Expression of Calbindin Immunoreactivity by Subpopulations of Primary Sensory Neurons in Chick Embryo Dorsal Root Ganglion Cells Grown in Coculture or Conditioned Medium

Abstract

Primary sensory neurons which innervate neuromuscular spindles in the chicken are calbindin-immunoreactive. The influence exerted by developing skeletal muscle on the expression of calbindin immunoreactivity by subpopulations of dorsal root ganglion (DRG) cells in the chick embryo was tested in vitro in coculture with myoblasts, in conditioned medium (CM) prepared from myoblasts and in control cultures of DRG cells alone. Control cultures of DRG cells grown at the 6^th embryonic day (E6) did not show any calbindin-immunostained ganglion cell. In coculture of myoblasts previously grown for 14 days, about 3% of calbindin-immunoreactive ganglion cells were detected while about 1% were observed in some cultures grown in CM. Fibroblasts from various sources were devoid of effect. Skin or kidney cells were more active than myoblasts to initiate calbindin expression by subpopulations of DRG cells in coculture or, to a lesser degree, in CM. The results suggest that cellular factors would rather induce calbindin expression in certain sensory neurons than ensure a selective neuronal survival.

Role of neuron‐target interactions in the development of a subpopulation of avian sensory neurons

“…They reported that immature (E6) chick sensory neurons do not express de novo calbindin-like immunoreactivity (a subpopulation-specific marker) in vitro unless they are cocultured with peripheral tissues. Although some subpopulation types (Bossart et al, 1988) may differentiate only in response to contact with peripheral tissues, while others can arise autonomously (present results; Ernsberger and Rohrer, 1988), this apparent contradiction may be the result of differences in culture media and substrata used in the three studies.…”

“…However, the neurons in that study may not all have been naive, since they were removed from the embryo only after their in vivo birthdays, and some may have been postmitotic for up to 1 day in vivo. In contrast, results inconsistent with the above conclusion were recently described by Bossart et al (1988). They reported that immature (E6) chick sensory neurons do not express de novo calbindin-like immunoreactivity (a subpopulation-specific marker) in vitro unless they are cocultured with peripheral tissues.…”

“…experimental alterations in neuron-target interactions appear to result in respecification or phenotypic modulation of adult rat sensory neurons (McMahon and Gibson, 1987). It has also been reported that the proportions of sensory neurons exhibiting different histochemically defined phenotypes can be altered under various in vitro conditions (Barakat and Droz, 1985;Barakat et al, 1986;Bossart et al, 1988). It is possible, therefore, that sensory neuron development is regulated in a manner analogous to that of autonomic neuron development, where the phenotype is labile for some time and can be modulated by peripheral cues.…”

Triiodothyronine Exerts a Trophic Action on Rat Sensory Neuron Survival and Neurite Outgrowth through Different Pathways

“…BDNF knockout mice are born with a 30% decrement in the normal complement of lumbar DRG neurons (Ernfors et al, 1994), and mice lacking the NT-3 receptor (TrkC) have virtually no large-fibre sensory afferents of the Ia class (Klein et al, 1994). Furthermore, the expression of particular phenotypic subpopulations of DRG sensory neurons is regulated by unidentified factors derived from central and peripheral targets (Bossart et al, 1988;Philippe et al, 1988;Barakat and Droz, 1989a. b; Barakat-Walter et al, 1991;Duc et al, 1991).…”