Noradrenergic modulation of the masseteric reflex in behaving cats. I. Pharmacological studies

The masseteric (jaw closure) reflex was utilized as a model system for assessing functional changes in central norepinephrine (NE) neurotransmission. This monosynaptic reflex was chosen because of its simple and well-defined circuitry, and because its motor component receives a dense NE innervation. Previous experiments in our laboratory described NE modulation of this reflex in the anesthetized rat. The present experiments examine the effects of NE on this response in the unanesthetized, behaving cat. The masseteric reflex was elicited by electrical stimulation of the mesencephalic trigeminal nucleus, and the response was recorded via electrodes permanently implanted in the masseter muscle. The amplitude of the reflex response was measured before and at various intervals following microinfusion (0.5 μl) of NE or of various NE agonists directly into the motor trigeminal nucleus (MoV). Microinfusions of NE (0.125-5.0 μg) produced dose-dependent increases in the amplitude of the elicited reflex response. These effects were evident within 1 min postinfusion and lasted up to 30 min; in all cases, the response amplitude returned to baseline levels. The increase seen in response to 0.5 μg NE was blocked by pretreatment with the α-1-adrenergic antagonist prazosin, but not by pretreatment with the serotonin (5-HT) antagonist methysergide. Methysergide did, however, completely block the increase in the amplitude seen in response to microinfusion of 5-HT. Infusion of the α-1-adrenergic agonist phenylephrine also increased the amplitude of the reflex response. By contrast, infusion of the β-adrenergic agonist isoproterenol had no effect, whereas clonidine, a presynaptic α-2-adrenergic agonist, decreased its amplitude. Neither saline infusion nor infusion of NE outside of the motor nucleus had any effect on the amplitude of the reflex response. These data indicate that NE augments the masseteric reflex response by a direct action in the MoV, probably via α-1-adrenergic receptors. Studies in the following paper examine whether physiological activation of this NE input also facilitates the reflex response.