The characteristic leaf damage caused by attack from Empoasca spp. was only observed on 35S-jmt-1 plants

rases catalyze the conversion of cAMP and cGMP into AMP and GMP, respectively, and are important for the homeostatic regulation of cyclic nucleotide-mediated signaling events. The PDEs are grouped into several families, two of which, PDEs 4 and 7, exclusively target cAMP. Rolipram, a PDE4-specific small molecule inhibitor, has antidepressant effects and was recently found to facilitate memory formation and synaptic plasticity in rodents. Rolipram was also shown to reverse synaptic 1 September 2011 | Volume 6 | Issue 9 | e25735 Cdk5, Synaptic Plasticity, and Behavior plasticity and memory deficits in CBP+/2 mice, a mouse model of Rubinstein-Taybi syndrome. Cyclin-dependent kinase 5 was initially classified as a cyclin-dependent kinase based on sequence homology to other Cdks that operate in the cell cycle. Cdk5 has been implicated in almost every aspect of brain development and neural function including neuronal migration, neurite extension, synaptic transmission, and synaptic plasticity. Intriguingly, Cdk5 gain-of-function mutations result in an increased number of synapses in vivo and the facilitation of LTP in slices, whereas the loss of Cdk5 activity in p35 knockout mice results in impaired hippocampal LTD. In contrast, an inducible Cdk5 conditional knockout mouse model exhibited facilitated LTP and enhanced memory formation via reduced degradation of the NR2B subunit of the NMDA receptor. Despite a greater understanding of how Cdk5 is critically important for synapse formation, the in vivo role for Cdk5 as a part of a signaling pathway crucial to hippocampal learning and memory remains unclear. In the current report, we found that Cdk5 loss of function in distinct hippocampal circuits resulted in impairments in various memory functions and synaptic plasticity, observations distinct from previously reported findings using a different Cdk5 mouse model. In addition, multiple PDE isoforms were PG-490 biological activity markedly upregulated, which led to the dysregulation of cAMP pathway and impaired CREB phosphorylation. Remarkably, the observed deficiencies in Cdk5 conditional knockout mice can be rescued by rolipram treatment. Taken together, these results indicate a key function for Cdk5 in regulating cAMP signaling via modulation of PDE expression to facilitate synaptic plasticity and hippocampaldependent memory formation. Results Associative and spatial memories are impaired in Cdk5f/ f/T29 mice To evaluate the consequences of Cdk5 ablation in hippocampal neurons, Cdk5f/f/T29 mice were generated using the Cre line T29-2, in which Cre is highly expressed in CA1 pyramidal neurons of the hippocampus, and subjected to various behavior tasks. The ablation of Cdk5 using T29-Cre does not lead to significant changes in overall brain architecture or cell survival. We noted in the T29Cre ” line that Cre-mediated Cdk5 knockout is relatively specific to area CA1 in young mice, with the deletion of Cdk5 spreading to ” cortical and other brain regions in older mice. Beginning at 5 months of age, Cdk5f/f/T29 mice suffered mild to severe seizures and died by 8 months, which might be due to the spreading of T29-Cre expression. Therefore, we used 2.5 to 3.5 month-old mice to perform all behavior tests. Cdk5f/f/T29 mice were trained using Pavlovian fear conditioning paradigm 24 hours prior to a memory test. Cdk5f/f/T29 mice exhibited significantly reduced freezing behavior compared to control littermates in the context-dependent memory test. Consistent with the notion that the hi