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At least 883 records · Page 49Linked to original sources
PubMed1985

Entropy concept in relation to brain waves and evoked potentials: critique of a physical approach.

Basar's view that the larger the number of synchronized and coupled participating neural generators, i.e., the lower the entropy of the neural systems, the lower the responsiveness of the system, and vice versa, was reconsidered experimentally and theoretically, in the light of current knowledge about the relationship between EEG states and evoked potentials. It was found that the morphology as well as the magnitude of the somatosensory evoked potentials was the same during synchronized (low entropy) and desynchronized (high entropy) EEG states in normal human subjects. Baclofen caused an increase in the somatosensory evoked potentials without affecting the EEG in unanaesthetized dogs. In the less complicated and more limited systems such as the skeletal muscle and monosynaptic reflex paradigms, an inverse relationship was established between the entropy state and responsiveness. This relationship can be simply explained by the neurophysiological facts such as Na-inactivation process at the excitable membranes and the refractory states of the neural generators. These results are consistent with those from the literature; the evoked potentials are usually large when recorded during synchronized EEG states and vice versa. It is suggested that, at least, the well established neurophysiological facts should not be ignored in physical approaches to neural mechanisms, especially when it concerns highly complex systems such as the brain.

Animals↗
PubMed1975

Responses of nucleus z neurons to vibration of hindlimb extensor muscles in the decerebrate cat.

1. Small sinusoidal changes of length, applied longitudinally to the ddifferented GS muscle, were uused as a specific stimulus to activate the muscle spindle receptors in precollicular decerebrate cats. In order to determine the relative contribution of the primary and secondary endings of muscle spindles to the response of the nucleus z neurons, the effects of muscle vibration on this unit activity were studied under conditions in which the segmental monosynaptic reflexes produced by stimulation of the primary endings of muscle spindles were continuously monitored. 2. Vibration of the GS muscle (at 180-200/sec and amplitudes up to 250-320 mu) affected the frequency and pattern of discharge in 50 out of 168 units recorded from the lower medulla...

Achilles Tendon↗
PubMed1992

Calcium as a counteractive agent to streptomycin induced respiratory depression: an in vivo electrophysiological observation.

Effect of streptomycin on respiratory function in cats was studied. It was observed that streptomycin at a dose of 40 mg/kg body weight intravenously (i.v.) caused respiratory failure or streptomycin induced respiratory depression (SIRD). This respiratory failure is not linked with Herring-Breuer stretch receptors because the effect remained unaltered in artificially ventilated cats. The involvement of central structures in SIRD can be discarded since intracarotid and intraventricular administration of streptomycin failed to produce any change in respiration. Studies on monosynaptic reflex, dorsal and ventral root activities of spinal phrenic and intercostal nerves, and on fusimotor and alpha-motor neuron activities of spinal intercostal and phrenic nerves in decerebrated cats indicated clearly that respiratory depression is not only due to blockade at neuromuscular junction but due to functional depression at the level of muscle receptors and spinal cord motor neurons. The respiratory depression induced by streptomycin was more or less completely reversed when calcium was administered intravenously from external source. It is speculated that streptomycin induced respiratory depression may be mediated through calcium inhibition which can be treated with external calcium in conjunction with artificial respiration.

Animals↗
PubMed2003

[Features of stepping pattern formation in decerebrated cats under epidural spinal cord stimulation].

The mechanisms of stepping pattern formation initiated by epidural spinal cord stimulation in decerebrated cats, were investigated. It is shown that the ability to produce the stepping pattern involve the L3-L5 segments. In flexor muscle, the formation of stepping pattern under optimal stimulation frequency (5-10 Hz) of these segments is provided by polysynaptic activity with the latency 80-110 ms. In extensor muscle, this process is realized through interaction of monosynaptic reflex and polysynaptic activity. The stepping pattern under epidural stimulation is determined by spinal structures with modulation influence of the peripheral feedback.

Animals↗
PubMedDate not supplied

[The effect of DOPA on the reciprocal inhibition of the innervation centers of antagonistic muscles in newborn rat pups].

