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Hong Jia - One of the best experts on this subject based on the ideXlab platform.
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electrically evoked inhibitory effects of the nucleus submedius on the jaw opening reflex are mediated by ventrolateral Orbital Cortex and periaqueductal gray matter in the rat
Neuroscience, 1999Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:Abstract In previous studies we have shown that electrical stimulation of the nucleus submedius inhibits the rat radiant heat-induced tail flick reflex, and that this antinociceptive effect is mediated by the ventrolateral Orbital Cortex and periaqueductal gray. The aim of the present study was to examine whether electrical stimulation of the nucleus submedius could inhibit the rat jaw-opening reflex, and to determine whether electrolytic lesions of the ventrolateral Orbital Cortex or the periaqueductal gray could attenuate the nucleus submedius-evoked inhibition. Experiments were performed on pentobarbital-anesthetized rats. The jaw-opening reflex elicited by electrical stimulation of the tooth pulp or the facial skin was monitored by recording the evoked digastric electromyogram. Conditioning stimulation was delivered unilaterally to the nucleus submedius 90 ms prior to each test stimulus to the tooth pulp. After that, electrolytic lesions were made in ventrolateral Orbital Cortex or periaqueductal gray, and the effect of nucleus submedius stimulation on the jaw-opening reflex was re-examined. Unilateral electrical stimulation of nucleus submedius was found to significantly depress the jaw-opening reflex (mean threshold of 28.0±1.4 μA, n =48), and the magnitude of inhibition increased linearly when the stimulus intensity was increased from 20 to 70 μA, resulting in depression of the digastric electromyogram amplitude from 18.4±5.4% to 74.0±4.9% of the control ( P n =37). The onset of inhibition occured 60 ms after the beginning of nucleus submedius stimulation and lasted about 100 ms, as determined by varying the conditioning-test time interval. Furthermore, ipsilateral lesions of the ventrolateral Orbital Cortex or bilateral lesions of the lateral or ventrolateral parts of periaqueductal gray eliminated the nucleus submedius-evoked inhibition of the jaw-opening reflex. These data suggest that the nucleus submedius plays an important role in modulation of orofacial nociception, and provide further support for a hypothesis that the antinociceptive effect of nucleus submedius stimulation is mediated by ventrolateral Orbital Cortex and activation of a descending inhibitory system in the periaqueductal gray.
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inhibitory effects of electrical stimulation of ventrolateral Orbital Cortex on the rat jaw opening reflex
Brain Research, 1998Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:In previous studies, we have shown that electrically or chemically evoked activation of the ventrolateral Orbital Cortex (VLO) depresses the rat tail-flick (TF) reflex, and this antinociceptive effect is mediated by the periaqueductal gray (PAG). The aim of the present study was to examine whether electrical stimulation of the VLO could inhibit the rat jaw-opening reflex (JOR), and to determine whether electrolytic lesions of the PAG could attenuate this VLO-evoked inhibition. Unilateral electrical stimulation of the VLO significantly depressed the JOR elicited by tooth pulp or facial skin stimuli, with a mean threshold of 30.5+/-2.3 microA (n=22). Increasing stimulation intensities from 30 to 80 microA resulted in greater reduction of the dEMG amplitude from 22.9+/-5.0% to 69.7+/-3.7% of the baseline value (P<0.01, n=22). The inhibitory effect appeared 50 ms after the beginning of VLO stimulation and lasted about 150 ms, as determined by varying the conditioning-test (C-T) time interval. Unilateral lateral or ventrolateral lesions of the PAG produced only a small attenuation of the VLO-evoked inhibition of the JOR, but bilateral lesions eliminated this inhibition. These findings suggest that the VLO plays an important role in modulation of orofacial nociceptive inputs, and provide further support for the hypothesis that the antinociceptive effect of VLO is mediated by PAG leading to activation of a brainstem descending inhibitory system and depression of nociceptive inputs at the trigeminal level. The role played by VLO in pain modulation is discussed in association with the proposed endogenous analgesic system consisting of medullary cord-Sm-VLO-PAG-medullary cord.
