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Biomedical subjects

M H Chase

Publications and source records attributed to M H Chase.

At least 91 records · Page 5Linked to original sources
PubMed1986

Hypothalamic substrates of self-stimulation in cats.

The purpose of this study was to gather anatomical data concerning sites for self-stimulation in the lateral hypothalamus in the cat. The study was conducted on 25 adult cats. In each cat, one to three monopolar stimulating electrodes were implanted bilaterally in the lateral hypothalamus in a region between sections Fr 10.0 and Fr 13.0, L 2.0 and L 5.0, and H -2.0 and H -6.0. A reference electrode was placed in the calvaria over the frontal sinus. Twenty-two of these cats learned to press a lever when each press was rewarded by a brief (0.3 s) electrical stimulus (2.0 to 7.0 V, 100/s, 1 ms duration per pulse) delivered to the hypothalamus. Postmortem anatomical analysis of the brains revealed that most of the positive rewarding sites were located in a midlateral hypothalamic zone, which included the medial forebrain bundle, and were localized to section Fr 11.5, between L 2.0 and L. 5.0, and H -3.0 and H -5.5.

Animals↗
PubMed1985

Aging of motoneurons and synaptic processes in the cat.

The aging of spinal cord alpha motoneurons was explored in old cats with intracellular recording techniques to determine the basic membrane properties of these neurons and their monosynaptic response following activation of group Ia afferent fibers. The conduction velocity of the motoneurons' axons decreased in old animals (14 to 15 years of age) compared with adult controls (1 to 3 years of age). The input resistance of the motoneurons increased in the old cats; no change occurred in the resting membrane potential or spike amplitude. There was a reduction in the delay between the initial segment and the somadendritic components of the antidromic spike. The half-width duration of the monosynaptic EPSP in the old cats increased, but its amplitude did not change. These data indicate that a host of different membrane properties of spinal cord motoneurons and their Ia-monosynaptic input are affected by the aging process. Analysis of the results suggests that the degradation of neuronal processes occurs in all motoneurons rather than preferentially affecting a specific population of motoneurons.

Action Potentials↗
PubMed1985

Sleep-waking modulation of respiratory sinus arrhythmia in aged and young adult cats.

Heart rate variation at the respiratory frequency was examined in young adult and aged cats during waking and quiet sleep. Respiratory sinus arrhythmia was found to be significantly enhanced during quiet sleep compared with waking in both groups of cats. Aged cats exhibited respiratory sinus arrhythmia comparable to that of young adult cats during both waking and quiet sleep.

Age Factors↗
PubMed1984

Ethanol-induced modulation of the membrane potential and synaptic activity of trigeminal motoneurons during sleep and wakefulness.

In the present study we investigated the direct actions of ethanol on the membrane properties and excitatory and inhibitory postsynaptic potentials of trigeminal motoneurons in chronic cats. During states of sleep and wakefulness, extracellular and intracellular recordings were carried out together with juxtacellular (somatic and dendritic) and intracellular pressure injections of 0.05-2.5 M ethanol solutions in femtoliter quantities. Juxtacellularly applied ethanol induced: a sequence of excitatory-inhibitory alterations in firing activity which were accompanied by depolarizing-hyperpolarizing shifts in the resting membrane potential; a decrease in the amplitude of action potentials; and a depression in excitatory and inhibitory postsynaptic potentials. Intracellular ethanol injections resulted in depolarization of the membrane potential and a decrease in the amplitude of action potentials as well as a reduction in the amplitude of excitatory and inhibitory postsynaptic potentials. Both juxtacellularly and intracellularly applied ethanol affected the membrane potential and synaptic activity in a fashion that was not dependent upon the animal's behavioral state of sleep or wakefulness.

Action Potentials↗
PubMed1984

Role of medullary reticular neurons in the inhibition of trigeminal motoneurons during active sleep.

