Expression of FGF-2 and FGF receptor type 1 in the adult rat brainstem: effect of colchicine

Abstract

In the adult rat brainstem, neuronal subpopulations of several motor and sensory nuclei display basic fibroblast growth factor (bFGF or FGF-2) immunoreactivity (IR; Grothe et al. J. Comp. Neurol. 305:328-336). In the present study we demonstrate that FGF-2-IR correlates with staining for the high-affinity FGF-receptor 1. Intracerebroventricular injection of colchicine leads to the disappearance or substantial reduction of FGF-2-IR in the hypoglossal, facial, trigeminal motor, trochlear, and mesencephalic trigeminal nuclei. In contrast, FGF-2-IR appears in many perikarya of the red nucleus and the medial nucleus of the trapezoid body, whereas in control rats both nuclei showed immunostained fibers and almost no immunoreactive cell bodies. This dramatic change of FGF-2-IR could be explained by the ability of colchicine to block fast axonal transport. Cranial nuclei may internalize FGF-2 at the periphery via high-affinity receptors and retrogradely transport the molecule to their perikarya. The red nucleus and the medial nucleus of the trapezoid body may synthesize FGF-2 and provide the growth factor to afferent or efferent neurons. The presence of FGF-2 mRNA in brainstem extract and the absence of the FGF-2 transcript in extracts of the hypoglossal nucleus corroborate this suggestion. The effect of colchicine on FGF-2-IR in the brainstem nuclei suggests that FGF-2 could be specifically retrogradely transported in other cranial nuclei, in addition to the hypoglossal system. Together with the ability of FGF-2 to stimulate neuronal survival, this result strongly supports the hypothesis that FGF-2 is acting as a neurotrophic factor on specific central neuron populations.