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inhibitory effects of glutamate induced activation of thalamic nucleus submedius are mediated by ventrolateral Orbital Cortex and periaqueductal gray in rats
European Journal of Pain, 1998Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:This study found that in lightly-anesthetized rats a unilateral micro-injection of glutamate (200 mm, 0.5 μ1) into the thalamic nucleus submedius (Sm) markedly depressed the radiant heat-evoked tail flick (TF) reflex. After injection, the mean TFL increased 25.6 ± 6.5% (n = 24) of the baseline at 5 min, up to a peak value (48.4 ± 7.2%) at 20 min, and recovered to the baseline level at 60 min. This inhibitory effect was dose-related and repeatable over a time interval of 1.0–1.5 h in the same animal. Furthermore, micro-injections of γ-aminobutyric acid (GABA) (100 mM) into the ipsilateral ventrolateral Orbital Cortex (VLO) (0.7μl), or bilaterally into the lateral or ventrolateral parts of the periaqueductal gray (PAG) (0.5 μ1 on each side), eliminated the Sm-evoked inhibition. After GABA was injected into VLO or PAG, the Sm applications of glutamate failed to produce any significant changes in TFL, with the TFL changes being similar to the saline control (p>0.05). These results confirmed our previous findings that electrical stimulation of Sm depressed the rat TF reflex and that this inhibitory effect was blocked by electrolytic lesion of the VLO or PAG. Therefore, the present study provides further support for the hypothesis that Sm plays an important role in modulation of nociception, and that its effects are mediated by the VLO-PAG pathway, leading to activation of the brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.
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inhibitory effects of electrically evoked activation of ventrolateral Orbital Cortex on the tail flick reflex are mediated by periaqueductal gray in rats
Pain, 1997Co-Authors: Yu-qiu Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:The present study found in lightly anesthetized rats that the radiant heat-evoked tail flick (TF) reflex was markedly inhibited by a unilateral electrical stimulation (a 20 ms train of 0.2 ms, 100 Hz, 30–100 μA pulses) of the ventrolateral Orbital Cortex (VLO), with the tail flick latency (TFL) being increased. The mean threshold of VLO stimulation for producing inhibition of the TF reflex was 39.2±8.7 μA (n=26), and this inhibitory effect increased following increasing stimulation intensity from 40 to 70 μA. The inhibition developed and remained during the stimulation and disappeared rapidly after termination of the stimulation. When the VLO was stimulated at an intensity of 100 μA in addition to the inhibition an after-facilitation of the TF reflex (a decrease in TFL) was observed at 5–10 s after termination of the stimulation. Bilateral electrolytic lesions of the lateral or ventrolateral parts of the periaqueductal gray matter (PAG) dramatically reduced or eliminated the VLO-evoked inhibition, and the after-facilitation as well. The difference was significant between the TFL changes produced by VLO stimulation before and after PAG lesion (P<0.01). The results suggest that the antinociception elicited by VLO stimulation is mediated by PAG, leading to activation of the brainstem descending inhibitory system which depresses the nociceptive transmission at the spinal level. The role played by VLO in pain modulation was discussed in association with the proposed endogenous analgesic system consisting of spinal cord-Sm-VLO-PAG-spinal cord.
