Local infusion of beta-endorphin (beta-END) into the medial preoptic area (MPOA) dose-dependently impaired the gating of the copulatory response and the execution of the sexual performance of sexually experienced, intact male rats. Local naloxone treatment prevented the impairment of the sexual response by beta-END, but failed to facilitate unimpaired copulation. Local infusion into the MPOA of equimolar doses of alpha-endorphin, dynorphin-A-(1-17) or met-enkephalin were less effective than beta-END. It is suggested that endogenous opioid systems in the MPOA are normally quiescent, and increased activity may be related to disrupted or inhibited male sexual behavior.

Students using online formative tests linked to microlectures receive higher grades especially in highly aligned summative tests.

No abstract

Exercise-induced loss of skeletal muscle K + can seriously impede muscle performance through membrane depolarization. Thus far, it has been assumed that the negative equilibrium potential and large membrane conductance of Cl − attenuate the loss of force during hyperkalaemia. We questioned this idea because there is some evidence that Cl − conductance was established with 9-anthracene carboxylic acid (9-AC). At 100 µM, 9-AC reduced the loss of force due to hyperkalaemia, while at 200 µM, 9-AC completely prevented loss of force. To study the role of the Na + −K + −2Cl − cotransporter (NKCC1) in this matter, we added 400 µM of the NKCC inhibitor bumetanide to the incubation medium. This did not affect the hyperkalaemia-induced loss of force. We conclude that Cl − exerts a permanent depolarizing influence on V m . This influence of Cl − on V m , in combination with a large membrane conductance, can apparently have two different effects on hyperkalaemia-induced loss of force. It might exert a stabilizing influence on force production during short periods of hyperkalaemia, but it can add to the loss of force during prolonged periods of hyperkalaemia.

No abstract