Forgot Password

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

Goat Anti-Mouse Trkb Polyclonal antibody, Unconjugated


Antibody ID


Target Antigen

Mouse TrkB mouse

Proper Citation

(R and D Systems Cat# AF1494, RRID:AB_2155264)


polyclonal antibody


vendor recommendations: Blocking/Neutralize; Immunocytochemistry; Immunohistochemistry; Western Blot; Blockade of Receptor-ligand Interaction, Immunohistochemistry, Western Blot

Host Organism



R and D Systems

Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability.

  • Dawes JM
  • Neuron
  • 2018 Feb 21

Literature context:


Human autoantibodies to contactin-associated protein-like 2 (CASPR2) are often associated with neuropathic pain, and CASPR2 mutations have been linked to autism spectrum disorders, in which sensory dysfunction is increasingly recognized. Human CASPR2 autoantibodies, when injected into mice, were peripherally restricted and resulted in mechanical pain-related hypersensitivity in the absence of neural injury. We therefore investigated the mechanism by which CASPR2 modulates nociceptive function. Mice lacking CASPR2 (Cntnap2-/-) demonstrated enhanced pain-related hypersensitivity to noxious mechanical stimuli, heat, and algogens. Both primary afferent excitability and subsequent nociceptive transmission within the dorsal horn were increased in Cntnap2-/- mice. Either immune or genetic-mediated ablation of CASPR2 enhanced the excitability of DRG neurons in a cell-autonomous fashion through regulation of Kv1 channel expression at the soma membrane. This is the first example of passive transfer of an autoimmune peripheral neuropathic pain disorder and demonstrates that CASPR2 has a key role in regulating cell-intrinsic dorsal root ganglion (DRG) neuron excitability.

Funding information:
  • NINDS NIH HHS - NS18400(United States)

Membrane-bound glucocorticoid receptors on distinct nociceptive neurons as potential targets for pain control through rapid non-genomic effects.

  • Shaqura M
  • Neuropharmacology
  • 2017 Jul 11

Literature context:


Glucocorticoids were long believed to primarily function through cytosolic glucocorticoid receptor (GR) activation and subsequent classical genomic pathways. Recently, however, evidence has emerged that suggests the presence of rapid non-genomic GR-dependent signaling pathways within the brain, though their existence in spinal and peripheral nociceptive neurons remains elusive. In this paper, we aim to systemically identify GR within the spinal cord and periphery, to verify their putative membrane location and to characterize possible G protein coupling and pain modulating properties. Double immunofluorescence confocal microscopy revealed that GR predominantly localized in peripheral peptidergic and non-peptidergic nociceptive C- and Aδ-neurons and existed only marginally in myelinated mechanoreceptive and proprioreceptive neurons. Within the spinal cord, GR predominantly localized in incoming presynaptic nociceptive neurons, in pre- and postsynaptic structures of the dorsal horn, as well as in microglia. GR saturation binding revealed that these receptors are linked to the cell membrane of sensory neurons and, upon activation, they trigger membrane targeted [35S]GTPγS binding, indicating G protein coupling to a putative receptor. Importantly, subcutaneous dexamethasone immediately and dose-dependently attenuated acute nociceptive behavior elicited in an animal model of formalin-induced pain hypersensitivity compared to naive rats. Overall, this study provides firm evidence for a novel neuronal mechanism of GR agonists that is rapid, non-genomic, dependent on membrane binding and G protein coupling, and acutely modulates nociceptive behavior, thus unraveling a yet unconsidered mechanism of pain relief.

Funding information:
  • NINDS NIH HHS - T32 NS061764(United States)
  • NINDS NIH HHS - U01 NS090595(United States)

Pericytes of Multiple Organs Do Not Behave as Mesenchymal Stem Cells In Vivo.

