Expression of tPA mRNA in the facial nucleus following facial nerve transection in the rat

Neurotrophic factor prosaposin (PS) is a precursor for saposins A, B, C, and D, which are activators for specific sphingolipid hydrolases in lysosomes. Both saposins and PS are widely contained in various tissues. The brain, skeletal muscle, and heart cells predominantly contain unprocessed PS rather than saposins. PS and PS-derived peptides stimulate neuritogenesis and increase choline acetyltransferase activity in neuroblastoma cells and prevent programmed cell death in neurons. We previously detected increases in PS immunoactivity and its mRNA in the rat facial nucleus following facial nerve transection. PS mRNA expression increased not only in facial motoneurons, but also in microglia during facial nerve regeneration. In the present study, we examined the changes in immunoreactivity of the PS receptors GPR37 and GPR37L1 in the rat facial nucleus following facial nerve transection. Following facial nerve transection, many small Iba1- and glial fibrillary acidic protein (GFAP)-positive cells with strong GPR37L1 immunoreactivity, including microglia and astrocytes, were observed predominately on the operated side. These results indicate that GPR37 mainly works in neurons, whereas GPR37L1 is predominant in microglia or astrocytes, and suggest that increased PS in damaged neurons stimulates microglia or astrocytes via PS receptor GPR37L1 to produce neurotrophic factors for neuronal recovery.

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Facial Nerve Transection Causes Expansion of Myelin Autoreactive T Cells in Regional Lymph Nodes and T Cell Homing to the Facial Nucleus

Autoimmunity ◽

10.3109/08916939209001912 ◽

1992 ◽

Vol 13 (2) ◽

pp. 117-126 ◽

Cited By ~ 63

Author(s):

Tomas Olsson ◽

Per Diener ◽

Åke Ljungdahl ◽

Bo Höjeberg ◽

Peter H. Van Der Meide ◽

...

Keyword(s):

T Cells ◽

T Cell ◽

Facial Nerve ◽

Lymph Nodes ◽

Nerve Transection ◽

Facial Nucleus ◽

Regional Lymph Nodes ◽

Autoreactive T Cells ◽

Cell Homing ◽

T Cell Homing

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Motor neuronal and glial apoptosis in the adult facial nucleus after intracranial nerve transection

Journal of Neurosurgery ◽

10.3171/jns.2006.104.3.411 ◽

2006 ◽

Vol 104 (3) ◽

pp. 411-418 ◽

Cited By ~ 8

Author(s):

Per Mattsson ◽

Kioumars Delfani ◽

Ann Marie Janson ◽

Mikael Svensson

Keyword(s):

Facial Nerve ◽

Motor Neurons ◽

Neuronal Apoptosis ◽

Neuronal Loss ◽

Terminal Deoxynucleotidyl Transferase ◽

Cresyl Violet ◽

Nerve Transection ◽

Facial Nucleus ◽

Double Labeling ◽

Intracranial Lesions

Object Intracranial lesions affecting the facial nerve are usually associated with significant morbidity and poor functional restitution, despite the fact that a peripheral nerve injury normally recovers well. Mechanistic explanations are needed to direct future therapies. Although neonatal motor neurons are known to die as a result of apoptosis after axotomy, this cell death mechanism has not been explicitly demonstrated after peripheral cranial nerve transection in adult mammals. Methods The authors induced substantial retrograde neuronal death in the adult rodent by transecting the facial nerve during its intracranial course. Neuronal apoptosis was demonstrated as shrunken facial motor neurons, retrogradely labeled with fluorogold and with nuclei positively labeled by terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick–end labeling (TUNEL). Glial apoptosis was demonstrated by double labeling with respect to cell type. On postinjury Days 7 and 14, the intracranial axotomy led to neuronal apoptosis, corresponding to a neuronal loss that was observed quantitatively in cresyl violet–stained tissue sections obtained using a stereological method. In contrast, no neuronal apoptosis was observed after creating a distal lesion of the facial nerve, which causes less neuronal loss. In addition, glial apoptosis was seen in the facial nucleus after both distal and proximal axotomy. Whereas the proximal intracranial axotomy led to TUNEL-positive nuclei in cells showing markers for oligodendrocytes and microglia, only the latter glial cell population was double labeled with TUNEL-positive nuclei after distal lesioning. Conclusions These findings may ultimately lead to new therapeutic strategies in patients suffering from facial nerve palsy due to an intracranial lesion.

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