The Experts below are selected from a list of 63 Experts worldwide ranked by ideXlab platform
Zhang Ying - One of the best experts on this subject based on the ideXlab platform.
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The influence of ibotenic acidinduced damage of Midbrain Reticular Formation on mental status and related factors in cats
Chinese critical care medicine, 1999Co-Authors: Zhang YingAbstract:Objective:To investigate the influence of damage of Midbrain Reticular Formation on the mental status and its potential mechanism(s).Methods:A model of Midbrain Reticular Formation damage was made by stereotaxic microinjection of ibotenic acid (IA) in cats.Mental status,electrophysiological activities,and ultrastructural changes were observed in the present study.Results:IA could selectively damage neuron cells of Midbrain Reticular Formation without marked influence on axonal conduction,and it elicits overexcitation response rather than permanent unconsciousness.Meanwhile,such model showed corresponding features in EEG and EP and ultrastructural changes.Conclusions:These data suggest that selective damage of neuron cells may not lead to permanent unconsciousness,and disorder of consciousness after Midbrain injury appears to be associated with impairment of conduction between efferent and efferent nerve fibers in Reticular Formation.
Raoul Di Perri - One of the best experts on this subject based on the ideXlab platform.
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Spinal input to the Midbrain Reticular Formation: pharmacological investigation.
Progress in Brain Research, 2008Co-Authors: Arturo Morillo, A. R. Dravid, Raoul Di PerriAbstract:Publisher Summary Studies on the D-lysergic acid diethylamide (LSD-25) indicate that this substance produces electrocortical arousal in the relaxed, conscious cat and that such an effect is not observed in the “encephale isole” or in the “cerveau isole” preparations. This chapter discusses the action of LSD-25 upon evoked potentials simultaneously recorded from the lateral funiculus of the spinal cord at upper cervical level and from the brain stem Reticular Formation at intercollicular level. Acute experiments were carried out in 18 intact adult cats. Under ether anesthesia, the animals were tracheotomized, one of their femoral veins was cannulated, and a sciatic nerve was dissected and cut. The animals were placed in a stereotaxic apparatus and nichrome wire electrodes were stereotaxically placed through a burr hole into the mesencephalic Reticular Formation at intercollicular level. The electrodes in the Midbrain were located contralaterally to the dissected sciatic nerve. Under visual inspection, electrodes were inserted into the lateral funiculus of the spinal cord at the level of the second cervical segment, ipsilateral to the sciatic stimulated. LSD-25 had no effect upon the evoked potentials in the lateral funiculus of the spinal cord but depressed the response in the Midbrain Reticular Formation.
Etienne Olivier - One of the best experts on this subject based on the ideXlab platform.
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Midbrain Reticular Formation circuitry subserving gaze in the cat.
Annals of the New York Academy of Sciences, 2002Co-Authors: Paul J. May, Susan Warren, Bingzhong Chen, Frances J. Richmond, Etienne OlivierAbstract:Physiological experiments in primates have identified a region of the Midbrain tegmentum, the central mesencephalic Reticular Formation (cMRF), which plays a role in gaze control.1 Specifically, stimulation of this region produces horizontal saccades; recordings from this region reveal neurons with saccade-related activity; and chemical inactivation of this region produces contralateral head tilt and spontaneous saccades. More rostral regions of the Midbrain Reticular Formation (MRF), just lateral to the interstitial nucleus of Cajal (InC), have neurons with vertical movement fields, and chemical inactivation of this region produces hypometric vertical saccades.2 In the macaque, there is an extensive overlap of tectoReticular terminals and reticulotectal cells in the region corresponding to the cMRF.3 The present study explored whether an area similar to the cMRF is present in the cat by analyzing the distribution of MRF neurons targeting the superior colliculus (SCol) and cervical spinal cord. These studies were carried out in eight adult cats under approved protocols adhering to the NIH guidelines. In the single-injection animals, 0.1-0.5 μl of a 10% BDA was injected into either the SCol or cervical cord. The SCol was approached dorsally, by aspirating the overlying cortex, while the cervical cord (C1) was approached through the foramen magnum. In the dual-tracer animals, both approaches were used to inject 5% Fast Blue into the SCol and 5% Fluoro-Gold into C1 (0.5 μl each). Standard perfusion and processing techniques were used.
Earl Carstens - One of the best experts on this subject based on the ideXlab platform.
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isoflurane blunts electroencephalographic and thalamic Reticular Formation responses to noxious stimulation in goats
Anesthesiology, 1999Co-Authors: Joseph F. Antognini, Earl CarstensAbstract:BACKGROUND: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. METHODS: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the Midbrain Reticular Formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. RESULTS: At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the Midbrain Reticular Formation, thalamic, and bifrontal-hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean +/- SD), total (-33+/-7%), delta (-47+/-12%), theta (-23+/-12%), and alpha (-21+/-6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (-35+/-5%), delta (-42+/-7%), theta (-35+/-8%), and alpha (-23+/-11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. CONCLUSIONS: Isoflurane blunted EEG and Midbrain Reticular Formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.
Kikuro Fukushima - One of the best experts on this subject based on the ideXlab platform.
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THE INTERSTITIAL NUCLEUS OF CAJAL IN THE Midbrain Reticular Formation AND VERTICAL EYE MOVEMENT
Neuroscience research, 1991Co-Authors: Kikuro FukushimaAbstract:Abstract Bilateral lesions of the Midbrain Reticular Formation within, and in the close vicinity of, the interstitial nucleus of Cajal (INC) result in the severe impairment of the ability to hold eccentric vertical eye position after saccades, phase advance and decreased gain of the vestibulo-ocular reflex (VOR) induced by sinusoidal vertical rotation. In addition, the INC region of alert animals contains many burst-tonic and tonic neurons whose activity is closely correlated with vertical eye movement, not only during spontaneous saccades, but also during the VOR, smooth pursuit and optokinetic eye movements. Although their activity is closely related to these conjugate vertical eye movements, it is different from the oculomotor motor neuron activity. These results indicate that the INC region is involved in, and indispensable for, some aspects of eye position generation during vertical eye movement. Further comparison of INC neuron discharge with eye movements during two special conditions indicates that the INC region alone cannot produce eye position signals. First, INC neuron discharge shows no response or an 80° phase advance (close to the expected value if there is no integration) in the dark compared to the light during sinusoidal vertical linear acceleration in alert cats. Second, during rapid-eye-movement (REM) sleep, the discharge of INC neurons is no longer correlated with eye position. These results imply that the INC is not the entire velocity-to-position integrator, but that it has to work with other region(s) to perform the integration. A close functional linkage has been described between vertical-eye-movement-related neurons in the INC region and vestibulo-ocular relay neurons related to the vertical semicircular canals in the vestibular nuclei. It has been suggested that both are the major constituents of the common neural integrator circuits for vertical eye movements.