Roles of the Drosophila SK Channel (dSK) in Courtship Memory

A role for SK channels in synaptic plasticity has been very well-characterized. However, in the absence of simple genetic animal models, their role in behavioral memory remains elusive. Here, we take advantage of Drosophila melanogaster with its single SK gene (dSK) and well-established courtship memory assay to investigate the contribution of this channel to memory. Using two independent dSK alleles, a null mutation and a dominant negative subunit, we show that while dSK negatively regulates the acquisition of short-term memory 30 min after a short training session, it is required for normal long-term memory 24 h after extended training. These findings highlight important functions for dSK in courtship memory and suggest that SK channels can mediate multiple forms of behavioral plasticity

Effects of metal ions on cyprinid fish immune response: In vitro effects of Zn2+ and Mn2+ on the mitogenic response of carp pronephros lymphocytes

International audienceLymphocytes from the pronephros of carp (Cyprinus carpio L) have been subjected to transformation by mitogens, concanavalin A (Con A), phytohemagglutinin (PHA), and lipopolysaccharides (LPS), with Zn or Mn at varying concentrations. Addition of Zn2+ (10−7 to 10−3 M) to mitogen-stimulated T and B cells enhanced [3H]thymidine incorporation. Addition of 10−5 M Zn2+ inhibited the response to Con A, PHA, and LPS. At this concentration, Zn was toxic. Addition of Mn2+ (10−7 to 10−3 M) to mitogen-stimulated lymphocytes enhanced [3H]thymidine incorporation. This effect was observed with Con A- and PHA-stimulated lymphocytes, but not with LPS-stimulated lymphocytes. In contrast, addition of 10−1 M Mn2+ to lymphocyte cultures exerted an inhibitor effect on the response to Con A or to PHA, while the response to LPS was unaffected. Addition of 10−1 M Mn2+ to Con A- or PHA-stimulated cultures at different times after initiation of stimulation indicated that Mn2+ was inhibitory only when it was added before the first 16 hr of cultures. The inhibition induced by 10−1 M Mn2+ could be reversed by adding 2 mM CaCl2 to the culture

Habenula lesions alter synaptic plasticity within the fimbria-accumbens pathway in the rat.

Both the habenula and the nucleus accumbens, and especially the glutamatergic innervation of the latter from the hippocampus, have been hypothesized to be involved, in different ways, in the pathophysiology of cognitive disturbances in schizophrenia. Lesions of the habenula produce disturbances of memory and attention in experimental animals. As the habenular nuclei have been shown to influence the release of many neurotransmitters, both in the hippocampus and the nucleus accumbens, we examined in this study the effects of bilateral habenula lesions on the plasticity of the fimbria-nucleus accumbens pathway, by means of the long-term depression phenomenon in freely moving rats. Long-term depression, induced within the shell region of the nucleus accumbens by low-frequency stimulation of the fimbria, was exaggerated and showed greater persistence in habenula-lesioned rats compared with sham-operated animals. These results indicate that plasticity in the fimbria-nucleus accumbens pathway is altered by habenula lesions in a way similar to previously-reported effects of stress and the psychosis-provoking agent ketamine. Moreover, they strengthen the views that the habenula belongs to systems, mediating higher cognitive functions, which involve the hippocampus and the nucleus accumbens. Finally, this study suggests that dysfunction of the habenula could contribute to cognitive alterations in diseases such as schizophrenia, where the habenula is reported to exhibit exaggerated calcification

Post-extinction fluoxetine treatment prevents stress-induced reemergence of extinguished fear

The post-extinction exposure of rats to a sub-conditioning procedure (SCP; i.e., retraining with a shock intensity that is too weak to induce by itself significant fear conditioning) has been reported to provoke the reemergence of extinguished fear. This phenomenon can be prevented by chronic fluoxetine treatment. We sought to examine another potential inducer of fear reemergence, acute stress, in rats and determine whether fluoxetine prevents this phenomenon. Because in previous studies fluoxetine was administered before extinction, we first analyzed its effect on the SCP-associated reemergence of auditory-cued conditioned fear in rats injected after extinction to avoid any interaction between fluoxetine and extinction learning. Next, we used the same protocol but replaced the SCP with acute stress. We found that the SCP and acute stress, which were carried out 3 weeks after fear extinction, similarly provoked the reemergence of extinguished fear in rats injected with vehicle during the 3-week period. In contrast, the animals treated with fluoxetine during this period behaved similarly to those not exposed to an inducer of fear reemergence. Our data establish acute stress as an inducer of fear reemergence. The results provide further support for the hypothesis that fluoxetine interfered with mechanisms that reactivated extinguished fear, even when administered after fear extinction