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involvement of the frontal ventrolateral Orbital Cortex in descending inhibition of nociception mediated by the periaqueductal gray in rats
Neuroscience Letters, 1997Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:Our previous findings which indicated that electrical stimulation of ventrolateral Orbital Cortex (VLO) can depress the rat tail flick (TF) reflex and that the VLO-evoked inhibitory effect is blocked by electrolytic lesions of periaqueductal gray (PAG) suggest a role of the VLO in the modulation of nociception. To further investigate the involvement of VLO in this nociceptive modulatory pathway, we tested the effects of microinjections of glutamate (200 mM, 0.7 μl) into the VLO on the TF reflex. An unilateral microinjection of glutamate into the VLO significantly depressed the TF reflex; and this effect was repeatable. Furthermore, bilateral microinjections of γ-aminobutyric acid (GABA; 100 mM, 0.5 μl on each side) into the ventrolateral parts of PAG could eliminate this VLO-evoked inhibition of the TF reflex. These results, along with our previous findings provide further support for a hypothesis that VLO, as a higher center in the frontal Cortex, plays an important role in modulation of nociception, and this role is mediated by PAG leading to activation of the brainstem descending inhibitory system which depresses the nociceptive information at the spinal level.
Joseph L Price - One of the best experts on this subject based on the ideXlab platform.
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Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression
Brain Structure and Function, 2008Co-Authors: Wayne C Drevets, Joseph L Price, Maura L. FureyAbstract:The neural networks that putatively modulate aspects of normal emotional behavior have been implicated in the pathophysiology of mood disorders by converging evidence from neuroimaging, neuropathological and lesion analysis studies. These networks involve the medial prefrontal Cortex (MPFC) and closely related areas in the medial and caudolateral Orbital Cortex (medial prefrontal network), amygdala, hippocampus, and ventromedial parts of the basal ganglia, where alterations in grey matter volume and neurophysiological activity are found in cases with recurrent depressive episodes. Such findings hold major implications for models of the neurocircuits that underlie depression. In particular evidence from lesion analysis studies suggests that the MPFC and related limbic and striato-pallido-thalamic structures organize emotional expression. The MPFC is part of a larger “default system” of cortical areas that include the dorsal PFC, mid- and posterior cingulate Cortex, anterior temporal Cortex, and entorhinal and parahippocampal Cortex, which has been implicated in self-referential functions. Dysfunction within and between structures in this circuit may induce disturbances in emotional behavior and other cognitive aspects of depressive syndromes in humans. Further, because the MPFC and related limbic structures provide forebrain modulation over visceral control structures in the hypothalamus and brainstem, their dysfunction can account for the disturbances in autonomic regulation and neuroendocrine responses that are associated with mood disorders. This paper discusses these systems together with the neurochemical systems that impinge on them and form the basis for most pharmacological therapies.
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complementary circuits connecting the Orbital and medial prefrontal networks with the temporal insular and opercular Cortex in the macaque monkey
The Journal of Comparative Neurology, 2008Co-Authors: Kadharbatcha S Saleem, Hideki Kondo, Joseph L PriceAbstract:The origin and termination of axonal connections between the Orbital and medial prefrontal Cortex (OMPFC) and the temporal, insular, and opercular Cortex have been analyzed with anterograde and retrograde axonal tracers, injected in the OMPFC or temporal Cortex. The results show that there are two distinct, complementary, and reciprocal neural systems, related to the previously defined “Orbital” and “medial” prefrontal networks. The Orbital prefrontal network, which includes areas in the central and lateral part of the Orbital Cortex, is connected with vision-related areas in the inferior temporal Cortex (especially area TEav) and the fundus and ventral bank of the superior temporal sulcus (STSf/v), and with somatic sensory-related areas in the frontal operculum (OPf) and dysgranular insular area (Id). No connections were found between the Orbital network and auditory areas. The Orbital network is also connected with taste and olfactory cortical areas and the perirhinal Cortex and appears to be involved in assessment of sensory objects, especially food. The medial prefrontal network includes areas on the medial surface of the frontal lobe, medial Orbital areas, and two caudolateral Orbital areas. It is connected with the rostral superior temporal gyrus (STGr) and the dorsal bank of the superior temporal sulcus (STSd). This region is rostral to the auditory parabelt areas, and there are only relatively light connections between the auditory areas and the medial network. This system, which is also connected with the entorhinal, parahippocampal, and cingulate/retrosplenial Cortex, may be involved in emotion and other self-referential processes. J. Comp. Neurol. 506:659–693, 2008. © 2007 Wiley-Liss, Inc.
