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The Journal of Neuroscience, May 3, 2006, 26(18)
This Week in The Journal
This Week in The Journal
Cellular/Molecular
Synaptic Sites of Endocannabinoid Synthesis
Takayuki Yoshida, Masahiro Fukaya, Motokazu Uchigashima, Eriko Miura, Haruyuki Kamiya, Masanobu Kano, and Masahiko Watanabe
(see pages 4740–4751)
The retrograde messenger endocannabinoid 2-arachidonoyl-glycerol (2-AG) is produced in postsynaptic cells only to act on CB1 receptors on presynaptic nerve terminals. In this week's Journal, Yoshida et al. examine—very closely—the subcellular localization of the 2-AG production machinery, diacylglycerol lipase-
(DAGL
Development/Plasticity/Repair
Neutralizing NG2 after Spinal Injury
Andrew M. Tan, Mario Colletti, Ann T. Rorai, J. H. Pate Skene, and Joel M. Levine
(see pages 4729–4739)
Axons trying to regenerate after spinal cord injury face a major obstacle in the form of the glial scar. It's not only figuring out what makes axons grow, but also avoiding things that may inhibit growth, such as myelin-associated growth inhibitors, semaphorins, and chondroitin sulfate proteoglycans (CSPGs). This week, Tan et al. tried to take the proteoglycan NG2 out of action. The authors transected rat spinal cords and then treated the animals with neutralizing or non-neutralizing anti-NG2 monoclonal antibodies (mAbs). Antibodies were infused into the spinal cord over several days from gelfoam pledglets. In rats treated with non-neutralizing mAbs, afferent mechanosensory neuron axons usually stopped within the lesion penumbra and failed to enter the core. Neutralizing mAbs, however, allowed the axons to grow through the core of the glial scar. When the sensory nerve was preconditioned with a lesion to stimulate growth, axons grew well past the glial scar and into the white matter.
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Axons labeled with cholera toxin B subunit (CTB; red) terminated caudal to the edge of a spinal cord lesion after treatment with non-neutralizing NG2 antibodies (top panel). However, treatment with neutralizing NG2 antibodies allowed axons to grow past the lesion core (bottom panel). See the article by Tan et al. for details.
Behavioral/Systems/Cognitive
Top-Down Auditory Map Plasticity
Daniel B. Polley, Elizabeth E. Steinberg, and Michael M. Merzenich
(see pages 4970–4982)
During early critical periods, topographical maps are formed in sensory cortex based on dedicated afferent sensory input, a bottom-up organization. By training rats to respond either to frequency or to intensity of the same auditory stimuli, Polley et al. tested whether auditory receptive field plasticity in the adult was also affected by top-down task-dependent factors such as attention. In the authors' protocol, the bottom-up signals remained constant but the top-down focus differed. The proportion of primary auditory cortex (AI) and suprarhinal auditory field (SRAF) dedicated to auditory frequencies in the target range expanded in rats trained in frequency recognition (FR), but not in rats trained in loudness recognition (LR). Conversely, in FR-trained—but not LR-trained—rats, auditory stimuli in the trained decibel range evoked more responses. Perhaps surprising, AI responded as robustly to top-down effects as the SRAF, a "higher" processing center.
Neurobiology of Disease
Refining A
Immunotherapy
Marcel Maier, Timothy J. Seabrook, Noel D. Lazo, Liying Jiang, Pritam Das, Christopher Janus, and Cynthia A. Lemere
(see pages 4717–4728)
In a second antibody-based study this week, Maier et al. attempt to refine immunotherapy for Alzheimer's disease (AD). Antibodies raised against A
DOI:
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