PubMed Health⌕ Search

Biomedical subjects

M H Chase

Publications and source records attributed to M H Chase.

At least 73 records · Page 4Linked to original sources
PubMed1991

A medullary inhibitory region for trigeminal motoneurons in the cat.

The present report describes the effects on trigeminal motoneurons of stimulation of a circumscribed site within the parvocellular region of the medullary reticular formation. This medullary site was selected because anatomical studies have shown that premotor interneurons project from this site to the trigeminal motorpool. Electrical stimulation of this site induced IPSPs (PcRF-IPSPs) in jaw-closer motoneurons. A population of these IPSPs, recorded contralateral to the site of stimulation, exhibited latencies shorter than 1.5 ms (mean 1.16 +/- 0.08 SD). Their mean amplitude was 1.72 mV +/- 1.13 SD and their mean duration was 3.52 ms +/- 2.15 SD. We believe that these PcRF-IPSPs arose as the result of activation of a monosynaptic pathway. A comparable inhibitory input from this site to ipsilateral jaw-closer motoneurons and to both contra and ipsilateral digastric motoneurons was also observed. We therefore conclude that this medullary PcRF site contains premotor interneurons that are capable of postsynaptically inhibiting motoneurons that innervate antagonistic jaw muscles.

Animals↗
PubMed1991

Strychnine antagonizes jaw-closer motoneuron IPSPs induced by reticular stimulation during active sleep.

In chronic, unanesthetized, normally respiring cats, stimulation of the nucleus reticularis pontis oralis induced inhibitory postsynaptic potentials (IPSPs) in masseter motoneurons during active sleep, but not during wakefulness or quiet sleep. Strychnine, when applied juxtacellularly by microiontophoresis to masseter motoneurons, specifically suppressed the active sleep-dependent IPSPs. In contrast, bicuculline did not suppress the active sleep-dependent IPSPs. These results indicate these IPSPs are mediated by the putative neurotransmitter glycine.

Action Potentials↗
PubMed1991

The postsynaptic inhibitory control of lumbar motoneurons during the atonia of active sleep: effect of strychnine on motoneuron properties.

The present study examined the effects of strychnine on the tonic hyperpolarization and the changes in membrane properties of lumbar motoneurons that occur during active sleep. To carry out these studies, intracellular recordings from lumbar motoneurons were combined with the juxtacellular microiontophoretic application of strychnine in chronic, undrugged, normally respiring cats. During active sleep, compared to quiet sleep, motoneurons that were not exposed to strychnine exhibited tonic hyperpolarization, a decrease in cell excitability, and an increase in membrane conductance; they were also bombarded by high-frequency, large-amplitude IPSPs. In conjunction with the juxtacellular application of strychnine, there was a marked reduction in the degree of hyperpolarization during active sleep; motoneuron excitability was no longer suppressed, and there was a reduction in the increase in membrane conductance. In addition, the large-amplitude IPSPs were blocked. These results identify glycine as the neurotransmitter responsible for the state-dependent changes in membrane properties and the hyperpolarization of motoneurons that takes place during active sleep.

Action Potentials↗
PubMed1990

Suppression of the PGO-related lumbar motoneuron IPSP by strychnine.

Intracellular recordings from lumbar motoneurons in chronic unanesthetized cats revealed that a distinct inhibitory postsynaptic potential (IPSP) occurs following pontogeniculooccipital (PGO) waves during active sleep. Strychnine, when applied juxtacellularly by microiontophoresis, was found to block this IPSP. These data suggest that glycine is likely to be the neurotransmitter that is responsible for the inhibition of lumbar motoneurons that occurs in conjunction with the PGO waves of active sleep.

Action Potentials↗
PubMed1990

Non-reciprocal postsynaptic inhibition of digastric motoneurons.

This study was undertaken to explore the effects, on digastric motoneurons, of electrical stimulation of a site within the parvocellular medullary reticular formation (PcRF). This site is located lateral to the hypoglossal nucleus and ventral to the dorsal motor nucleus of the vagus nerve. Within this site are somas of premotor interneurons that project to trigeminal motor nuclei. Stimulation of this site resulted in the generation of IPSPs in digastric motoneurons. We postulate that these IPSPs were due to the activation of a monosynaptic path from the PcRF to digastric motoneurons. The present results, in conjunction with those previously reported which indicate that the PcRF also induces monosynaptic IPSPs in masseter motoneurons, demonstrate that this is a site of origin for the postsynaptic inhibitory control of motoneurons that innervate both jaw opening and closing muscles.

