocka et al., 1995). Besides the findings of this genetic model, in the GHB model of typical absence seizures, elevated levels of prodynorphin were found in the hippocampus, suggesting involvement of the limbic circuitry in this pharmacologic model (Lasoń et al., 1983).
30 years of dynorphins - New insights on their functions in neuropsychiatric diseases
2009, Pharmacology and Therapeutics