X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

c-Fos (9F6) Rabbit mAb antibody

RRID:AB_10692514

Antibody ID

AB_2247211

Target Antigen

c-Fos (9F6) Rabbit mAb bovine, human, rat, porcine, hamster, mouse, h, m, r, (hm, b, pg)

Proper Citation

(Cell Signaling Technology Cat# 2250, RRID:AB_2247211)

Clonality

monoclonal antibody

Comments

Applications: W, IF-IC, F, ChIP. Consolidation on 9/2016: AB_10692514, AB_10828199.

Host Organism

rabbit

Vendor

Cell Signaling Technology

Cat Num

2250 also 2250S, 2250P

Publications that use this research resource

Amygdala EphB2 Signaling Regulates Glutamatergic Neuron Maturation and Innate Fear.

  • Zhu XN
  • J. Neurosci.
  • 2016 Sep 28

Literature context:


Abstract:

The amygdala serves as emotional center to mediate innate fear behaviors that are reflected through neuronal responses to environmental aversive cues. However, the molecular mechanism underlying the initial neuron responses is poorly understood. In this study, we monitored the innate defensive responses to aversive stimuli of either elevated plus maze or predator odor in juvenile mice and found that glutamatergic neurons were activated in amygdala. Loss of EphB2, a receptor tyrosine kinase expressed in amygdala neurons, suppressed the reactions and led to defects in spine morphogenesis and fear behaviors. We further found a coupling of spinogenesis with these threat cues induced neuron activation in developing amygdala that was controlled by EphB2. A constitutively active form of EphB2 was sufficient to rescue the behavioral and morphological defects caused by ablation of ephrin-B3, a brain-enriched ligand to EphB2. These data suggest that kinase-dependent EphB2 intracellular signaling plays a major role for innate fear responses during the critical developing period, in which spinogenesis in amygdala glutamatergic neurons was involved. SIGNIFICANCE STATEMENT: Generation of innate fear responses to threat as an evolutionally conserved brain feature relies on development of functional neural circuit in amygdala, but the molecular mechanism remains largely unknown. We here identify that EphB2 receptor tyrosine kinase, which is specifically expressed in glutamatergic neurons, is required for the innate fear responses in the neonatal brain. We further reveal that EphB2 mediates coordination of spinogenesis and neuron activation in amygdala during the critical period for the innate fear. EphB2 catalytic activity plays a major role for the behavior upon EphB-ephrin-B3 binding and transnucleus neuronal connections. Our work thus indicates an essential synaptic molecular signaling within amygdala that controls synapse development and helps bring about innate fear emotions in the postnatal developing brain.