In experiments on 5--7- and 16-day rat puppies with acute lesion of the spinal cord, by means of monosynaptic tests, studies have been made of the effect of DOPA on reciprocal inhibition of antagonist muscles. Test stimuli were applied to n. tibialis, conditioned ones--to n. peroneus. It was shown that the pattern of the effects depends on the action of the drug on the magnitude of the initial monosynaptic reflex used as a test. It the latter was initially inhibited, the conditioned stimulation resulted within the first 1-8 msec not in the development of postsynaptic inhibition, but in evident facilitation, which was longer in 5--7-day animals. The level of presynaptic inhibition was somewhat lower than the initial one, but exhibited longer duration. In case of facilitation of a control test after DOPA injection, configuration of reciprocal inhibition curves did not significantly differ from that obtained before administration of the drug.

Aging↗
PubMedDate not supplied

[Pharmacologic profile of protirelin tartrate].

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1979

H-reflex latency in uremic neuropathy: correlation with NCV and clinical findings.

Sixty-two uremic patients on dialysis of varying durations were tested bilaterally for posterior tibial nerve H-reflex latency, at 3-month intervals. Bilateral nerve conduction velocities (NCVs) of the peroneal, tibial, and sural nerves were concomitantly determined in all subjects. Proprioception sense, vibration perception threshold at the great toes, and deep tendon reflexes at the knee and ankle were determined in all subjects on the day of electrodiagnostic testing. The sensitivity of the H-reflex latency in detection of the onset and severity of uremic neuropathy was assessed. H-reflex latency changes were compared to NCV and clinical test results. The following was found: (1) of the parameters studied, the H-reflex latency appeared to be the most sensitive indicator of early uremic polyneuropathies, (2) electrodiagnostic tests were more sensitive to the onset of neuropathies than the clinical testing parameters studied, and (3) the sural sensory nerve appeared to be involved earlier than peroneal and tibial motor nerves in neuropathies studied.

Adolescent↗
PubMed1987

[Changes in transmission efficiency in synapses of the dorsal horn of the cat spinal cord during repeated activation of cutaneous afferents].

Inhibition dynamics of certain components of the spinal cord potentials under low frequency stimulation of cutaneous nerves was studied in acute experiments on cats. The experimental data obtained were approximated by the theoretical curve on the assumption that the two-pool model of the transmitter storage was applicable. An increase of the mediator replenishment intensity during rhythmical stimulation has been demonstrated. The results obtained were similar to those obtained from monosynaptic reflex investigations, that demonstrates the likeness of action mechanisms for different afferent synapses.

Afferent Pathways↗
PubMed1978

Reciprocal Ia inhibition in spastic paralysis in man.

Reciprocal reflex connections were studied in capsular hemiplegia and spastic paresis with spinal cord lesions, using Lloyd's technique. Effects of conditioning stimulation of the tibial or peroneal nerve on the H reflex in the antagonists were examined. Stimulus intensity was controlled with reference to the threshold of the M wave. Weaker stimulation than this threshold was regarded as stimulation of group I afferents. It aroused no subjection sensation in intact subjects. Early and strong inhibition, comparable to Ia inhibition in the cat (Lloyd 1946), was observed from weak stimulation of the tibial nerve on the pre-tibial (flexor) H reflex, but not from the peroneal nerve on the triceps surae (extensor) H reflex in capsular hemiplegia. Alcohol block of extensor motor points resulted in reduction of spasticity without further paralysis in the blocked muscle and a remarkable increase in strength of the antagonist pre-tibial muscles. These results suggest that an extensor spasticity withe flexor weakness, which is common in capsular hemiplegia, may be due to an imbalance of reflex activities via Ia muscle afferents, and that a part of flexor weakness can be restored by "disinhibition' by reduction of Ia inflow from extensor muscles. Ia inhibition was also observed in one third of cases with spinal cord lesions at rest. It returned to normal after recovery from spastic paresis by radical therapy in some cases.

Brain↗
PubMed1986

Comparative study of various H1-blockers on neuropharmacological and behavioral effects including 1-(2-ethoxyethyl)-2-(4-methyl-1-homopiperazinyl)benzimidazole difumarate (KB-2413), a new antiallergic agent.

