PubMed Health⌕ Search

Biomedical subjects

Y Sahara

Publications and source records attributed to Y Sahara.

26 records · Page 2Linked to original sources
PubMed1988

Single-unit activity in bulbar reticular formation during food ingestion in chronic cats.

1. Single-unit activity was recorded from 215 neurons in the medial bulbar reticular formation during the masticatory sequence, from intake to deglutition, of 3 kinds of food (cat food pellets, canned fish, and milk) in 8 chronically prepared, unanesthetized, spontaneously respiring cats with their head fixed to a stereotaxic apparatus without pain or pressure. The firing patterns were compared to the simultaneously recorded EMGs of the jaw-closing and -opening muscles and to the jaw movement. 2. Fifty neurons changed their firing patterns during mastication. Nine neurons increased and one neuron decreased or stopped firing coincident with the masticatory sequence without an apparent rhythmical modulation of frequency corresponding with the masticatory rhythm (nonphasic group). The firing pattern of the remaining 40 neurons was modulated in phase with jaw movement (phasic group); 34 neurons either showed a spike burst or attained the highest firing frequency during the jaw-opening phase (opening type), while 6 neurons did so during the jaw-closing phase (closing type). The firing patterns of each neuron were essentially the same regardless of the kind of food ingested, except for 2 opening-type neurons that showed a rhythmical burst during mastication of solid food and tonic activity during lapping milk. 3. For 16 phasic neurons, there were significant correlations between some aspects of the firing pattern and a parameter of the movement during ingestion of solid food and/or milk. With one exception, these relationships did not appear to be due to sensory feedback. 4. We detected a monosynaptic excitatory projection from 3 opening-type neurons to the anterior digastric motoneurons, and monosynaptic inhibitory projections to the temporal or masseter motoneurons from 3 other opening-type neurons, by spike-triggered averaging of the full-wave rectified EMG of the jaw-closing and -opening muscles. No monosynaptic projections from the closing-type neurons or nonphasic group neurons to either jaw-opener or -closer motoneurons were detected. 5. The instantaneous firing frequency of all 3 inhibitor premotor neurons was positively correlated with the opening velocity, and the firing of 2 was also related to the jaw displacement.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Activity during active sleep of bulbar reticular neurons firing rhythmically during mastication in cats.

Unitary activity was recorded from 17 bulbar reticular neurons, which fired rhythmically during mastication, in unanesthetized, spontaneously respiring cats during sleep and wakefulness. All these neurons showed the highest mean firing rate during food ingestion, and none of them showed any tonic discharge during active sleep. The results are discussed in terms of a functional differentiation of bulbar reticular inhibitory neurons projecting to jaw-closer motoneurons in relation to phasic inhibition during mastication and tonic inhibition during active sleep of jaw-closer motoneurons.

Animals↗
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

Phase-linked variations in the amplitude of the digastric nerve jaw-opening reflex response during fictive mastication in the rabbit.

The diagastric nerve reflex response to stimulation of the upper lip was studied in urethan-anesthetized rabbits paralysed with pancuronium bromide. Rhythmic bursts of masticatory activity were evoked in the nerve by repetitive electrical stimulation of the motor cortex. The amplitude and latency of the reflex responses during fictive mastication were compared with preceding control values. When stimuli close to threshold were given, the largest and earliest responses occurred during the digastric burst. When intense stimuli were employed, the largest responses were out of phase with the burst, although the latency was still shortest when the motoneurons were rhythmically active. Since the pattern is essentially the same as that seen during normal mastication, we conclude that the cyclical modulation of reflex amplitude and latency is not the result of sensory feedback generated by the movements themselves but is instead governed by the central motor program.

Animals↗
PubMed1982

Bulbar reticular unit activity during food ingestion in the cat.

During food ingestion in cats, the activity of single bulbar reticular neurons showed rhythmical spike bursts during the active jaw opening phase of mastication. By utilizing spike-triggered averaging techniques, certain reticular cells were strongly suggested to be inhibitory neurons projecting to jaw closer motoneurons. We propose that these bulbar reticular neurons participate in the central generation of masticatory jaw movements by rhythmically inhibiting jaw closer motoneurons during mastication.

Animals↗
PubMedDate not supplied

Dynorphin increases in the dorsal spinal cord in rats with a painful peripheral neuropathy.

It is known that painful tissue injury evokes an increase in dynorphin in spinal neurons. It is not known, however, whether dynorphinergic systems respond similarly to the pain that accompanies peripheral neuropathy. Radioimmunoassays and immunocytochemistry were used to evaluate changes in dynorphin A(1-8) in the spinal cord of rats with a painful peripheral neuropathy. The neuropathy is the result of a constriction injury that is created by tying loose ligatures around the common sciatic nerve. Signs of abnormal pain sensations, hyperalgesia, allodynia (pain after normally innocuous stimuli), and spontaneous pain (or dysesthesia), are first detected 2-5 days after injury, reach peak severity in about 10 days, and persist for 2-3 months (Bennett, G. J.; Xie, Y.-K. Pain 33:87-107; 1988). Dynorphin increased by 5 days in cells in laminae I-II and V-VII in the lumbar spinal cord ipsilateral to the injury. This increase, maximal at 10 days (262%), was still present 20 days after the injury but was now seen only in neurons in the deep laminae (V-VII). Thus, the spinal dynorphinergic system appears to respond to neuropathic pain. Furthermore, our results suggest that dynorphinergic cells in the superficial and deep laminae may have different roles in nociception.

Animals↗