We sought to identify those cells involved in the generation of atonia of the masseter muscles during active sleep. A neuronal population was examined in the medullary reticular formation which has been shown to project monosynaptically to trigeminal motoneurons and provide inhibitory input to them. These neurons exhibited a pattern of state-dependent discharge which was characterized by a tonic increase in firing frequency which paralleled the tonic decrease in somatomotor reflex activity (within the trigeminal system) in the continuum of wakefulness to quiet (NREM) sleep to active sleep. This population of cells discharged at extremely high rates during active sleep, especially during periods of rapid eye movements, when postsynaptic inhibitory control of motoneurons is most prominent. We therefore suggest that these medullary units are the inhibitory neurons which are responsible for the postsynaptic inhibition of trigeminal motoneurons during active sleep.

Animals↗
PubMed1983

Subthreshold excitatory activity and motoneuron discharge during REM periods of active sleep.

A striking paradox of the rapid eye movement periods of active sleep, which are typically characterized by the exacerbation of somatomotor atonia, is the occurrence of muscle twitches and jerks. The purpose of this study was to examine the specific motoneuron membrane potential processes responsible for these myoclonic patterns of activity. In lumbar motoneurons, examined intracellularly in the cat prepared for long-term study, these processes consisted of recurrent depolarizing membrane potential shifts and spontaneous action potentials that were either full-sized or of partial amplitude. In addition, the invasion of antidromically induced spikes into the soma was often blocked. Hyperpolarizing potentials were evident in the intervals between spontaneous spikes. Hyperpolarization was also observed immediately before depolarization and spike activity, in contrast to the gradual depolarization of the motoneuron membrane potential that always occurred during wakefulness. Thus, during rapid eye movement periods, in conjunction with muscle twitches and jerks, a strong excitatory input is superimposed on a background of inhibitory input. The unique patterns of membrane potential change that arise thus seem to result from the simultaneous coactivation of excitatory and inhibitory processes.

Action Potentials↗
PubMed1983

Effects of juxta- and intracellular microinjection of ethanol on trigeminal motoneurons in the chronic cat.

The direct cellular effects of ethanol on trigeminal motoneurons were studied in chronic cats during sleep and wakefulness. Intracellular and extracellular recordings were obtained while simultaneously injecting ethanol microdroplets onto the surface (juxtacellularly) or within the soma (intracellularly) of these motoneurons. Juxtacellular ethanol injection resulted in a suppression of neuronal excitability as well as a reduction in the amplitude of action potentials and monosynaptically-induced excitatory postsynaptic potentials. Intracellular ethanol injection led to a slight increase in excitability (i.e. membrane depolarization); concurrently, however, there was a reduction in the amplitude of spike and synaptic potentials. We conclude that the predominant response of trigeminal motoneurons to the direct application of ethanol entails a dose-dependent reduction in membrane excitability in addition to a depression of excitatory synaptic transmission. This pattern of ethanol action was observed throughout the states of quiet sleep and active sleep as well as when the animal was awake.

Animals↗
PubMed1983

Synaptic mechanisms and circuitry involved in motoneuron control during sleep.

Spontaneous amplitude fluctuations of the brainstem monosynaptic trigeminal jaw-closing reflex were examined in the freely moving chronic cat during wakefulness, quiet sleep, and active sleep. The largest amplitude responses occurred during active wakefulness; they decreased in size during quiet sleep. The lowest amplitude responses occurred during active sleep. A chronic cat preparation was developed in order to record intracellularly from identified trigeminal motoneurons for prolonged period of time throughout the states of sleep and wakefulness. The membrane potential of trigeminal motoneurons exhibited fluctuations that were correlated with changes in the animal's behavioral state. The fundamental pattern consisted of (a) slight hyperpolarization during quiet sleep, compared to arousal or alert wakefulness, (b) little if any hyperpolarization during quiet sleep compared to quiet wakefulness, and (c) dramatic hyperpolarization when active sleep was compared to quiet sleep. Sustained spike activity of trigeminal motoneurons, when present during wakefulness, decreased in frequency or tended to occur in bursts when the animal was in quiet sleep. During active sleep, activity ceased except for a few isolated spikes or short-duration bursts of action potentials. Based on an analysis of antidromically induced spike potentials and monosynaptically induced postsynaptic potentials, it was concluded that postsynaptic inhibition of trigeminal motoneurons during active sleep acts to suppress somatic reflex activity and produce muscular atonia. A companion study of the membrane potential of lumbar motoneurons in the chronic, unanesthetized, undrugged, normally respiring cat was performed during sleep and wakefulness. The antidromic field potential, antidromic and orthodromic spike, EPSP, membrane input resistance, and rheobasic current of lumbar motoneurons were studied during sleep and wakefulness. No change in motoneuron excitability occurred when quiet wakefulness was compared to quiet sleep. Postsynaptic inhibition resulted in decrease in excitability during active sleep. Further phasic decreases in excitability, also due to postsynaptic inhibition, occurred during active sleep in conjunction with clusters of rapid eye movements. The mesencephalon, pons, and medulla were explored in a conditioning-test paradigm in an attempt to find a site where electrical stimulation induced a pattern of somatomotor reflex and motoneuron membrane potential modulation comparable to that which occurs spontaneously during sleep and wakefulness. In unanesthetized, freely moving cats during wakefulness and quiet sleep, electrical stimulation within and in the vicinity of the nucleus pontis oralis produced facilitation of the masseteric reflex, whereas during active sleep the identical stimulus resulted in potent suppression of the reflex.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1982

