Studies in the preceding paper demonstrated that the amplitude of the masseteric reflex in behaving cats is augmented by pharmacological manipulations that increase norepinephrine (NE) tone in the motor trigeminal nucleus (MoV) through exogenous means. The present studies examine whether such a relationship also exists under physiological conditions, i.e., whether physiological increases in NE synaptic activity are correlated with increases in the reflex amplitude. The masseteric reflex was elicited in behaving cats by electrical stimulation of the mesencephalic trigeminal nucleus (MesV) and the response recorded via electrodes permanently placed in the masseter muscle. Following baseline measures of the reflex amplitude, the reflex was again elicited while cats were exposed to various environmental stimuli known to activate NE neurons: 15 min of 100-dB white noise, confrontation with a dog, or auditory clicks presented repetitively at various intervals prior to MesV stimulation. Presentation of the white noise or the dog significantly facilitated the reflex response for the duration of the exposure. The clicks produced reflex facilitation at 100 and 150 msec following their presentation and reflex suppression at 20 msec. Two approaches were then employed to determine whether NE mediated, at least in part, augmentation of the reflex produced by these environmental conditions. In the first, cats were given either the α-1-noradrenergic antagonist prazosin (5 mg/kg, i.p.) or the serotonin antagonist methysergide (0.5 mg/kg, i.p.). In all cases, prazosin blocked the reflex augmentation whereas methysergide was without effect. In the second study, directed at anatomically localizing these effects, the catecholamine neurotoxin 6-hydroxydopamine (4 μg in 1 μl) was infused unilaterally into the MoV to produce denervation of the NE input to the motor component of the reflex arc. One week later, the reflex was tested on both the intact and denervated sides while the cat was re-exposed to the aforementioned conditions. The normal augmentation was either blocked or markedly diminished on the denervated side while remaining unchanged on the intact side. In both the pharmacological and neurotoxin experiments the suppression produced by the 20-msec click-reflex interval was maintained, indicating that these effects were not attributable to nonspecific damage. These data represent the first demonstration that the release of NE, at a specific site and under physiological conditions, facilitates behavioral output in the intact organism. Furthermore, the neurotoxin experiment goes beyond correlation and establishes that a cause-and-effect relationship exists between increased NE activity and augmentation of the reflex response.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Neuroscience|
|State||Published - 1990|
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