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News tips from the Journal of Neuroscience

1. Neurosteroids and Tonic GABAergic Inhibition
Jamie Maguire and Istvan Mody

Fluctuations in progesterone levels during the ovarian cycle can alter the subunit composition of GABAA receptors. In this weeks Journal, Maguire and Mody link this effect to neurosteroid production. The authors focused on the d subunit that underlies GABA-mediated tonic inhibition of dentate granule cells in the hippocampus. The progesterone receptor antagonist RU486 had no effect on GABAA subunit expression in cycling mice. However, finasteride, which inhibits synthesis of neurosteroids from progesterone, prevented upregulation of the d subunit and blocked the enhancement of GABAA receptor-mediated tonic inhibition that normally occurs during diestrous. Similar effects were seen in males or ovariectomized females that were treated with progesterone, as well as in mice subjected to an acute stress (2 min of increased CO2 ). Acute stress increases neurosteroids, and treatment of brain slices with the neurosteroid THDOC (3a,5a-tetrahydrodeoxycorticosterone) also increased tonic GABAergic inhibition.


2. Engineering Astrocytes as Injury Repairmen
William B. J. Cafferty, Shih-Hung Yang, Philip J. Duffy, Shuxin Li, and Stephen M. Strittmatter

Unfortunately, the CNS throws up a number of roadblocks to axonal regeneration. One of these, chondroitin sulfate proteoglycans (CSPGs), is a major component of the glial scar that forms at the site of a CNS injury. This week, Cafferty et al. exploit the bacterial enzyme chondroitinase ABC (ChABC), which can digest CSPGs, to reopen the roadway. The authors made a transgenic mouse that expressed ChABC in astrocytes under the control of the gfap promoter. After dorsal hemisection of the spinal cord, corticospinal tract axons in wild-type mice stopped abruptly rostral to the lesion. In the transgenic mice, however, axons extended into th
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Contact: Sara Harris
sharris@sfn.org
202-962-4000
Society for Neuroscience
27-Feb-2007


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