Animals↗
PubMed1990

Medullary control of lumbar motoneurons during carbachol-induced motor inhibition.

The present study examined the effects of stimulation of the medullary nucleus reticularis gigantocellularis (NRGc) on the Ia-monosynaptic reflex and the membrane potential of lumbar motoneurons. Stimulation of the NRGc was carried out in acute decerebrate cats during motor suppression induced by the intrapontine microinjection of carbachol. During carbachol-induced motor suppression, compared with control conditions (prior to the administration of carbachol), NRGc stimulation resulted in a statistically significant reduction in the Ia-monosynaptic reflex. This effect was maximal at an interval of 45 ms following NRGc stimulation. NRGc stimulation also induced, in lumbar motoneurons, a large amplitude (3.17 mV +/- 0.36 [S.E.M.]), long duration (54.73 ms +/- 3.52 [S.E.M.]) inhibitory postsynaptic potential whose peak coincided with the interval of maximum reflex suppression. These results suggest that carbachol activates pontine neurons that excite cells of the medullary NRGc. We believe that these medullary neurons, in addition to those of the nucleus pontis oralis (NPO)7, participate in the modulation of the descending inhibitory pathway that is responsible for the phenomenon of response-reversal and generalized atonia during naturally occurring active (i.e. REM) sleep.

Animals↗
PubMed1990

The atonia and myoclonia of active (REM) sleep.

Postsynaptic inhibition is a principal process responsible not only for the atonia of the somatic musculature during active sleep but also for the phasic episodes of decreased motoneuron excitability that accompany bursts of REMs during this state. These postsynaptic processes are dependent upon the presence of active sleep-specific IPSPs, which are apparently mediated by glycine. The phasic excitation of motoneurons during REM periods is due to excitatory postsynaptic potentials that, when present, encounter a motoneuron already subjected to enhanced postsynaptic inhibition. These EPSPs are mediated by a non-NMDA neurotransmitter. Thus, from the perspective of motoneurons, active sleep can be characterized as a state abundant in the availability of strikingly potent patterns of postsynaptic inhibition and, during REM periods, not only by enhanced postsynaptic excitation, but also by enhanced postsynaptic inhibition. The site of origin of these inhibitory and excitatory drives is, at present, less clearly defined. There is a consensus that the structure(s) from which the inhibitory drives emanate are located in the lower brainstem, with a cholinoceptive trigger zone situated in the dorsolateral pontine tegmentum in or in the vicinity of the nucleus pontis oralis. We have suggested that from this cholinoceptive trigger zone there emanates an excitatory drive that directly, or through interneurons, excites a medullary are in or in the vicinity of the nucleus reticularis gigantocellularis. Thus, a cascade of cholinoceptively activated excitatory activity proceeds to eventually activate inhibitory interneurons whose activation results in motoneuron inhibition and muscle atonia during active sleep. Resolution of the precise location and mechanisms of interaction of the supraspinal inhibitory and excitatory motoneuron control mechanism constitutes a major goal of future experiments and the next major challenge for researchers in this field.

Brain Stem↗
PubMed1989

Cable properties of spinal cord motoneurons in adult and aged cats.

1. The electrophysiological properties of spinal cord alpha-motoneurons were investigated in adult cats (1-3 yr old) and old cats (14-15 yr old) using intracellular recording techniques. Voltage transients following depolarizing pulses of current were analyzed according to the procedure described by Ito and Oshima (15). The input resistance of each cell, together with the passive electrical time constants, were used to estimate the electrotonic length and total cell capacitance of each motoneuron. 2. Adult and old motoneurons both exhibited an undershoot of the membrane potential following the cessation of a subthreshold depolarizing current pulse (15). The average time constant for the decay of this undershoot in membrane potential was statistically indistinguishable in motoneurons of adult and aged animals. 3. The average membrane time constant of motoneurons in aged cats was 19% longer than that of motoneurons in adult cats. 4. The average total cell capacitance of motoneurons in aged cats was 16% smaller than that of motoneurons in adult cats. 5. The average electrotonic length of old motoneurons was statistically indistinguishable from that of motoneurons in adult cats. 6. From these results, we conclude that there is an age-dependent increase in the membrane resistance and an age-dependent decrease in cell surface area of alpha-motoneurons of the lumbar spinal cord in aged cats. Both of these phenomena are believed to contribute to the age-dependent increase in input resistance that has been previously reported to occur in motoneurons in aged cats (18).

