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The Journal of Neuroscience, July 18, 2007, 27(29)

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This Week in The Journal
This Week in The Journal

Formula Cellular/Molecular

BMP Signaling and Synaptic Plasticity

Mu Sun, Mark J. Thomas, Rachel Herder, M. Lisa Bofenkamp, Scott B. Selleck, and Michael B. O'Connor

(see pages 7740–7750)

Bone morphogenic protein (BMP) has diverse functions in cell signaling from development to cell death. This week, Sun et al. focused on its possible role in synaptic plasticity by targeting the endogenous BMP antagonist chordin. The BMPRII receptor protein was expressed throughout the hippocampus in wild-type mice, as was chordin. Brain slices from mice lacking Chordin (Chrd–/–) had enhanced paired-pulse facilitation and an increased frequency of miniature EPSCs, consistent with a presynaptic site of action for BMP. Nerve terminals in Chrd–/– mice also had an increase in docked vesicles. Perfusion of BMP2 in wild-type slices mimicked the effects seen in slices from Chrd–/– mice. The effects on plasticity and behavior were complex. Long-term potentiation was enhanced in Chrd–/– slices with high-frequency stimulation, but not with theta burst or pairing protocols; and mutant mice showed improved learning in the water maze, but impairment in the Y maze.

Formula Development/Plasticity/Repair

Reducing Oligodendrocyte Apoptosis after Spinal Cord Injury

Tae Y. Yune, Jee Y. Lee, Gil Y. Jung, Sun J. Kim, Mei H. Jiang, Young C. Kim, Young J. Oh, George J. Markelonis, and Tae H. Oh

(see pages 7751–7761)

Traumatic spinal cord injury (SCI) leads not only to neuronal loss, but also to apoptosis of oligodendrocytes and subsequent demyelination. This week, Yune et al. tried to connect the dots between neuroprotection afforded by the antibiotic minocycline, inhibition of microglia activation, and apoptotic signaling through the p75 neurotrophin receptor (p75NTR). Five days after a contusion injury at T10/11 in adult rats, the spinal cord showed elevated levels of pro-nerve growth factor (proNGF). Phosphorylated p38 protein-activated mitogen kinase (p-p38MAPK), an indicator of microglia activation, also increased after SCI. In vitro, the activated microglia produced proNGF, which binds to the p75NTR receptor and triggers apoptosis in oligodendrocytes. By several measures, minocycline treatment was effective. It reduced p-p38MAPK and proNGF in microglia as well as p75NTR expression in oligodendrocytes; it reduced axonal and myelin loss after injury; and treated rats had better recovery of hindlimb locomotor function.

Formula Behavioral/Systems/Cognitive

News for the Left-Handed

Stefan Klöppel, Anna Vongerichten, Thilo van Eimeren, Richard S. J. Frackowiak, and Hartwig R. Siebner

(see pages 7847–7853)

Most of us (90%) do just about every complex manual task with our right hand. Being left-handed in a right-handed world has its advantages and disadvantages. One seeming disadvantage is that some lefties are forced as children to become right-handed. In this week's Journal, Klöppel et al. investigated the changes that occur as a consequence of retraining, not only for handwriting but also for more general manual tasks. Using fMRI (functional magnetic resonance imaging), the authors compared brain activity between right-handers, left-handers, and converted left-handers. Converted left-handers performing a simple button press displayed increased activity in the SM1 (primary sensorimotor hand area) and the caudal PMd (dorsal premotor cortex) of the nondominant left hemisphere. Thus, the switch in handedness resulted in a reorganization of the executive motor system controlling even simple hand movements. However, higher-order sensorimotor areas were not affected by retraining. So is it better to fight than switch?


Figure 1
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Handwriting samples of subjects asked to write "ll" on an electronic tablet. The "converted" left-hander was able to write with both hands. See the article by Klöppel et al. for details.

 
Formula Neurobiology of Disease

The Benefits of Sleep in a Mouse Model of HD

Patrick N. Pallier, Elizabeth S. Maywood, Zhiguang Zheng, Johanna E. Chesham, Alexei N. Inyushkin, Richard Dyball, Michael H. Hastings, and A. Jennifer Morton

(see pages 7869–7878)

We usually think of Huntington's disease (HD) as involving abnormal movements (chorea) and cognitive impairments. However, these patients also show disrupted circadian rhythms. Thus, Pallier et al. compared HD model R6/2 mice with wild-type mice to see how disrupted circadian rhythms might affect cognitive performance. As expected, activity–rest cycles in R6/2 mice became irregular with age, as did expression of the circadian proteins mPER1 and mPER2 in the suprachiasmatic nucleus (SCN). In slices, however, the electrophysiological and molecular clockwork of the SCN appeared intact in R6/2 mice, suggesting that the intrinsic SCN circuitry was functioning normally. Hypnotic doses of sedative drug normalized the sleep–wake cycle and improved cognitive performance on the two-choice swim test in the R6/2 mice and regulated their expression of SCN circadian genes. Although not a cure for HD, symptomatic treatment for disrupted sleep would appear to have its benefits.


Related articles in J. Neurosci.:

Presynaptic Contributions of Chordin to Hippocampal Plasticity and Spatial Learning
Mu Sun, Mark J. Thomas, Rachel Herder, M. Lisa Bofenkamp, Scott B. Selleck, and Michael B. O'Connor
J. Neurosci. 2007 27: 7740-7750. [Abstract] [Full Text]  

Minocycline Alleviates Death of Oligodendrocytes by Inhibiting Pro-Nerve Growth Factor Production in Microglia after Spinal Cord Injury
Tae Y. Yune, Jee Y. Lee, Gil Y. Jung, Sun J. Kim, Mei H. Jiang, Young C. Kim, Young J. Oh, George J. Markelonis, and Tae H. Oh
J. Neurosci. 2007 27: 7751-7761. [Abstract] [Full Text]  

Can Left-Handedness be Switched? Insights from an Early Switch of Handwriting
Stefan Klöppel, Anna Vongerichten, Thilo van Eimeren, Richard S. J. Frackowiak, and Hartwig R. Siebner
J. Neurosci. 2007 27: 7847-7853. [Abstract] [Full Text]  

Pharmacological Imposition of Sleep Slows Cognitive Decline and Reverses Dysregulation of Circadian Gene Expression in a Transgenic Mouse Model of Huntington's Disease
Patrick N. Pallier, Elizabeth S. Maywood, Zhiguang Zheng, Johanna E. Chesham, Alexei N. Inyushkin, Richard Dyball, Michael H. Hastings, and A. Jennifer Morton
J. Neurosci. 2007 27: 7869-7878. [Abstract] [Full Text]  




This Article
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Google Scholar
Right arrow Search for Related Content

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