The effects of subcutaneous injections of glucocorticoids on amoeboid microglia in postnatal rats

C. Kaur, C. H. Wu, C. Y. Wen, E. A. Ling

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Subcutaneous injections of glucocorticoids into postnatal rats resulted in a drastic reduction in the number of amoeboid microglial cells in the corpus callosum as shown by their labelling with the monoclonal antibodies of the OX-series, ED1, lectin and rhodamine isothiocynate (RhIc). In rats receiving 2 or 3 injections of glucocorticoids and killed at the age of 4 or 7 days, between 40 to 60% of the callosal amoeboid microglial cells were depleted when compared with the corresponding control animals. The cells that survived the glucocorticoid treatments became ramified, while those in the controls of the same age group remained round or amoeboidic. In rats killed at 2 or 3 weeks of age, the microglia became extremely ramified with a concomitant diminution in their immunostaining, particularly in the glucocorticoid-injected rats. In rats receiving glucocorticoid injections along with RhIc, the RhIc-laden amoeboid microglia appeared round and amoeboidic and were intensely stained with OX-42, suggesting their activation and upregulation of complement type 3 receptors when compared with rats receiving only glucocorticoids. Compared with the control, cellular proliferation continued in rats given glucocorticoid injection as indicated by the occurrence of many bromodeoxyuridine-labelled cells in the corpus callosum at the age of 6 days. Ultrastructural studies confirmed the presence of mitotic cells identified as amoeboid microglia because of their labelling with isolectin. A striking ultrastructural feature in glucocorticoids-injected rats was the wide occurrence of amoeboid microglial cells that had ingested a variable number of lectin-labelled cells. It is concluded from this study that the drastic reduction of amoeboid microglia after glucocorticoid injections can be attributed to the suppression of their precursor cells, monocytes. Another possible explanation is the acceleration of their degeneration process, probably greatly enhanced by glucocorticoids; the degenerating amoeboid microglia were readily eliminated by the surviving amoeboid microglial cells through endocytosis. Glucocorticoids also accelerated the maturation process of the persisting amoeboid microglia to become ramified in form.

Original languageEnglish
Pages (from-to)449-459
Number of pages11
JournalArchives of Histology and Cytology
Volume57
Issue number5
Publication statusPublished - 1994

Fingerprint

Microglia
Subcutaneous Injections
Glucocorticoids
Rhodamines
Corpus Callosum
Lectins
Injections
Macrophage-1 Antigen
Bromodeoxyuridine
Endocytosis
Monocytes
Up-Regulation
Age Groups
Monoclonal Antibodies
Cell Proliferation

ASJC Scopus subject areas

  • Anatomy
  • Histology

Cite this

The effects of subcutaneous injections of glucocorticoids on amoeboid microglia in postnatal rats. / Kaur, C.; Wu, C. H.; Wen, C. Y.; Ling, E. A.

In: Archives of Histology and Cytology, Vol. 57, No. 5, 1994, p. 449-459.

Research output: Contribution to journalArticle

@article{d2d747facddd465cbdd1c0d99caae77e,
title = "The effects of subcutaneous injections of glucocorticoids on amoeboid microglia in postnatal rats",
abstract = "Subcutaneous injections of glucocorticoids into postnatal rats resulted in a drastic reduction in the number of amoeboid microglial cells in the corpus callosum as shown by their labelling with the monoclonal antibodies of the OX-series, ED1, lectin and rhodamine isothiocynate (RhIc). In rats receiving 2 or 3 injections of glucocorticoids and killed at the age of 4 or 7 days, between 40 to 60{\%} of the callosal amoeboid microglial cells were depleted when compared with the corresponding control animals. The cells that survived the glucocorticoid treatments became ramified, while those in the controls of the same age group remained round or amoeboidic. In rats killed at 2 or 3 weeks of age, the microglia became extremely ramified with a concomitant diminution in their immunostaining, particularly in the glucocorticoid-injected rats. In rats receiving glucocorticoid injections along with RhIc, the RhIc-laden amoeboid microglia appeared round and amoeboidic and were intensely stained with OX-42, suggesting their activation and upregulation of complement type 3 receptors when compared with rats receiving only glucocorticoids. Compared with the control, cellular proliferation continued in rats given glucocorticoid injection as indicated by the occurrence of many bromodeoxyuridine-labelled cells in the corpus callosum at the age of 6 days. Ultrastructural studies confirmed the presence of mitotic cells identified as amoeboid microglia because of their labelling with isolectin. A striking ultrastructural feature in glucocorticoids-injected rats was the wide occurrence of amoeboid microglial cells that had ingested a variable number of lectin-labelled cells. It is concluded from this study that the drastic reduction of amoeboid microglia after glucocorticoid injections can be attributed to the suppression of their precursor cells, monocytes. Another possible explanation is the acceleration of their degeneration process, probably greatly enhanced by glucocorticoids; the degenerating amoeboid microglia were readily eliminated by the surviving amoeboid microglial cells through endocytosis. Glucocorticoids also accelerated the maturation process of the persisting amoeboid microglia to become ramified in form.",
author = "C. Kaur and Wu, {C. H.} and Wen, {C. Y.} and Ling, {E. A.}",
year = "1994",
language = "English",
volume = "57",
pages = "449--459",
journal = "Archives of Histology and Cytology",
issn = "0914-9465",
publisher = "Japan Society of Histological Documentation",
number = "5",

}

TY - JOUR

T1 - The effects of subcutaneous injections of glucocorticoids on amoeboid microglia in postnatal rats

AU - Kaur, C.