Aging↗
PubMed1989

Evidence that glycine mediates the postsynaptic potentials that inhibit lumbar motoneurons during the atonia of active sleep.

Postsynaptic inhibition of somatic motoneurons underlies the atonia of active sleep. This inhibitory control depends, in large measure, on the bombardment of motoneurons during active sleep by a unique class of large-amplitude inhibitory postsynaptic potentials (IPSPs). These potentials are present only during this behavioral state and have therefore been designated as active sleep-specific IPSPs (AS-IPSPs). The present study was concerned with determining the neurotransmitter that mediates these AS-IPSPs. Lumbar motoneurons were recorded intracellularly during quiet and active sleep in intact, undrugged, normally respiring cats. The frequency and waveform parameters of the inhibitory postsynaptic potentials recorded from these motoneurons were examined following the microiontophoretic juxta-cellular administration of strychnine (a glycine receptor antagonist) and picrotoxin and bicuculline (GABA receptor antagonists). Microiontophoretically applied strychnine abolished the AS-IPSPs and a majority of smaller-amplitude IPSPs. Neither picrotoxin nor bicuculline modified the frequency, amplitude, or rising phase of the AS-IPSPs or the smaller-amplitude IPSPs. We conclude that the postsynaptic inhibitory drive that impinges on motoneurons during active sleep is principally mediated by glycine or a glycinergic substance.

Animals↗
PubMed1988

Renshaw cells are inactive during motor inhibition elicited by the pontine microinjection of carbachol.

The present study was undertaken to determine whether the postsynaptic inhibition of motoneurons that occurs following the pontine microinjection of carbachol in the decerebrate cat is due to the activity of Renshaw cells. Thirty-two out of 37 Renshaw cells (86%) were spontaneously active prior to the administration of carbachol, whereas only 2 out of 13 Renshaw cells (15%) discharged during carbachol-induced motor inhibition. In addition, discrete inhibitory synaptic potentials were observed in 33% of the Renshaw cells from which intracellular recordings were obtained after carbachol administration, indicating that these cells were actively inhibited. The finding that a population of Renshaw cells, which inhibit motoneurons, were themselves inhibited during a period of profound motoneuron inhibition was quite unexpected. These results support the conclusion that Renshaw cells are not the inhibitory interneurons that are responsible for the powerful inhibition of motoneurons that occurs following the pontine microinjection of carbachol.

Action Potentials↗
PubMed1988

Alterations of group Ia-motoneuron monosynaptic EPSPs in aged cats.

The fashion in which the aging process affects synaptic transmission was explored in old cats. The synapses between Ia-afferent fibers and spinal cord alpha-motoneurons were studied employing intracellular recording techniques. The amplitude and time course of Ia-motoneuron monosynaptic excitatory postsynaptic potentials (Ia-EPSPs) recorded from motoneurons of the gastrocnemius medialis motor pool were determined in adult (1-3 years of age) and in old (14-15 years of age) cats. These Ia-EPSPs were evoked by the stimulation of the gastrocnemius medialis nerve in pentobarbital-anesthetized cats. No statistically significant change was found in the amplitude of these synaptic potentials in the old cats compared with the adult controls. In contrast, their time course was markedly modified; both rise-time and half-width were significantly longer in the old cats. In addition, the rate-of-rise of these Ia-EPSPs was significantly slower in the old cats. No breaks or inflections were observed on the rising phase of the potentials in the adult cats, whereas they were present in a subpopulation of potentials in the old cats. There was also a reduction, in the old cats, in the conduction velocity of the peripheral portion of the Ia-afferent fibers. These data indicate that Ia synaptic transmission is considerably affected during old age. It is suggested that these effects in aged cats may be due to modifications in presynaptic as well as postsynaptic processes.

Aging↗
PubMed1987

Effect of inhibitory amino acid antagonists on IPSPs induced in lumbar motoneurons upon stimulation of the nucleus reticularis gigantocellularis during active sleep.

