Characterization of sensory deficits in TrkB knockout mice

P. Perez-Pinera, O. García-Suarez, A. Germanà, B. Díaz-Esnal, F. de Carlos, I. Silos-Santiago, M. E. del Valle, J. Cobo, J. A. Vega

Research output: Contribution to journalArticlepeer-review


The sensory deficit in TrkB deficient mice was evaluated by counting the neuronal loss in lumbar dorsal root ganglia (DRG), the absence of sensory receptors (cutaneous-associated to the hairy and glabrous skin - muscular and articular), and the percentage and size of the neurocalcin-positive DRG neurons (a calcium-binding protein which labels proprioceptive and mechanoceptive neurons). Mice lacking TrkB lost 32% of neurons, corresponding to the intermediate-sized and neurocalcin-positive ones. This neuronal lost was accomplished by the absence of Meissner corpuscles, and reduction of hair follicle-associated sensory nerve endings and Merkel cells. The mutation was without effect on Pacinian corpuscles, Golgi's organs and muscle spindles. Present results further characterize the sensory deficit of the TrkB-/- mice demonstrating that the intermediate-sized neurons in lumbar DRG, as well as the cutaneous rapidly and slowly adapting sensory receptors connected to them, are under the control of TrkB for survival and differentiation. This study might serve as a baseline for future studies in experimentally induced neuropathies affecting TrkB positive DRG neurons and their peripheral targets, and to use TrkB ligands in the treatment of neuropathies in which cutaneous mechanoreceptors are primarily involved.

Original languageEnglish (US)
Pages (from-to)43-47
Number of pages5
JournalNeuroscience Letters
Issue number1
StatePublished - Mar 5 2008
Externally publishedYes


  • Dorsal root ganglion
  • Sensory corpuscles
  • TrkB deficient mice

ASJC Scopus subject areas

  • Neuroscience(all)


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