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I L Stafford

Publications and source records attributed to I L Stafford.

4 recordsLinked to original sources
PubMed1991

Single-unit and physiological analyses of brain norepinephrine function in behaving animals.

In behaving cats, the single-unit activity of locus coeruleus noradrenergic neurons is strongly activated by a variety of challenges (stressors). For example, exposing cats to a dog or to loud white noise, dramatically increases the activity of these neurons and simultaneously produces strong activation of the sympathetic nervous system. Similarly, glucoregulatory, thermoregulatory, and cardiovascular challenges also coactivate noradrenergic neurons and the sympathetic nervous system. A related research program utilized a simple brainstem response (the monosynaptic jaw closure reflex) to explore the physiological significance of this response of brain noradrenergic neurons. Conditions which activate these neurons were also shown to potentiate the elicited jaw closure-reflex response. Importantly, when the noradrenergic input to the motor side of this reflex pathway was destroyed with a neurotoxin, the conditions which previously potentiated the reflex were now ineffective. These data represent the first demonstration that the release of norepinephrine, at a specific site, and under physiological conditions, facilitates behavioral output in the intact organism.

Action Potentials↗
PubMed1990

Noradrenergic modulation of the masseteric reflex in behaving cats. II. Physiological studies.

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 gain 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 alpha-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.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1990

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 microliters) of NE or of various NE agonists directly into the motor trigeminal nucleus (MoV). Microinfusions of NE (0.125-5.0 micrograms) 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 micrograms NE was blocked by pretreatment with the alpha-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 alpha-1-adrenergic agonist phenylephrine also increased the amplitude of the reflex response. By contrast, infusion of the beta-adrenergic agonist isoproterenol had no effect, whereas clonidine, a presynaptic alpha-2-adrenergic agonist, decreased its amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