title: Characterization of sensory deficits in TrkB knockout mice.
abstract: 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.
authors.affiliation: Departamentos de Morfología y Biología Celular, Universidad de Oviedo, Spain.
authors.forename: P
authors.initials: P
authors.lastname: Perez-Pinera
authors.forename: O
authors.initials: O
authors.lastname: García-Suarez
authors.forename: A
authors.initials: A
authors.lastname: Germanà
authors.forename: B
authors.initials: B
authors.lastname: Díaz-Esnal
authors.forename: F
authors.initials: F
authors.lastname: de Carlos
authors.forename: I
authors.initials: I
authors.lastname: Silos-Santiago
authors.forename: M E
authors.initials: ME
authors.lastname: del Valle
authors.forename: J
authors.initials: J
authors.lastname: Cobo
authors.forename: J A
authors.initials: JA
authors.lastname: Vega
mesh_terms: D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D048429:Cell Size; D002470:Cell Survival / Q000235:genetics; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000166:cytology / Q000378:metabolism* / Q000503:physiopathology; D007150:Immunohistochemistry; D008465:Mechanoreceptors / Q000378:metabolism* / Q000503:physiopathology; D018862:Merkel Cells / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009414:Nerve Growth Factors / Q000378:metabolism; D051596:Neurocalcin / Q000378:metabolism; D009475:Neurons, Afferent / Q000166:cytology / Q000378:metabolism*; D010523:Peripheral Nervous System Diseases / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D011434:Proprioception / Q000235:genetics; D020813:Receptor, trkB / Q000172:deficiency* / Q000235:genetics; D011984:Sensory Receptor Cells / Q000378:metabolism / Q000503:physiopathology; D020886:Somatosensory Disorders / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D014110:Touch / Q000235:genetics
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D009414:Nerve Growth Factors; D051596:Neurocalcin; D020813:Receptor, trkB; C073922:neurotrophin 4