These novel observations with an adenosine A(1) receptor agonist suggest that this pharmacological action could contribute to antipsychotic effects in addition to thymoleptic effects. (C) 2009 Elsevier Ltd. All rights reserved.”
“Purpose: We determine the prevalence of premature ejaculation

in patients with hyperthyroidism and observed intravaginal ejaculation latency time alterations before and after hyperthyroidism treatment.

Materials Selleckchem 10058-F4 and Methods: Between January 2004 and June 2007, 49 patients with hyperthyroidism and no history of hyperthyroidism treatment were enrolled in the study. After obtaining a detailed sexual anamnesis an erectile function questionnaire was completed and a patient self-reported outcome measure of difficult control over ejaculation was examined. We assessed stopwatch measurements of intravaginal ejaculation latency time performed by the patient or partner. Patient anxiety status was also evaluated. Changes in the mentioned measurements induced by hyperthyroidism treatment were examined 8 weeks after the achievement of euthyroidism.

Results: In the 43 eligible patients mean +/- SD age was 48.0 +/- 8.8 years. Premature ejaculation was

observed in 31 of the 43 patients (72.1%). Mean intravaginal ejaculation latency time in patients with hyperthyroidism was 72.8 +/- 83.3 seconds. Of 4SC-202 concentration the 43 patients 30 (69.8%) were considered to have definite premature ejaculation according this website to stopwatch measurements. In patients with hyperthyroidism who had definite premature ejaculation anxiety scores were determined to be higher. A positive correlation was noted between serum thyroid stimulating hormone and intravaginal ejaculation latency time in the patients. In 24 patients who completed the followup visits we noted statistically

significant improvement in intravaginal ejaculation latency time after the achievement of euthyroidism.

Conclusions: Excess thyroid hormone and premature ejaculation are clinically interrelated conditions. Hyperthyroidism should be considered a novel and reversible etiological risk factor for premature ejaculation.”
“Reduced synaptic inhibition due to dysfunction of ionotropic GABA(A) receptors has been proposed as one factor in cerebral ischaemia-induced excitotoxic cell death. However, the participation of the inhibitory metabotropic GABA(B) receptors in these pathological processes has not been extensively investigated. We used oxygen-glucose deprivation (OGD) and NMDA-induced excitotoxicity as models to investigate whether ischaemia-like challenges alter the protein levels of GABA(B1) and GABA(B2) receptor subunits in rat organotypic hippocampal slice cultures.