Noradrenergic hyperinnervation of the motor trigeminal nucleus: alterations in membrane properties and responses to synaptic input

The physiological consequences of the noradrenergic (NE) hyperinnervation of the rat brain stem produced by neonatal administration of 6-hydroxydopamine (6-OHDA) was studied in the motor trigeminal nucleus. Stimulation of the region of the lateral lemniscus, the source of the noradrenergic innervation of the nucleus, facilitated the masseteric reflex for up to 200 msec in both normal and hyperinnervated animals. The peak facilitation was 71% larger in the NE hyperinnervated animals and was reduced by systemically administered alpha- and beta-adrenergic receptor antagonists. Intracellular recordings revealed that the mean resting potential of NE hyperinnervated trigeminal motoneurons was 3 mV more hyperpolarized than that of normal cells. The mean input resistance of NE hyperinnervated motoneurons was reduced from 1.83 +/- 0.15 to 1.22 +/- 0.19 M Omega. NE hyperinnervation increased the amplitude of the monosynaptic EPSP evoked by stimulation of primary afferent cell bodies in the mesencephalic trigeminal nucleus (MesV) by 65%. The mean rise time of the EPSP was increased in NE hyperinnervated motoneurons while the mean half-width was unchanged, suggesting a shift in the distribution of primary afferent terminals away from the motoneuron soma. Stimulation of the lateral lemniscus region produced a predominantly depolarizing PSP with a time course similar to that of the reflex facilitation. The amplitude of the depolarization in NE hyperinnervated motoneurons was not significantly different from that of controls. During this lateral lemniscus region-evoked PSP, stimulation of MesV produced an EPSP of increased amplitude, associated with a decrease or no change in input resistance.