The present study was performed to generate data implicating glycine or gamma-aminobutyric acid as neurotransmitter candidates mediating the IPSPs which are recorded in lumbar motoneurons following electrical stimulation of the nucleus reticularis gigantocellularis (NRGc) during the atonia of active sleep. Accordingly, intracellular records were obtained from lumbar motoneurons in unanesthetized, normally respiring cats during naturally occurring states of active sleep, while inhibitory amino acid antagonists were microiontophoretically released next to the recorded cell. Electrical stimuli, applied to the NRGc during active sleep under drug-free conditions, evoked inhibitory postsynaptic potentials (IPSPs) in all of the lumbar motoneurons which were examined. These NRGc-induced IPSPs exhibited an average latency-to-onset of 26.6 +/- 1.3 ms, a latency-to-peak of 42.5 +/- 1.3 ms, an average amplitude of 3.9 +/- 0.4 mV and a duration of 34.4 +/- 2.1 ms. Strychnine, when applied microiontophoretically, abolished or markedly suppressed these NRGc-induced IPSPs. In contrast, the microiontophoretic application of picrotoxin or bicuculline methiodide failed to block these IPSPs. To the extent that strychnine may be considered to be a specific antagonist of glycine, the present results suggest that glycine (or a structurally related amino acid) participates in the generation of NRGc-induced IPSPs during the atonia of active sleep.

Animals↗
PubMed1987

Effect of inhibitory amino acid antagonists on masseteric reflex suppression during active sleep.

We examined the pharmacological basis for the suppression of the masseteric (jaw-closer) reflex which occurs during the behavioral state of active sleep. Accordingly, the masseteric reflex was recorded in intact, unanesthetized, normally respiring cats during naturally occurring states of wakefulness and active sleep. The amplitude of the reflex during these states was determined before and after strychnine, picrotoxin, and bicuculline methiodide were applied, by microinjection, to the trigeminal motor nucleus. The effectiveness of each drug in blocking the active sleep-related suppression of the masseteric reflex was examined and compared with the degree of suppression evoked, during wakefulness, by stimulation of the inferior alveolar nerve. Microinjection of strychnine (50 microM to 20 mM) reduced the degree of suppression of the masseteric reflex during active sleep, but was markedly more effective in blocking reflex suppression that was induced by stimulating the inferior alveolar nerve. Picrotoxin and bicuculline methiodide (10 microM to 5 mM) produced a nonspecific increase in the amplitude of the masseteric reflex during both states. Thus, these substances did not appear to reduce the degree of reflex suppression induced by inferior alveolar nerve stimulation or that occurring spontaneously during active sleep. We concluded that strychnine-sensitive postsynaptic inhibition does participate in the suppression of masseter motor activity during active sleep, but that it is not the exclusive factor responsible for atonia of the masseter musculature during this state.

Amino Acids↗
PubMed1987

Behavioral state-specific inhibitory postsynaptic potentials impinge on cat lumbar motoneurons during active sleep.

High-gain intracellular records were obtained from lumbar motoneurons in intact, undrugged cats during naturally occurring states of wakefulness, quiet sleep, and active sleep. Spontaneous, discrete, inhibitory postsynaptic potentials (IPSPs) were found to impinge on lumbar motoneurons during all states of sleep and wakefulness. IPSPs which occurred during wakefulness and quiet sleep were of relatively low amplitude and had a low frequency of occurrence. During the state of active sleep there occurred a great increase in inhibitory input. This was the result of the appearance of large-amplitude IPSPs and of an increase in the frequency of low-amplitude IPSPs which were indistinguishable from those recorded during wakefulness and quiet sleep. In addition to a difference in amplitude, the time course of the large IPSPs recorded during active sleep further differentiated them from the smaller IPSPs recorded during wakefulness, quiet sleep, and active sleep; i.e., their rise-time and half-width were of longer duration and their rate-of-rise was significantly faster. We suggest that the large, active sleep-specific IPSPs reflect the activity of a group of inhibitory interneurons which are inactive during wakefulness and quiet sleep and which discharge during active sleep. These as yet unidentified interneurons would then serve as the last link in the brain stem-spinal cord inhibitory system which is responsible for producing muscle atonia during the state of active sleep.

Action Potentials↗
PubMed1987

Motoneuron properties during motor inhibition produced by microinjection of carbachol into the pontine reticular formation of the decerebrate cat.