AU - Wu, C. H.

AU - Wen, C. Y.

AU - Ling, E. A.

PY - 1994

Y1 - 1994

N2 - Subcutaneous injections of glucocorticoids into postnatal rats resulted in a drastic reduction in the number of amoeboid microglial cells in the corpus callosum as shown by their labelling with the monoclonal antibodies of the OX-series, ED1, lectin and rhodamine isothiocynate (RhIc). In rats receiving 2 or 3 injections of glucocorticoids and killed at the age of 4 or 7 days, between 40 to 60% of the callosal amoeboid microglial cells were depleted when compared with the corresponding control animals. The cells that survived the glucocorticoid treatments became ramified, while those in the controls of the same age group remained round or amoeboidic. In rats killed at 2 or 3 weeks of age, the microglia became extremely ramified with a concomitant diminution in their immunostaining, particularly in the glucocorticoid-injected rats. In rats receiving glucocorticoid injections along with RhIc, the RhIc-laden amoeboid microglia appeared round and amoeboidic and were intensely stained with OX-42, suggesting their activation and upregulation of complement type 3 receptors when compared with rats receiving only glucocorticoids. Compared with the control, cellular proliferation continued in rats given glucocorticoid injection as indicated by the occurrence of many bromodeoxyuridine-labelled cells in the corpus callosum at the age of 6 days. Ultrastructural studies confirmed the presence of mitotic cells identified as amoeboid microglia because of their labelling with isolectin. A striking ultrastructural feature in glucocorticoids-injected rats was the wide occurrence of amoeboid microglial cells that had ingested a variable number of lectin-labelled cells. It is concluded from this study that the drastic reduction of amoeboid microglia after glucocorticoid injections can be attributed to the suppression of their precursor cells, monocytes. Another possible explanation is the acceleration of their degeneration process, probably greatly enhanced by glucocorticoids; the degenerating amoeboid microglia were readily eliminated by the surviving amoeboid microglial cells through endocytosis. Glucocorticoids also accelerated the maturation process of the persisting amoeboid microglia to become ramified in form.

AB - Subcutaneous injections of glucocorticoids into postnatal rats resulted in a drastic reduction in the number of amoeboid microglial cells in the corpus callosum as shown by their labelling with the monoclonal antibodies of the OX-series, ED1, lectin and rhodamine isothiocynate (RhIc). In rats receiving 2 or 3 injections of glucocorticoids and killed at the age of 4 or 7 days, between 40 to 60% of the callosal amoeboid microglial cells were depleted when compared with the corresponding control animals. The cells that survived the glucocorticoid treatments became ramified, while those in the controls of the same age group remained round or amoeboidic. In rats killed at 2 or 3 weeks of age, the microglia became extremely ramified with a concomitant diminution in their immunostaining, particularly in the glucocorticoid-injected rats. In rats receiving glucocorticoid injections along with RhIc, the RhIc-laden amoeboid microglia appeared round and amoeboidic and were intensely stained with OX-42, suggesting their activation and upregulation of complement type 3 receptors when compared with rats receiving only glucocorticoids. Compared with the control, cellular proliferation continued in rats given glucocorticoid injection as indicated by the occurrence of many bromodeoxyuridine-labelled cells in the corpus callosum at the age of 6 days. Ultrastructural studies confirmed the presence of mitotic cells identified as amoeboid microglia because of their labelling with isolectin. A striking ultrastructural feature in glucocorticoids-injected rats was the wide occurrence of amoeboid microglial cells that had ingested a variable number of lectin-labelled cells. It is concluded from this study that the drastic reduction of amoeboid microglia after glucocorticoid injections can be attributed to the suppression of their precursor cells, monocytes. Another possible explanation is the acceleration of their degeneration process, probably greatly enhanced by glucocorticoids; the degenerating amoeboid microglia were readily eliminated by the surviving amoeboid microglial cells through endocytosis. Glucocorticoids also accelerated the maturation process of the persisting amoeboid microglia to become ramified in form.

UR - http://www.scopus.com/inward/record.url?scp=0028587822&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028587822&partnerID=8YFLogxK

M3 - Article

C2 - 7734174

AN - SCOPUS:0028587822

VL - 57

SP - 449

EP - 459

JO - Archives of Histology and Cytology

JF - Archives of Histology and Cytology

SN - 0914-9465

IS - 5

ER -