17 beta estradiol/癲癇性発作

Estrogens change the susceptibility to seizures in humans and experimental animals. In this study, the effect of estrone and 17 beta-estradiol on kainate-induced seizures and neurotoxicity was investigated in male mice. Pre-treatment with estrone (250-1000 micrograms/kg) at 24 and 2 hours before

Evidence shows neurosteroids play a key role in regulating epileptogenesis. Neurosteroids such as testosterone modulate seizure susceptibility through its transformation to metabolites which show proconvulsant and anticonvulsant effects, respectively. Reduction of testosterone by aromatase generates

The acute effects of 17 beta-estradiol on brain excitability were studied in vitro and in vivo utilizing rat hippocampal slices and a cat cerveau isolé preparation. The hippocampal slices were perfused with 17 beta-estradiol (10(-7)-10(-10) M) for 30 min. No effects were observed on synaptic

A time course study that examined the effects of the female estrous cycle on the chronic slow spike-and-wave discharges (SSWDs), gamma-aminobutyric B receptor (GABA(B)R) binding, and GABA(B)R protein expression was conducted in Long Evans hooded rats treated during development with a cholesterol

We investigated the effects of 17 beta-estradiol (E2) and progesterone (PG) on seizure sensitivity in two genetically epilepsy-prone strains, the DBA/2J and the C57/EL hybrid. In the DBA/2J, subject to audiogenic seizures when juvenile, oophorectomy produced a marked decrease in seizure sensitivity,

BACKGROUND Alcohol abuse, especially when experienced in multiple cycles of chronic abuse and withdrawal, leads to a sensitization of central nervous system hyperexcitability that may culminate in overt expression of seizures. In spite of the growing prevalence of alcohol abuse and dependence in

BACKGROUND Epilepsy and menopause have complicated interactions. Treatment of epilepsy may cause exacerbation of osteoporosis and alter the effects of hormone replacement therapy (HRT) whereas HRT may influence the frequency of seizures. METHODS An extensive search was performed in the Cochrane

OBJECTIVE Seizures with ictal laughter (also termed gelastic seizures) have been associated with hypothalamic hamartomas and precocious puberty. It is not known, however, where in the brain such seizures originate. We describe a child with gelastic seizures and a hypothalamic lesion (probably a

The target of the current study is to formulate letrozole loaded nanoemulsion (LET-NE) for the direct nose to brain delivery to reduce peripheral effects of letrozole (LET). LET-NE is compared against intraperitoneally administered free LET in kainic acid (KA) induced status epilepticus (SE) in

The ovarian steroid hormone estradiol, in addition to its function in the maintenance and regulation of reproductive capacity, can alter neuronal excitability. Estradiol is proconvulsant, increases neuronal excitability and decreases the threshold for seizure activity. Over one-third to one-half of

Ongoing studies from this laboratory have demonstrated marked potentiating actions of the sex steroid 17 beta-estradiol (E2) on glutamate-induced excitation. In the present study, systemic injection of a physiological dose of E2 was demonstrated to augment significantly excitatory responses of

The neurosteroid 3 alpha-hydroxy-5 alpha-pregnan-20-one (3 alpha, 5 alpha-THP) acts as a potent allosteric modulator and a direct activator of the GABA-chloride channel complex. This neurosteroid has also been found to protect against seizures that arise from blockade of the GABA-chloride channel

Catamenial epilepsy is a common phenomenon in female epileptic patients that is, in part, influenced by the 17-β-estradiol level during the menstrual cycle, which modulates the strength of the epileptic seizures. However, the underlying mechanism(s) for catamenial epilepsy remains unknown. In the

Given the well-documented involvement of estrogens in the modulation of hippocampal functions in both physiological and pathological conditions, the present study investigates the effects of 17-beta estradiol (E2) administration in the rat model of hippocampal neurodegeneration induced by