Phasic changes in motoneuron membrane potential during REM periods of active sleep.

Most of the phasically occurring periods of rapid eye movements (REMs) of active sleep are accompanied by enhanced suppression of somatomotor activity; however, during some of the REM episodes there are muscular twitches and jerks. The membrane potential changes underlying these motor processes were examined by recording intracellularly from lumbar motoneurons in cats that were undrugged, unanesthetized and normally respiring. Summated hyperpolarizing potentials were evident during REM episodes in conjunction with a decrease in motoneuron excitability. During other episodes of REMs there occurred summated depolarizing potentials which occasionally produced action potentials. These depolarizing events were in most cases preceded by a brief period of hyperpolarization. Thus, it appears that there is inhibitory input to lumbar motoneurons during all REM periods of active sleep; in some episodes the simultaneous coactivation of excitatory input leads to depolarization of the membrane and action potential generation.

Action Potentials↗
PubMed1982

Hyperpolarizing membrane responses induced in lumbar motoneurons by stimulation of the nucleus reticularis pontis oralis during active sleep.

Intracellular recordings were obtained from lumbar motoneurons in unanesthetized, undrugged, normally respiring cats during the states of wakefulness, quiet sleep and active sleep. The objective was to examine the state-dependent control of spinal cord motoneurons exerted by the pontomesencephalic reticular formation. Accordingly, electrical stimulation was applied to the nucleus reticularis pontis oralis while the membrane potential of lumbar motoneurons was recorded. Short latency depolarizing and/or hyperpolarizing potentials were observed throughout sleep and wakefulness; no state-dependent pattern was found in the direction of polarization or amplitude for these early potentials. However, a long latency hyperpolarizing potential emerged exclusively during active sleep; it was characterized by a peak latency of 45 +/- 1 (S.E.M.) ms, a duration of 40 +/- 2 ms, and an amplitude of 3 +/- 0.5 mV. This active sleep-selective potential was capable of inhibiting spontaneous motoneuron activity. These and previously obtained data support the notion that excitation of the nucleus reticularis pontis oralis results in somatomotor inhibition at the level of the spinal cord and brainstem selectively during the state of active sleep.

Animals↗
PubMed1981

Postsynaptic control of lumbar motoneuron excitability during active sleep in the chronic cat.

A correlated intracellular and extracellular study of lumbar motoneuron excitability during sleep and wakefulness was performed in the chronic, unanesthetized, undrugged, normally respiring cat. Experiments were designed to reveal the extent to which hypotonia during active sleep in mammals is dependent on postsynaptic inhibition of somatic motoneurons. Variations in the antidromic field potential, antidromic and orthodromic spike, EPSP, membrane input resistance and rheobasic current were studied. No change in motoneuron excitability occurred when quiet wakefulness was compared to quiet sleep. A decrease in excitability was present, due to postsynaptic inhibition, during active sleep. Further phasic decreases in excitability, also due to postsynaptic inhibition, occurred during active sleep in conjunction with clusters of rapid eye movements.

Action Potentials↗