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Goat anti-Chicken IgY H&L (DyLight® 488) secondary antibody

RRID:AB_10681017

Antibody ID

AB_10681017

Target Antigen

Goat anti-Chicken IgY H&L (DyLight® 488) secondary antibody chicken/bird, chicken

Proper Citation

(Abcam Cat# ab96947, RRID:AB_10681017)

Clonality

polyclonal antibody

Comments

validation status unknown, seller recommendations provided in 2012: Immunofluorescence; Immunocytochemistry; Immunohistochemistry - fixed; Immunohistochemistry; Flow Cytometry; Flow Cyt, ICC/IF, IHC-P

Host Organism

goat

Vendor

Abcam

Cat Num

ab96947

Publications that use this research resource

A Circuit for Integration of Head- and Visual-Motion Signals in Layer 6 of Mouse Primary Visual Cortex.

  • Vélez-Fort M
  • Neuron
  • 2018 Apr 4

Literature context:


Abstract:

To interpret visual-motion events, the underlying computation must involve internal reference to the motion status of the observer's head. We show here that layer 6 (L6) principal neurons in mouse primary visual cortex (V1) receive a diffuse, vestibular-mediated synaptic input that signals the angular velocity of horizontal rotation. Behavioral and theoretical experiments indicate that these inputs, distributed over a network of 100 L6 neurons, provide both a reliable estimate and, therefore, physiological separation of head-velocity signals. During head rotation in the presence of visual stimuli, L6 neurons exhibit postsynaptic responses that approximate the arithmetic sum of the vestibular and visual-motion response. Functional input mapping reveals that these internal motion signals arrive into L6 via a direct projection from the retrosplenial cortex. We therefore propose that visual-motion processing in V1 L6 is multisensory and contextually dependent on the motion status of the animal's head.

Funding information:
  • NIGMS NIH HHS - R01 GM065388-01(United States)

Axon Death Pathways Converge on Axundead to Promote Functional and Structural Axon Disassembly.

  • Neukomm LJ
  • Neuron
  • 2017 Jul 5

Literature context:


Abstract:

Axon degeneration is a hallmark of neurodegenerative disease and neural injury. Axotomy activates an intrinsic pro-degenerative axon death signaling cascade involving loss of the NAD+ biosynthetic enzyme Nmnat/Nmnat2 in axons, activation of dSarm/Sarm1, and subsequent Sarm-dependent depletion of NAD+. Here we identify Axundead (Axed) as a mediator of axon death. axed mutants suppress axon death in several types of axons for the lifespan of the fly and block the pro-degenerative effects of activated dSarm in vivo. Neurodegeneration induced by loss of the sole fly Nmnat ortholog is also fully blocked by axed, but not dsarm, mutants. Thus, pro-degenerative pathways activated by dSarm signaling or Nmnat elimination ultimately converge on Axed. Remarkably, severed axons morphologically preserved by axon death pathway mutations remain integrated in circuits and able to elicit complex behaviors after stimulation, indicating that blockade of axon death signaling results in long-term functional preservation of axons.