1. Silencing Cell-Cycle Reentry in Postmitotic Neurons
Angeles Almeida, Juan P. Bolańos, and Sergio Moreno
Increasing evidence suggests that cell-cycle proteins can be reactivated and contribute to cell demise. For example, the Cdk1–cyclin B1 complex can be reactivated in Alzheimer's disease. The E3-ubiquitin ligase anaphase-promoting complex (APC) marks mitotic cyclins such as B1 for degradation, and APC is activated by Cdh1 at the end of mitosis. Because Cdh1–APC remains active in postmitotic cells, Almeida et al. tested whether Cdh1 can keep cyclin B1 in check, thus preventing cell-cycle reentry. The answer seems to be yes.
2. Monosynaptic Whisker Control in the Rat
Valery Grinevich, Michael Brecht, and Pavel Osten
Whiskers, the primary somatosensory tool in rodents, move independently during object exploration. This does not seem to be consistent with existing anatomical evidence for purely polysynaptic innervation of motor neurons by vibrissa motor cortex (VMC) neurons. This week, Grinevich et al. reexamined the possibility of direct innervation. Injection of retrograde tracers into whisker follicles revealed motor neurons within 250 µm of the VMC terminals, a distance well within the dendritic tree of motor neurons. Electron microscopy confirmed a monosynaptic VMC-to-FN pathway.
3. Antidepressant Responsiveness and 5-HT Synthesis
Luigi Cervo, Alessandro Canetta, Eleonora Calcagno, Silvia Burbassi, Giuseppina Sacchetti, Silvio Caccia, Claudia Fracasso, Diego Albani, Gianluigi Forloni, and Roberto W. Invernizzi
Although selective serotonin (5-HT) reuptake inhibitors (SSRIs) benefit many patients, some patients are nonresponders. This week, Cervo et al. explored a possible genetic cause for SSRI responsiveness. The SSRI citalopram reduced immobility time in C57BL/6J and 129/Sv mice but had no effect in DBA/2J or BALB/c mice, suggesting that genetic differences in serotonin synthesis could contribute to the efficacy of SSRIs.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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