  • Guimarães-Camboa N
  • Cell Stem Cell
  • 2017 Mar 2

Literature context:


Pericytes are widely believed to function as mesenchymal stem cells (MSCs), multipotent tissue-resident progenitors with great potential for regenerative medicine. Cultured pericytes isolated from distinct tissues can differentiate into multiple cell types in vitro or following transplantation in vivo. However, the cell fate plasticity of endogenous pericytes in vivo remains unclear. Here, we show that the transcription factor Tbx18 selectively marks pericytes and vascular smooth muscle cells in multiple organs of adult mouse. Fluorescence-activated cell sorting (FACS)-purified Tbx18-expressing cells behaved as MSCs in vitro. However, lineage-tracing experiments using an inducible Tbx18-CreERT2 line revealed that pericytes and vascular smooth muscle cells maintained their identity in aging and diverse pathological settings and did not significantly contribute to other cell lineages. These results challenge the current view of endogenous pericytes as multipotent tissue-resident progenitors and suggest that the plasticity observed in vitro or following transplantation in vivo arises from artificial cell manipulations ex vivo.

Funding information:
  • NCI NIH HHS - R01 CA095287()
  • NHLBI NIH HHS - DP1 HL117649()
  • NHLBI NIH HHS - R01 HL070867()
  • NHLBI NIH HHS - R01 HL119967()
  • NHLBI NIH HHS - R01 HL123747()
  • NHLBI NIH HHS - R01 HL130452()
  • NIH HHS - DP1 OD006428()
  • NINDS NIH HHS - P30 NS047101()

Genetic Tracing of Cav3.2 T-Type Calcium Channel Expression in the Peripheral Nervous System.

  • Bernal Sierra YA
  • Front Mol Neurosci
  • 2017 Mar 31

Literature context:


Characterizing the distinct functions of the T-type ion channel subunits Cav3.1, 3.2 or 3.3 has proven difficult due to their highly conserved amino-acid sequences and the lack of pharmacological blockers specific for each subunit. To precisely determine the expression pattern of the Cav3.2 channel in the nervous system we generated two knock-in mouse strains that express EGFP or Cre recombinase under the control of the Cav3.2 gene promoter. We show that in the brains of these animals, the Cav3.2 channel is predominantly expressed in the dentate gyrus of the hippocampus. In the peripheral nervous system, the activation of the promoter starts at E9.5 in neural crest cells that will give rise to dorsal root ganglia (DRG) neurons, but not sympathetic neurons. As development progresses the number of DRG cells expressing the Cav3.2 channel reaches around 7% of the DRG at E16.5, and remains constant until E18.5. Characterization of sensory neuron subpopulations at E18.5 showed that EGFP+ cells are a heterogeneous population consisting mainly of TrkB+ and TrkC+ cells, while only a small percentage of DRG cells were TrkA+. Genetic tracing of the sensory nerve end-organ innervation of the skin showed that the activity of the Cav3.2 channel promoter in sensory progenitors marks many mechanoreceptor and nociceptor endings, but spares slowly adapting mechanoreceptors with endings associated with Merkel cells. Our genetic analysis reveals for the first time that progenitors that express the Cav3.2 T-type calcium channel, defines a sensory specific lineage that populates a large proportion of the DRG. Using our Cav3.2-Cre mice together with AAV viruses containing a conditional fluorescent reporter (tdTomato) we could also show that Cre expression is largely restricted to two functionally distinct sensory neuron types in the adult ganglia. Cav3.2 positive neurons innervating the skin were found to only form lanceolate endings on hair follicles and are probably identical to D-hair receptors. A second population of nociceptive sensory neurons expressing the Cav3.2 gene was found to be positive for the calcitonin-gene related peptide but these neurons are deep tissue nociceptors that do not innervate the skin.

Funding information:
  • European Research Council - 294678()

Dynamic expression of transcription factor Brn3b during mouse cranial nerve development.

  • Sajgo S
  • J. Comp. Neurol.
  • 2016 Apr 1

Literature context:


During development, transcription factor combinatorial codes define a large variety of morphologically and physiologically distinct neurons. Such a combinatorial code has been proposed for the differentiation of projection neurons of the somatic and visceral components of cranial nerves. It is possible that individual neuronal cell types are not specified by unique transcription factors but rather emerge through the intersection of their expression domains. Brn3a, Brn3b, and Brn3c, in combination with each other and/or transcription factors of other families, can define subgroups of retinal ganglion cells (RGC), spiral and vestibular ganglia, inner ear and vestibular hair cell neurons in the vestibuloacoustic system, and groups of somatosensory neurons in the dorsal root ganglia. The present study investigates the expression and potential role of the Brn3b transcription factor in cranial nerves and associated nuclei of the brainstem. We report the dynamic expression of Brn3b in the somatosensory component of cranial nerves II, V, VII, and VIII and visceromotor nuclei of nerves VII, IX, and X as well as other brainstem nuclei during different stages of development into adult stage. We find that genetically identified Brn3b(KO) RGC axons show correct but delayed pathfinding during the early stages of embryonic development. However, loss of Brn3b does not affect the anatomy of the other cranial nerves normally expressing this transcription factor.