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definition of the Orbital Cortex in relation to specific connections with limbic and visceral structures and other cortical regions
Annals of the New York Academy of Sciences, 2007Co-Authors: Joseph L PriceAbstract:The orbitofrontal Cortex is often defined topographically as the Cortex on the ventral surface of the frontal lobe. Unfortunately, this definition is not consistently used, and it obscures distinct connectional and functional systems within the Orbital Cortex. It is difficult to interpret data on the Orbital Cortex that do not take these different systems into account. Analysis of cortico-cortical connections between areas in the Orbital and medial prefrontal Cortex indicate two distinct networks in this region. One system, called the Orbital network, involves most of the areas in the central Orbital Cortex. The other system, has been called the medial prefrontal network, though it is actually more complex, since it includes areas on the medial wall, in the medial Orbital Cortex, and in the posterolateral Orbital Cortex. Some areas in the medial Orbital Cortex are involved in both networks. Connections to other brain areas support the distinction between the networks. The Orbital network receives several sensory inputs, from olfactory Cortex, taste Cortex, somatic sensory association Cortex, and visual association Cortex, and is connected with multisensory areas in the ventrolateral prefrontal Cortex and perirhinal Cortex. The medial network has outputs to the hypothalamus and brain stem and connects to a cortical circuit that includes the rostral part of the superior temporal gyrus and dorsal bank of the superior temporal sulcus, the cingulate and retrosplenial Cortex, the entorhinal and posterior parahippocampal Cortex, and the dorsomedial prefrontal Cortex.
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cortical abnormalities in bipolar disorder investigated with mri and voxel based morphometry
NeuroImage, 2006Co-Authors: Allison C Nugent, Joseph L Price, Michael P Milham, Earle E Bain, Linda Mah, Dara M Cannon, Sean Marrett, Carlos A Zarate, Daniel S Pine, Wayne C DrevetsAbstract:Bipolar disorder (BD) has been associated with abnormalities of brain structure. Specifically, in vivo volumetric MRI and/or post mortem studies of BD have reported abnormalities of gray matter (GM) volume in the medial prefrontal Cortex (PFC), amygdala, hippocampal subiculum and ventral striatum. These structures share anatomical connections with each other and form part of a "visceromotor" network modulating emotional behavior. Areas of the lateral Orbital, superior temporal and posterior cingulate cortices project to this network, but morphometric abnormalities in these areas have not been established in BD. The current study assessed tissue volumes within these areas in BD using MRI and voxel-based morphometry (VBM). MRI images were obtained from 36 BD subjects and 65 healthy controls. To account for possible neurotrophic and neuroprotective effects of psychotropic medications, BD subjects were divided into medicated and unmedicated groups. Images were segmented into tissue compartments, which were examined on a voxel-wise basis to determine the location and extent of morphometric changes. The GM was reduced in the posterior cingulate/retrosplenial Cortex and superior temporal gyrus of unmedicated BD subjects relative to medicated BD subjects and in the lateral Orbital Cortex of medicated BD subjects relative to controls. White matter (WM) was increased in the Orbital and posterior cingulate cortices, which most likely reflected alterations in gyral morphology resulting from the reductions in the associated GM. The morphometric abnormalities in the posterior cingulate, superior temporal and lateral Orbital cortices in BD support the hypothesis that the extended network of neuroanatomical structures subserving visceromotor regulation contains structural alterations in BD. Additionally, localization of morphometric abnormalities to areas known to exhibit increased metabolism in depression supports the hypothesis that repeated stress and elevated glucocorticoid secretion may result in neuroplastic changes in BD.
