Target contact regulates the calcium responsiveness of the secretory machinery during synaptogenesis.

Neuron B19 of Helisoma is selective in synaptogenesis. Presynaptic mechanisms underlying this selectivity were tested. Acetylcholine-sensitive assay cells were micromanipulated into contact with B19 somata to assess its secretory state. Prior to appropriate muscle target contact, spontaneous synaptic currents were detected; however, action potential-evoked release of neurotransmitter was detected only following hours of muscle contact. Photolysis of a calcium cage, DM-nitrophen, accelerated the frequency of synaptic currents in muscle-contacted, but not novel neuron-contacted, B19 somata. These studies demonstrate that contact with appropriate target muscle enhances the responsiveness of this neuron's secretory machinery to internal calcium levels, thereby imparting the presynaptic cell with the ability to couple action potentials with neurotransmitter release.     

Albertona balkanica from Early Miocene of Snegotin (Serbia) – implications for the distribution and evolution of Miocene Ochotonidae

Remains of Albertona balkanica from the Early Miocene clays of eastern Serbia have shifted the range boundary of this species in direction of Central Europe. The peculiarities in tooth morphology were used for comparison and defining of the possible evolutionary connection with other representatives of fossil Ochotonidae. Due to the similarity with fauna of Aliveri in Greece, the association of small mammals of Snegotin (which includes Albertona) was included in the MN4 zone.     

Therapy effect of antiulcer agents on new chronic cysteamine colon lesion in rat

After demonstration that cysteamine induced duodenal lesions in gastrectomized rats, while a number of antiulcer drugs mitigated these lesions, it was shown that one single intrarectal (i.r.) cysteamine application produced severe colon lesions in acute studies in rats. Thus, the further focus was on the protracted effect of cysteamine challenge (400 mg/kg b.w. i.r.) and therapy influence in chronic experiments in female rats. Regularly, cysteamine colon lesions were markedly mitigated by ranitidine (10), omeprazole (10), atropine (10), methylprednisolone (1), sulphasalazine (50; mg/kg), pentadecapeptide BPC 157 (PL-10, PLD-116; 10 microg or 10 ng/kg). Specifically, after 1 or 3 months following initial challenge (cysteamine 400 mg/kg i.r.) in female rat, the therapy [BPC 157 (PL-10, PLD-116 (10.0 microg or 10.0 ng/kg; i.g., i.p., i.r.), ranitidine, omeprazole, atropine, methylprednisolone, sulphasalazine (i.p.)] reversed the protracted cysteamine colon injury: the 1 week-regimen (once daily application) started after 1 month post-cysteamine, as well as the 2 weeks-regimen (once daily application), which started after 3 months. The effect on recidive lesion was also tested. These cysteamine lesions may reappear after stopping therapy (after stopping therapy for 3 weeks at the end of 2-weeks regimen started in 3 months-cysteamine female rats) in sulphasalazine group, while this reappearance is markedly antagonized in pentadecapeptide BPC 157 (PL-10, PLD-116)-rats (cysteamine-colon lesion still substantially low).