Noradrenergic facilitation of motor neurons: localization of adrenergic receptors in neurons and nonneuronal cells in the trigeminal motor nucleus.

Both alpha- and beta-adrenergic receptors (ARs) are involved in the facilitation of the monosynaptic jaw-closing reflex in the trigeminal motor nucleus (MoV) caused by norepinephrine (NE). The amplitude of muscle spindle afferent-evoked EPSPs in masseter motor neurons is 65% greater when noradrenergic axons to the motor nucleus are concomitantly activated and seems to be due to a presynaptic mechanism (Vornov, J. J., and J. Sutin. 1986. J. Neurosci. 6: 30-37). To determine the subtypes of ARs located on motor neurons and other cells, the cytotoxic lectin Ricin communis was injected into the masseter nerve of the trigeminal motor root to eliminate motor neurons in the masseter subnucleus of MoV. Autoradiography following incubation of tissue sections in the alpha 1 ligand 125IBE 2254 (125I-HEAT) or the nonselective beta ligand [125I]iodocyanopindolol (125ICYP) showed a decrease in alpha 1-AR binding related to the motor neuron degeneration and an increase in beta-AR binding associated with the glial reaction. To determine the extent to which glial proliferation was responsible for the increase in beta-ARs, cytosine arabinofuranoside (AraC) was administered to inhibit mitosis. Following AraC treatment, the total number of glial cells in the ricin-treated MoV was similar to that in normal MoV. Both beta-AR density and GFAP immunoreactivity remain increased, but to a lesser degree than following the ricin treatment alone. AraC also partially prevented the increase of immunolabeled or histochemically visualized microglia and capillary endothelial cells. The coincidence of the increases in beta-AR binding and GFAP in a region devoid of neurons argues that reactive astrocytes and other nonneuronal cells express beta-ARs in vivo. To determine whether the increase in astroglial beta-ARs was due to an up-regulation resulting from transynaptic degeneration of NE terminals, NE content was measured in MoV tissue punches, and NE terminals were visualized by immunocytochemical labeling of dopamine-beta-hydroxylase. NE content and NE terminal density remained unchanged following ricin-induced motor neuron degeneration.