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Orbitomedial prefrontal cortical projections to distinct longitudinal columns of the periaqueductal gray in the rat.
The Journal of comparative neurology, 2000Co-Authors: Nicole S. Floyd, Amon T Ferry, Joseph L Price, Kevin A. Keay, Richard BandlerAbstract:We utilised retrograde and anterograde tracing procedures to study the origin and termination of prefrontal cortical (PFC) projections to the periaqueductal gray (PAG) in the rat. A previous study, in the primate, had demonstrated that distinct subgroups of PFC areas project to specific PAG columns. Retrograde tracing experiments revealed that projections to dorsolateral (dlPAG) and ventrolateral (vlPAG) periaqueductal gray columns arose from medial PFC, specifically prelimbic, infralimbic, and anterior cingulate cortices. Injections made in the vlPAG also labeled cells in medial, ventral, and dorsolateral Orbital Cortex and dorsal and posterior agranular insular Cortex. Other Orbital and insular regions, including lateral and ventrolateral Orbital, ventral agranular insular, and dysgranular and granular insular Cortex did not give rise to appreciable projections to the PAG. Anterograde tracing experiments revealed that the projections to different PAG columns arose from specific PFC areas. Projections from the caudodorsal medial PFC (caudal prelimbic and anterior cingulate cortices) terminated predominantly in dlPAG, whereas projections from the rostroventral medial PFC (rostral prelimbic Cortex) innervated predominantly the vlPAG. As well, consistent with the retrograde data, projections arising from select Orbital and agranular insular cortical areas terminated selectively in the vlPAG. The results indicate: (1) that rat Orbital and medial PFC possesses an organisation broadly similar to that of the primate; and (2) that subdivisions within the rat Orbital and medial PFC can be recognised on the basis of projections to distinct PAG columns.
Jingshi Tang - One of the best experts on this subject based on the ideXlab platform.
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activation of serotonin 1a receptors in ventrolateral Orbital Cortex depresses persistent nociception a presynaptic inhibition mechanism
Neurochemistry International, 2010Co-Authors: Fuquan Huo, Tao Chen, Fensheng Huang, Jie Feng, Jingshi TangAbstract:The present study examined the effect of serotonin 1A (5-HT(1A)) receptor activation in the ventrolateral Orbital Cortex (VLO) upon formalin-evoked flinching behavior and spinal Fos expression, and further determined whether activation of 5-HT(1A) receptors affected the spontaneous GABAergic miniature inhibitory postsynaptic currents (mIPSCs) in rat VLO slice by pharmacologically separated neurons to understand the possible mechanism underlying this effect. Microinjection of the 5-HT(1A) receptors agonist 8-OH-DPAT (8-hydro-2-(di-n-propylamino) tetralin) into the VLO depressed the formalin-evoked nociceptive behavior flinching response and the Fos expression in the lumbar spinal cord dorsal, which was antagonized by pre-treatment with 5-HT(1A) receptors antagonist NAN-190 (1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine hydrobromide). Furthermore, application of 8-OH-DPAT into VLO slice inhibited GABAergic mIPSC frequency in a dose-dependent manner without effects on amplitude of the GABAergic mIPSCs, this effect was blocked by NAN-190. These results provide evidence for the involvement of 5-HT(1A) receptors in VLO in the modulation of persistent inflammatory nociception, and suggest that a presynaptic inhibition of the GABA release may contribute to the 5-HT(1A) receptor-mediated descending antinociception.
