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DIG-AP antibody

RRID:AB_2313640

Antibody ID

AB_2313640

Target Antigen

Proper Citation

(Roche Cat# 11 093 274 910, RRID:AB_2313640)

Clonality

unknown

Vendor

Roche

Cat Num

11 093 274 910

Publications that use this research resource

A Central Extended Amygdala Circuit That Modulates Anxiety.

  • Ahrens S
  • J. Neurosci.
  • 2018 Jun 13

Literature context:


Abstract:

Both the amygdala and the bed nucleus of the stria terminalis (BNST) have been implicated in maladaptive anxiety characteristics of anxiety disorders. However, the underlying circuit and cellular mechanisms have remained elusive. Here we show that mice with Erbb4 gene deficiency in somatostatin-expressing (SOM+) neurons exhibit heightened anxiety as measured in the elevated plus maze test and the open field test, two assays commonly used to assess anxiety-related behaviors in rodents. Using a combination of electrophysiological, molecular, genetic, and pharmacological techniques, we demonstrate that the abnormal anxiety in the mutant mice is caused by enhanced excitatory synaptic inputs onto SOM+ neurons in the central amygdala (CeA), and the resulting reduction in inhibition onto downstream SOM+ neurons in the BNST. Notably, our results indicate that an increase in dynorphin signaling in SOM+ CeA neurons mediates the paradoxical reduction in inhibition onto SOM+ BNST neurons, and that the consequent enhanced activity of SOM+ BNST neurons is both necessary for and sufficient to drive the elevated anxiety. Finally, we show that the elevated anxiety and the associated synaptic dysfunctions and increased dynorphin signaling in the CeA-BNST circuit of the Erbb4 mutant mice can be recapitulated by stress in wild-type mice. Together, our results unravel previously unknown circuit and cellular processes in the central extended amygdala that can cause maladaptive anxiety.SIGNIFICANCE STATEMENT The central extended amygdala has been implicated in anxiety-related behaviors, but the underlying mechanisms are unclear. Here we found that somatostatin-expressing neurons in the central amygdala (CeA) controls anxiety through modulation of the stria terminalis, a process that is mediated by an increase in dynorphin signaling in the CeA. Our results reveal circuit and cellular dysfunctions that may account for maladaptive anxiety.

Funding information:
  • NCI NIH HHS - P30 CA045508()
  • NIMH NIH HHS - R01 MH101214()
  • NINDS NIH HHS - R01-NS058956(United States)

Sonic Hedgehog Is a Remotely Produced Cue that Controls Axon Guidance Trans-axonally at a Midline Choice Point.

  • Peng J
  • Neuron
  • 2018 Jan 17

Literature context:


Abstract:

At the optic chiasm choice point, ipsilateral retinal ganglion cells (RGCs) are repelled away from the midline by guidance cues, including Ephrin-B2 and Sonic Hedgehog (Shh). Although guidance cues are normally produced by cells residing at the choice point, the mRNA for Shh is not found at the optic chiasm. Here we show that Shh protein is instead produced by contralateral RGCs at the retina, transported anterogradely along the axon, and accumulates at the optic chiasm to repel ipsilateral RGCs. In vitro, contralateral RGC axons, which secrete Shh, repel ipsilateral RGCs in a Boc- and Smo-dependent manner. Finally, knockdown of Shh in the contralateral retina causes a decrease in the proportion of ipsilateral RGCs in a non-cell-autonomous manner. These findings reveal a role for axon-axon interactions in ipsilateral RGC guidance, and they establish that remotely produced cues can act at axon guidance midline choice points.

Differential projections of the densocellular and intermediate parts of the hyperpallium in the pigeon (Columba livia).

  • Atoji Y
  • J. Comp. Neurol.
  • 2018 Jan 1

Literature context:


Abstract:

The visual Wulst in birds shows a four-layered structure: apical part of the hyperpallium (HA), interstitial part of HA (IHA), intercalated part of hyperpallium (HI), and densocellular part of hyperpallium (HD). HD also connects with the hippocampus and olfactory system. Because HD is subjacent to HI, the two have been treated as one structure in many studies, and the fiber connections of HD have been examined by afferents and efferents originating outside HD. However, to clarify the difference between these two layers, they need to be treated separately. In the present study, the fiber connections of HD and HI were analyzed with tract-tracing techniques using a combination of injections of cholera toxin subunit B (CTB) for retrograde tracing and biotinylated dextran amine (BDA) for anterograde tracing. When the two tracers were bilaterally injected in HD, a major reciprocal connection was seen with the dorsolateral subdivision (DL) of the hippocampal formation. When CTB and BDA were bilaterally injected in HI, strong reciprocal connections were found between HI and HA. Next, projection neurons in HD and HI were examined by double staining for CTB combined with vesicular glutamate transporter 2 (vGluT2) mRNA in situ hybridization. After CTB was injected in DL or HA, many neurons revealed CTB+/vGluT2+ in HD or HI, respectively. Furthermore, in situ hybridization showed that DL and HA contained neurons expressing various subunits of ionotropic glutamate receptors: AMPA, kainate, and NMDA types. These results suggest that glutamatergic neurons in HD and HI project primarily to DL and HA, respectively.

Funding information:
  • NCRR NIH HHS - RR 17072(United States)

Area-specific substratification of deep layer neurons in the rat cortex.

  • Watakabe A
  • J. Comp. Neurol.
  • 2012 Nov 1

Literature context:


Abstract:

Gene markers are useful tools to identify cell types for fine mapping of neuronal circuits. Here we report area-specific sublamina structure of the rat cerebral cortex using cholecystokinin (cck) and purkinje cell protein4 (pcp4) mRNAs as the markers for excitatory neuron subtypes in layers 5 and 6. We found a segregated expression, especially pronounced in layer 6, where corticothalamic and corticocortical projecting neurons reside. To examine the relationship between gene expression and projection target, we injected retrograde tracers into several thalamic subnuclei, ventral posterior (VP), posterior (PO), mediodorsal (MD), medial and lateral geniculate nuclei (MGN and LGN); as well as into two cortical areas (M1 and V1). This combination of tracer-in situ hybridization (ISH) experiments revealed that corticocortical neurons predominantly express cck and corticothalamic neurons predominantly express pcp4 mRNAs in all areas tested. In general, cck(+) and pcp4(+) cells occupied the upper and lower compartment of layer 6a, respectively. However, the sublaminar distribution and the relative abundance of cck(+) and pcp4(+) cells were quite distinctive across areas. For example, layer 6 of the prelimbic cortex was almost devoid of cck(+) neurons, and was occupied instead by corticothalamic pcp4(+) neurons. In the lateral areas, such as S2, there was an additional layer of cck(+) cells positioned below the pcp4(+) compartment. The claustrum, which has a tight relationship with the cortex, mostly consisted of cck(+)/pcp4(-) cells. In summary, the combination of gene markers and retrograde tracers revealed a distinct sublaminar organization, with conspicuous cross-area variation in the arrangement and relative density of corticothalamic connections.

Funding information:
  • NCI NIH HHS - R01CA130202(United States)
  • NIH HHS - R24 OD010435(United States)