CHL1-deficient and wild-type male mice do not differ in locomotor recovery from spinal cord injury

Abstract

STUDY DESIGNAnimal studyOBJECTIVESFemale mice deficient in the adhesion molecule CHL1 recovered better than their wild-type female littermates after spinal cord injury (SCI). This observation was unexpected, because CHL1 increases neurite outgrowth in vitro in a homophilic, neuron-dependent manner. Yet, in SCI, CHL1 is upregulated in the glial scar which reduces axonal regrowth, showing that CHL1 on glia can block regrowth of CHL1 positive axons. This notion that was verified in co-cultures of astrocytes and neurons. Since these SCI experiments were confined to females in the previous study, we now sought to assess SCI in CHL1-deficient male mice.SETTINGSW.M. Keck Center for Collaborative Neuroscience at RutgersMETHODSMale CHL1-deficient and wild-type littermate mice received thoracic weight-drop SCI. Locomotor recovery was analyzed weekly by the Basso Mouse Scale and a single frame motion analysis up to six weeks after SCI, when lesion volumes were measured immunohistologically. Hematological analysis was performed at 24 hours after injury.RESULTSCHL1-deficient males did not recover better or worse than their male wild-type littermates. Primary and secondary lesion volumes were similar in the two genotypes under all conditions. In the peripheral blood at 24 h after SCI, leukocyte numbers in mutant males were slightly higher than in wild-type males, but monocyte and lymphocyte numbers did not differ between genders. Neutrophil numbers were higher in males than in females.CONCLUSIONThese results indicate that CHL1-deficient males and females differ in the number of neutrophils slightly in numbers of leukocytes, but not lymphocytes or monocytes.