Peptides
Amyloid accumulation is associated with Alzheimer's disease, but little is known about the normal function of amyloids. The authors showed that peptide and protein hormones stored in pituitary secretory granules form amyloid-like aggregates in vitro. The amyloid fibrils could release monomers, indicating that they are not stable. Moreover, mouse pituitary tissue showed colocalization of an amyloid-specific dye with pituitary hormones. These findings indicate a biological function for amyloid aggregates in hormone storage.
Synaptic plasticity
CaMKII controls the direction of plasticity at parallel fiber–Purkinje cell synapses van Woerden, G. M. et al. Nature Neurosci. 12, 823–825 (2009)
Calcium/calmodulin-dependent protein kinase II (CAMKII) isoform α is important for the induction of long-term depression at cerebellar parallel fibre–Purkinje cell synapses, but the role of βCAMKII at these synapses is unknown. Here, whole-cell recordings revealed that paired parallel and climbing fibre stimulation induced long-term depression in Purkinje cells from wild-type mice but long-term potentiation in Purkinje cells from Camk2b−/− mice. Parallel fibre stimulation alone had the opposite result. This indicates that βCAMKII regulates bidirectional synaptic plasticity at parallel fibre–Purkinje cell synapses.
Repair
Reassessment of corticospinal tract regeneration in Nogo-deficient mice Lee, J. K. et al. J. Neurosci. 29, 8649–8654 (2009)
The axon growth inhibitor Nogo (also known as reticulon 4) has been studied as a potential target for stimulating axon regeneration after injury. However, different Nogo-deficient mouse lines have yielded mixed findings, with both no and extensive regeneration found — the latter was later shown to be due to a labelling artefact. The authors re-examined the line showing extensive regeneration and investigated a different line, which was deficient of all Nogo isoforms. They found no evidence of enhanced axon regeneration after spinal cord injury in either line compared with a wild-type line, suggesting that Nogo might not be a viable therapeutic target.
Psychiatric disorders
Interaction between the serotonin transporter gene ( 5-HTTLPR ), stressful life events, and risk of depression Risch, N. et al. JAMA 301, 2462–2471 (2009)
The increased risk of depression that results from an interaction between stressful life events and a polymorphism in the serotonin transporter gene (5-HTTLPR; also known as SLC6A4) is often used as a prime example of gene–environment interactions. However, some studies could not replicate this effect. This meta-analysis showed that the 5-HTTLPR polymorphism was not associated with depression, nor was there an interaction between stressful life events and 5-HTTLPR genotype. This result highlights the importance of sample size and study design in gene–environment association studies.
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In Brief. Nat Rev Neurosci 10, 545 (2009). https://doi.org/10.1038/nrn2694
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DOI: https://doi.org/10.1038/nrn2694