News tips from the Journal of Neuroscience

September 07, 2004

1. A zebrafish L1 homolog in regeneration:
L1.1 is involved in spinal cord regeneration in adult zebrafish Becker et al.

Expression of the cell adhesion molecule L1 is generally correlated with regenerative success, but it only appears in mammalian axotomized central neurons when axons are within a permissive peripheral nerve graft. The fish homolog L1.1 is upregulated after spinal transection, and is thought to aid in their robust axon regeneration and functional recovery. Without L1.1, brainstem neurons did not regenerate spinal axons or form functional synapses, and normal constant swimming behavior was nearly abolished.

2. Getting the attention of motion-sensitive neurons:
Attentional modulation of motion integration of individual neurons in the middle temporal visual area (MT) Cook et al.

Two highly-trained monkeys performed a motion detection task under two different attentional states. For cells that had robust responses to the motion stimulus, attention modulated the response function without a shift in the time or shape of the response. Thus their results suggest that attention increases the sensitivity of neurons without affecting the temporal characteristics of the response.

3. JNK signaling after ischemia:
The JNK signaling pathway mediates Bax activation and subsequent neuronal apoptosis through interaction with bim after transient focal cerebral ischemia Okuno et al.

Following ischemia, the c-Jun N-terminal protein kinase (JNK) pathway may be an early step leading to neuronal apoptosis via mitochondrial apoptosis-related proteins. Proapoptotic proteins of the BcL-2 family, like Bax, can be activated by BH3-only proteins, like Bim, resulting in Bax integration into the outer mitochondrial membrane, formation of channels, release of cytochrome c, and apoptotic cell death. A selective inhibitor of JNK reduced apoptosis in the ischemic core, blocked interactions between JNK, BimL and Bax, and the translocation of Bax from the cytoplasm to mitochondria.
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Society for Neuroscience

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