It is well established that cholinergic agonists, when injected into the pontine reticular formation in cats, produce a generalized suppression of motor activity (1, 3, 6, 14, 18, 27, 33, 50). The responsible neuronal mechanisms were explored by measuring ventral root activity, the amplitude of the Ia-monosynaptic reflex, and the basic electrophysiological properties of hindlimb motoneurons before and after carbachol was microinjected into the pontine reticular formation of decerebrate cats. Intrapontine microinjections of carbachol (0.25-1.0 microliter, 16 mg/ml) resulted in the tonic suppression of ventral root activity and a decrease in the amplitude of the Ia-monosynaptic reflex. An analysis of intracellular records from lumbar motoneurons during the suppression of motor activity induced by carbachol revealed a considerable decrease in input resistance and membrane time constant as well as a reduction in motoneuron excitability, as evidenced by a nearly twofold increase in rheobase. Discrete inhibitory postsynaptic potentials were also observed following carbachol administration. The changes in motoneuron properties (rheobase, input resistance, and membrane time constant), as well as the development of discrete inhibitory postsynaptic potentials, indicate that spinal cord motoneurons were postsynaptically inhibited following the pontine administration of carbachol. In addition, the inhibitory processes that arose after carbachol administration in the decerebrate cat were remarkably similar to those that are present during active sleep in the chronic cat. These findings suggest that the microinjection of carbachol into the pontine reticular formation activates the same brain stem-spinal cord system that is responsible for the postsynaptic inhibition of alpha-motoneurons that occurs during active sleep.

Action Potentials↗
PubMed1987

Basic electrophysiological properties of spinal cord motoneurons during old age in the cat.

1. The electrophysiological properties of alpha-motoneurons in old cats (14-15 yr) were compared with those of adult cats (1-3 yr). These properties were measured utilizing intracellular recording and stimulating techniques. 2. Unaltered in the old cat motoneurons were the membrane potential, action potential amplitude, and slopes of the initial segment (IS) and soma dendritic (SD) spikes, as well as the duration and amplitude of the action potential's afterhyperpolarization. 3. In contrast, the following changes in the electrophysiological properties of lumbar motoneurons were found in the old cats: a decrease in axonal conduction velocity, a shortening of the IS-SD delay, an increase in input resistance, and a decrease in rheobase. 4. In spite of these considerable changes in motoneuron properties in the old cat, normal correlations between different electrophysiological properties were maintained. The following key relationships, among others, were the same in adult and old cat motoneurons: membrane potential polarization versus action potential amplitude, duration of the afterhyperpolarization versus motor axon conduction velocity, and rheobase versus input conductance. 5. A review of the existing literature reveals that neither chronic spinal cord section nor deafferentation (13, 21) in adult animals produce the changes observed in old cats. Thus we consider it unlikely that a loss of synaptic contacts was responsible for the modifications in electrophysiological properties observed in old cat motoneurons. 6. We conclude that during old age there are significant changes in the soma-dendritic portion of cat motoneurons, as indicated by the modifications found in input resistance, rheobase, and IS-SD delay, as well as significant changes in their axons, as indicated by a decrease in conduction velocity.

Action Potentials↗
PubMed1986

Effect of stimulation of the nucleus reticularis gigantocellularis on the membrane potential of cat lumbar motoneurons during sleep and wakefulness.

The present study was performed in order to determine the effect of electrical stimulation of the medullary nucleus reticularis gigantocellularis (NRGc) on the membrane potential of spinal cord motoneurons during sleep and wakefulness. Accordingly, intracellular recordings were obtained from lumbar motoneurons in unanesthetized normally respiring cats during naturally occurring states of wakefulness, quiet sleep and active sleep. Electrical stimuli applied to the NRGc evoked synaptic potentials which occurred at short latency (less than 10 ms) and did not exhibit consistent changes in their waveforms during any states of sleep or wakefulness. During wakefulness and quiet sleep, longer latency (greater than 20 ms) low-amplitude hyperpolarizing potentials occasionally followed NRGc stimulation. However, during active sleep, NRGc stimulation produced, in all motoneurons, relatively large hyperpolarizing potentials that were characterized by a mean amplitude of 3.5 +/- 0.4 mV (mean +/- S.E.M.), a mean latency-to-peak of 43.0 +/- 0.8 ms, and an average duration of 34.4 +/- 1.7 ms. These potentials were capable of blocking the generation of orthodromic spikes elicited by sciatic nerve stimulation. When anodal current or chloride was passed through the recording electrode, the hyperpolarizing potentials decreased in amplitude, and in some cases their polarity was reversed. These results indicate that the active sleep-specific hyperpolarizing potentials were inhibitory postsynaptic potentials. Thus, the NRGc possesses the capability of providing a postsynaptic inhibitory drive that is directed toward lumbar motoneurons which is dependent on the occurrence of the behavioral state of active sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