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Migration of cultured fetal spinal cord astrocytes into adult host cervical cord and medulla following transplantation into thoracie spinal cord
Author(s) -
Goldberg W. J.,
Bernstein J. J.
Publication year - 1988
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490190106
Subject(s) - spinal cord , transplantation , anatomy , medulla , pathology , cord , biology , lesion , fetal tissue transplantation , medicine , fetus , neuroscience , surgery , pregnancy , genetics
Cell suspensions from 14‐days‐gestation rat spinal cord, which had previously been soaked for 1 hr in a 2 μg/ml solution of Phaseolus vulgaris leucoagglutinin (PHAL), were cultured on collagen gels containing laminin for 2 weeks. Pieces of the gel and attached cells were then transplanted into the dorsal column of adult host thoracic spinal cord. At 1, 2, and 3 months postimplantation (MPI), animals were sacrificed, and the spinal cords were removed, embaedded in paraffin, and sectioned at 8 μm for immunohistochemistry at the light microscopic level. Sections were double labeled for PHAL and utilized as a marker for transplant‐derived cells and glial fibrillar acidic protein (GFAP), a specific marker for astrocytes. Trnasplant‐derived astorcytes (PHAL‐GFAP positive cells) migrated from the transplantation site in both rostral and caudal directions and were observed within the host dorsal column ipsilateral to the transplantation site. At 2 months, latera migration into the contralateral dorsal coumn and ipsilateral dorsal horn was observed. At 3 MPI transplant‐derived astrocytes were observed in host medulla (nucleus gracilis). Transplant‐derived astrocytes were also observed on the glial limitans as far as nucleus gracilis. A migration rate of 0.72 mm/day was calculated, assuming a 14‐day delay in the initiation of migration. The ramifications of such extensive migration are discussed with regard to return of function and amelioration of lesion‐induced deficits.