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V J WILSON

Publications and source records attributed to V J WILSON.

26 records · Page 2Linked to original sources
PubMed1959

Recurrent facilitation of spinal reflexes.

Antidromic volleys in muscle nerves may facilitate monosynaptic reflexes originating from neighboring motoneurons. This facilitation has been studied in spinal cats. It is at its peak with a conditioning-test interval of 20 to 30 msec., and can last 50 to 100 msec. The threshold of facilitation is about the same as that of recurrent inhibition. Both phenomena appear to be activated by stimulation of the large motor axons. The latency of facilitation seems to be longer than that of recurrent inhibition by approximately 1 msec., suggesting the presence of at least one more synaptic delay. Facilitation often follows an inhibition of variable depth and duration. Frequently, however, the facilitation is not preceded by inhibition, and therefore it cannot be a rebound effect. The pharmacological properties of facilitation resemble those of recurrent inhibition. Dihydro-beta-erythroidine(1) partially blocks facilitation; the peak is decreased and occurs earlier, and the duration is shortened. Eserine increases the duration of facilitation and inhibition and sometimes enhances their magnitude. It is concluded that recurrent facilitation is mediated by the cholinergic axon collaterals, and that at least two interneurons are located between collateral and motoneuron. Possible mechanisms of facilitation are discussed.

Animals↗
PubMed1958

Action of meprobamate on spinal monosynaptic reflexes and on inhibitory pathways.

Meprobamate was administered intravenously to spinal cats, in cumulative doses of 30 to 40 mg./kg. each. Initial doses may have a variable action on monosynaptic reflexes. At times some reflexes are depressed, while others are enhanced or unaffected. When dose levels of 100 mg./kg. or higher are reached, monosynaptic reflexes, both flexor and extensor, are depressed. Monosynaptic reflexes can be strongly depressed by meprobamate, their input-output relations often remaining unchanged. In such cases there is thus no change in the spatial summation requirements of those motoneurons remaining in the excitable zone. Inhibitory pathways, both direct and disynaptic, are highly resistant to the action of meprobamate. The drug does not distinguish between the direct and disynaptic pathways. It is suggested that meprobamate acts as a general depressant of excitatory synaptic transmission.

Animals↗
PubMed1958

Early post-tetanic potentiation and low frequency depression of some group I reflex actions.

Group I reflex functions, namely monosynaptic reflex transmission, facilitation of synergists, and direct and disynaptic inhibition, show early post-tetanic potentiation following conditioning with a brief, high frequency, tetanus. Of these reflex functions, monosynaptic transmission always shows low frequency depression. Direct inhibitory pathways, and therefore inhibitory junctions, are insensitive to low frequency depression. The fact that direct inhibition can be potentiated shows it to be sufficiently labile that a decrease in efficacy at inhibitory junctions during repetitive activity should be revealed. Disynaptic inhibition often shows low frequency depression. As it is likely that inhibitory junctions in the direct and disynaptic pathways are similar, the low frequency depression of disynaptic inhibition is probably due to the properties of the excitatory relay between afferent fibers and interneurons in that pathway. Facilitation between synergists is often more depressed when the conditioning and testing volleys are nearly simultaneous than when they are separated by 1 to 1.5 msec. This result indicates that an early and rapid phase of action, responsible for homonymous and heteronymous transmission, is more sensitive to low frequency depression than is residual facilitation. In general, reflex transmission is more sensitive than are other aspects of action by group I fibers to events concurrent with and following repetitive activation.

Reflex↗
PubMed1957

Reflex depression in rhythmically active monosynaptic reflex pathways.

A study has been made of the depression that occurs when a monosynaptic reflex pathway is subjected to repetitive stimulation. Reflex depression has a dual origin. High frequency or early depression is postsynaptic in origin and results from subnormality in the motoneurons. Low frequency, late, or enduring depression is presynaptic in origin. The conditioning volley-test volley technique and the frequency-mean monosynaptic reflex amplitude relation yield similar information concerning reflex depression. Each method has its advantages and for some purposes one or the other of the methods necessarily must be employed. The results of a variety of experiments are consistent with the proposition that reflex depression in the monosynaptic reflex pathway originates by action in the group IA afferent fibers of muscle origin that are responsible for monosynaptic reflex transmission. Depression is present at a frequency of 0.1 per second (6 per minute) and absent at a frequency of 0.05 per second (3 per minute). Thus it is impractical for most purposes to employ repetition rates that satisfy the requirement for designation as "single shock" stimulations. The temporal course of enduring depression has been determined. It is identical with that for a number of other phenomena observable in monosynaptic reflex pathways, which suggests a common origin. The mechanism of low frequency or enduring depression is discussed in the light of this suggestion.

Depression↗
PubMed1955

Post-tetanic potentiation of polysynaptic reflexes of the spinal cord.

The phenomenon of post-tetanic potentiation has been studied in the cat spinal cord with particular reference to polysynaptic responses. Following tetanization of dorsal roots, these reflexes show an increased response, as measured in terms of their voltage-time area, with a predominant change in the earlier reflex pathways. Both of these changes in the reflex discharge have a time course of 15 to 25 seconds. Post-tetanic potentiation is also observed in response to stimulation of a dorsal rootlet following tetanization of another rootlet in the same or in a neighboring segment. This effect can be explained by post-tetanic changes in the terminals of secondary, and possibly higher order, internuncial cells, essentially similar to those changes in the primary afferent terminals which give rise to potentiation of the monosynaptic reflex.

Animals↗