Expression analysis of the regenerating gene (Reg) family members Reg-IIIβ and Reg-IIIγ in the mouse during development.

  • Matsumoto S
  • J. Comp. Neurol.
  • 2012 Feb 15

Literature context:


The regenerating gene/regenerating islet-derived (Reg) family is a group of small secretory proteins. Within this family, Reg type-III (Reg-III) consists of: Reg-IIIα, -β, -γ, and -δ. To elucidate the physiological relevance of Reg-III, we examined the localization and ontogeny of Reg-IIIβ and Reg-IIIγ in mice at different time points spanning from embryonic day 13.5 to 7 weeks old, using in situ hybridization and immunohistochemistry. Our results showed that Reg-IIIβ was expressed in specific subsets of primary sensory neurons and motor neurons, and that expression was transient during the embryonic and perinatal periods. Reg-IIIβ expression was also observed in absorptive epithelial cells of the intestine. In contrast, Reg-IIIγ expression was mainly observed in epithelial cells of the airways and intestine, but not in the nervous system, and expression levels showed a gradually increasing pattern along with development. In the airways Reg-IIIγ was expressed in goblet and Clara-like cells, whereas in the intestine Reg-IIIγ was expressed in the absorptive epithelial cells and Paneth cells, and was found to be expressed in development before these organs had been exposed to the outside world. The present findings imply that Reg-IIIβ and Reg-IIIγ expression is regulated along divergent pathways. Furthermore, we also suggest that expression of Reg-IIIγ in the airway and intestinal epithelia may occur to protect these organs from exposure to antigens or other factors (e.g., microbes) in the outer world, whereas the transient expression of Reg-IIIβ in the nervous system may be associated with the development of the peripheral nervous system including such processes as myelination.

Funding information:
  • Medical Research Council - (United Kingdom)
  • Medical Research Council - MC_U117570528(United Kingdom)

Expression of kin of irregular chiasm-like 3/mKirre in proprioceptive neurons of the dorsal root ganglia and its interaction with nephrin in muscle spindles.

  • Komori T
  • J. Comp. Neurol.
  • 2008 Nov 1

Literature context:


Kin of irregular chiasm-like 3 (Kirrel3), a mammalian homolog of the kirre gene of Drosophila melanogaster, belongs to the immunoglobulin superfamily. Previously, we have reported that Kirrel3 is expressed in the developing and adult central nervous system. In the present study we investigated the expression of Kirrel3 in the mouse dorsal root ganglia (DRG) and their projection targets. In the adult DRGs, Kirrel3 mRNA was detected in 21.5 +/- 2.3% of total DRG neurons and the expression was mainly prevalent in the medium- and large-sized neurons. In addition, Kirrel3 mRNA predominantly colocalized with tyrosine kinase receptor (Trk) C-immunoreactivity. In the developing DRGs, Kirrel3 mRNA was first detected in a few cells at embryonic day (E) 11.5, gradually increased, and reached the adult level at E17.5. During the development, Kirrel3 was expressed in most TrkC-positive DRG neurons. The expression of Kirrel3 was observed in TrkC-positive nerve fibers around neurotrophin 3 (NT3)-positive intrafusal muscle fibers of muscle spindles at E17.5. However, Kirrel3 was not expressed in TrkC-positive nerve fibers projecting to the spinal cord throughout development. Furthermore, nephrin was expressed in the NT3-positive intrafusal muscle fibers and was in close apposition with Kirrel3-immunoreactivity. Coimmunoprecipitation assay revealed that nephrin interacted with Kirrel3 in the developing muscles. These results suggest that Kirrel3 might play a role in the axonal pathfinding, cell recognition, and synapse formation of DRG neurons on appropriate target cells, including the targeting of proprioceptive neurons on muscle spindles through the interaction with nephrin.