Premium
The neurotrophic analogue of ACTH(4–9) reduces the perineuronal microglial reaction after rat facial nerve crush
Author(s) -
Ulenkate Herman J. L. M.,
Verhagen Marc A. M. T.,
Gispen WillemHendrik,
Jennekens Frans G. I.
Publication year - 1993
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440090307
Subject(s) - perineuronal net , regeneration (biology) , microglia , facial nerve , biology , axon , neuroglia , neuroscience , anatomy , central nervous system , immunology , inflammation , microbiology and biotechnology
Following peripheral nerve cursh, microglial cells proliferate and migrate to motoneuron cell bodies of the injured nerves. Newly formed glial processes displace nerve terminals from the cell bodies. This process is known as synaptic stripping. In animal models of peripheral nerve diseases, the ACTH(4–9) analogue, ORG2766, was shown to facilitate axonal regeneration and to protect against experimental neuropathy. In the present study we examined the effect of ORG2766 on the microglial reaction. After facial nerve crush, rats were treated with either ORG2766 on the microglial reaction. After facial nerve crush, rats were treated with either ORG2766 (75 μg/kg/48 h) or saline and were killed on day 2–6 after operation. Blind counting of the number of perineuronal glial cells in the facial nucleus was used to assess the effect of ORG2766 treatment on the microglial reaction. In the saline‐treated animals the number of perineuronal glial cells per motoneuron cell body on the curshed side increased significantly. This number increased up to day 5 after operation and decreased significantly from day 5 to 6. After initial increase in the peptide‐treated animals, however, the number of perineuronal glial cells remained constant form day 3 onwards. Hece, on post‐operation days 4 and 5, this number was significantly less than that seen in saline‐treated animals. Microglial cells proliferate, presumably through signalling by injured motoneurons. It is suggested that the decrease in the number of perineuronal glial cells in the ORG2766‐treated animals is the result of a peptide‐induced reduction in the release of mediating signals/cytokines or, alternatively, increased protection of motoneurons by stress proteins. Further research should address the mechanism of action of ORG2766 in animal models of motoneuron disease. © 1993 Wiley‐Liss, Inc.