In a conditioned avoidance response tested in rats, all of the H1-blockers employed caused a dose-related inhibition at doses 5-20 mg/kg (i.v.) except for ketotifen that elicited significant suppression even at a dose of 1 mg/kg. No inhibition was seen after administration of 1-(2-ethoxyethyl)-2-(4-methyl-1-homopiperazinyl)benzimidazole difumarate (KB-2413). ED50s were ranged from 4.1 to 7.4 mg/kg in diphenhydramine, pyrilamine and promethazine. In laminectomized rats, diphenhydramine, pyrilamine, promethazine and ketotifen suppressed the amplitudes of monosynaptic reflex potentials at doses higher than 2 mg/kg (i.v.). In the case of chlorpheniramine, significant inhibition was observed at a dose of 20 mg/kg. In a polysynaptic reflex, similar but less prominent inhibitions were affected by those drugs. However, KB-2413 did not influence spinal reflexes even at a dose of 20 mg/kg. In the rat phrenic nerve-diaphragm preparation, perfusion of H1-blockers at a concentration of 10(-5) M decreased the amplitudes of end-plate potentials except for chlorpheniramine and KB-2413. At 10(-4) M, all the test drugs caused significant inhibition. When the action potential of superior cervical ganglion was measured by the sucrose gap method, promethazine inhibited the action potential significantly at 10(-6) M, but the rest of the test drugs depressed the potentials at 10(-5) M. In spontaneous EEG, all H1-blockers caused a marked drowsy pattern at lower doses (2-5 mg/kg) except for chlorpheniramine, while in higher doses (10-20 mg/kg) epileptic signs in EEG with or without convulsive behavior were noticed. However, after KB-2413 (5-20 mg/kg) neither drowsy nor seizure pattern was observed, in EEG or behavior.

Action Potentials↗
PubMed1988

Physiological aspects of synaptic plasticity: the Ia/motoneuron connection as a model.

Damage to peripheral nerves results in substantial changes in the function of spinal synapses that mediate the monosynaptic reflex. These alterations consist independently of those caused by axotomy of the postsynaptic neuron and those produced by axotomy of the presynaptic neuron. Synaptic transmission is depressed following interruption of either limb of the segmental reflex loop. These reductions in EPSP amplitude are largely reversed following reinnervation of the peripheral tissue by the cut fibers, whether or not the regenerating fiber finds the correct muscle. Alterations in synaptic transmission following damage to the spinal cord itself are more variable than those noted after peripheral nerve damage. Although segmental EPSPs are generally enhanced following spinal injury (if in fact changes do occur), these increases are superimposed on motoneuron hyperpolarization, making the net changes in reflex transmission unpredictable. Furthermore, the extent of motoneuron depolarization is also influenced by the amount of temporal summation of EPSPs during the high-frequency activation of group Ia fibers known to occur, for example, during normal walking. Because EPSP amplitude is not constant during such activation and is modulated differently at connections on different motoneurons, changes in effective levels of synaptic transmission after such lesions are very difficult to predict. Thus it is not surprising that it is not possible to make close correlations between changes in amplitude of EPSPs and reflex behavior following injury (but see chapter by M.E. Goldberger and M. Murray, this volume). These alterations in synaptic transmission can occur at a considerable physical distance from the site of injury, peripheral or central. They illustrate the interdependence in elements of the nervous system, which can also be seen as changes in properties of motoneurons themselves (e.g., input resistance, after-hyperpolarization, rheobase) following many of these injuries. Altered cell properties complicate the functional interpretation of synaptic changes obtained after injury but must be considered in evaluating the sequelae of lesions in the peripheral and central nervous system.

Animals↗
PubMed1987

Effect of cooling on H- and T-reflexes in normal subjects.

The local application of cold has been used to decrease spasticity and facilitate neuromuscular function, but previous attempts to identify its effect on the stretch reflex have not been entirely successful. We examined the effects of cold on the Hoffmann (H) reflex and on the tendon tap (T) reflex in 16 subjects. A series of H/M recruitment curves and T-reflexes were recorded via surface EMG electrodes before and during cooling of the triceps surae. Skin and intramuscular temperatures were recorded with average decreases of 18.4C and 12.1C, respectively. Peak-to-peak amplitude of the M, H, and T compound action potentials (CAPs) was measured. In all cases, the amplitude of the maximal M-wave decreased (p less than 0.001) in response to cooling. These changes in the recording of CAPs should be considered when cooling experiments result in alterations in H or T waveforms. When using the M-wave as a covariant in our analysis, there were no significant changes in the H-reflex amplitude; the height of CAPs elicited by T decreased (p = 0.025). Our findings do not support earlier claims that simple cooling facilitates the excitatory alpha motoneuron pool as measured by the H-reflex; we do confirm that muscle spindle activity, as measured by the T-reflex, is decreased by muscle cooling.

Adult↗