The dopamine D1 receptor agonist SKF81297 has dose-related effects on locomotor activity but is without effect in a CER trace conditioning procedure conducted with two versus four trials

In an appetitively motivated procedure, we have previously reported that systemic treatment with the dopamine (DA) D1 receptor agonist SKF81297 (0.4 and 0.8 mg/kg) depressed acquisition at a 2s inter-stimulus-interval (ISI), suitable to detect trace conditioning impairment. However since DA is involved in reinforcement processes, the generality of effects across appetitively- and aversively-motivated trace conditioning procedures cannot be assumed. The present study tested the effects of SKF81297 (0.4 and 0.8 mg/kg) in an established conditioned emotional response (CER) procedure. Trace-dependent conditioning was clearly shown in two experiments: while conditioning was relatively strong at a 3-s ISI, it was attenuated at a 30-s ISI. This was shown after two (Experiment 1) or four (Experiment 2) conditioning trials conducted in - as far as possible - the same CER procedure. Contrary to prediction, in neither experiment was there any indication that trace conditioning was attenuated by treatment with 0.4 or 0.8 mg/kg SKF81297. In the same rats, locomotor activity was significantly enhanced at the 0.8 mg/kg dose of SKF81297. These results suggest that procedural details of the trace conditioning variant in use are an important determinant of the profile of dopaminergic modulation

Reports of the AAAI 2010 spring symposia

Original paper can be found at : https://www.aaai.org/ Copyright Association for the Advancement of Artificial Intelligence [Full text of this article is not available in the UHRA]The Association for the Advancement of Artificial Intelligence, in cooperation with Stanford University's Department of Computer Science, presented the 2010 Spring Symposium Series Monday through Wednesday, March 22-24, 2010, at Stanford University. The titles of the seven symposia were Artificial Intelligence for Development; Cognitive Shape Processing; Educational Robotics and Beyond: Design and Evaluation; Embedded Reasoning: Intelligence in Embedded Systems; Intelligent Information Privacy Management; It's All in the Timing: Representing and Reasoning about Time in Interactive Behavior; and Linked Data Meets Artificial Intelligence.Peer reviewe

Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder. Ten percent of cases are inherited; most involve unidentified genes. We report here 13 mutations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene on chromosome 16 that were specific for familial ALS. The FUS/TLS protein binds to RNA, functions in diverse processes, and is normally located predominantly in the nucleus. In contrast, the mutant forms of FUS/TLS accumulated in the cytoplasm of neurons, a pathology that is similar to that of the gene TAR DNA-binding protein 43 (TDP43), whose mutations also cause ALS. Neuronal cytoplasmic protein aggregation and defective RNA metabolism thus appear to be common pathogenic mechanisms involved in ALS and possibly in other neurodegenerative disorders

Jobs, work and citizens' income : four strategies and a new regime

Digitised version produced by the EUI Library and made available online in 2020