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the thalamic nucleus submedius and ventrolateral Orbital Cortex are involved in nociceptive modulation a novel pain modulation pathway
Progress in Neurobiology, 2009Co-Authors: Jingshi Tang, Fuquan HuoAbstract:Recently, a series of studies have given rise to and provided evidence for the hypothesis that the nucleus submedius (Sm) in the medial thalamus is involved in modulation of nociception. The Sm, ventrolateral Orbital Cortex (VLO) and the periaqueductal gray (PAG) constitute a pain modulatory pathway, activation of which leads to activation of the PAG-brainstem descending inhibitory system and depression of the nociceptive inputs in the spinal cord and trigeminal nucleus. Other studies have indicated that the Sm-VLO-PAG pathway plays an important role in the analgesia induced by electroacupuncture stimulation of the acupuncture point (acupoint) for exciting small diameter fiber (A-delta and C group) afferents. Opioid peptides, serotonin, dopamine, glutamate and their related receptors are involved in Sm- and/or VLO-mediated descending antinociception, and a GABAergic disinhibitory mechanism participates in mediating the antinociception induced by activation of mu-opioid receptors, serotonin 1(A) receptors, and dopamine D(2)-like receptors. This review describes these findings, which provide important new insights into the roles of the thalamus and cerebral Cortex in descending pain modulation.
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synaptic connections between gabaergic elements and serotonergic terminals or projecting neurons in the ventrolateral Orbital Cortex
Cerebral Cortex, 2009Co-Authors: Fuquan Huo, Jing Wang, Tao Chen, Ting Zhang, Jingshi TangAbstract:The ventrolateral Orbital Cortex (VLO) is part of an endogenous analgesic system, consisting of the spinal cord-thalamic nucleus submedius-VLO periaqueductal gray (PAG)-spinal cord loop. The present study examined morphological connections of GABAergic (gamma-aminobutyric acidergic) neurons and serotonergic projection terminals from the dorsal raphe nucleus (DR), as well as the relationship between GABAergic terminals and VLO neurons projecting to the PAG, by using anterograde and retrograde tracing combined with immunofluorescence, immunohistochemistry, and electron microscopy methods. Results indicate that the majority (93%) of GABAergic neurons in the VLO also express the 5-HT(1A) (5-hydroxytryptamine 1A) receptor, and serotonergic terminals originating from the DR nucleus made symmetrical synapses with GABAergic neuronal cell bodies and dendrites within the VLO. GABAergic terminals also made symmetrical synapses with neurons expressing GABA(A) receptors and projecting to the PAG. These results suggest that a local neuronal circuit, consisting of 5-HTergic terminals, GABAergic interneurons, and projection neurons, exists in the VLO, and provides morphological evidence for the hypothesis that GABAergic modulation is involved in 5-HT(1A) receptor activation-evoked antinociception.
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electrically evoked inhibitory effects of the nucleus submedius on the jaw opening reflex are mediated by ventrolateral Orbital Cortex and periaqueductal gray matter in the rat
Neuroscience, 1999Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:Abstract In previous studies we have shown that electrical stimulation of the nucleus submedius inhibits the rat radiant heat-induced tail flick reflex, and that this antinociceptive effect is mediated by the ventrolateral Orbital Cortex and periaqueductal gray. The aim of the present study was to examine whether electrical stimulation of the nucleus submedius could inhibit the rat jaw-opening reflex, and to determine whether electrolytic lesions of the ventrolateral Orbital Cortex or the periaqueductal gray could attenuate the nucleus submedius-evoked inhibition. Experiments were performed on pentobarbital-anesthetized rats. The jaw-opening reflex elicited by electrical stimulation of the tooth pulp or the facial skin was monitored by recording the evoked digastric electromyogram. Conditioning stimulation was delivered unilaterally to the nucleus submedius 90 ms prior to each test stimulus to the tooth pulp. After that, electrolytic lesions were made in ventrolateral Orbital Cortex or periaqueductal gray, and the effect of nucleus submedius stimulation on the jaw-opening reflex was re-examined. Unilateral electrical stimulation of nucleus submedius was found to significantly depress the jaw-opening reflex (mean threshold of 28.0±1.4 μA, n =48), and the magnitude of inhibition increased linearly when the stimulus intensity was increased from 20 to 70 μA, resulting in depression of the digastric electromyogram amplitude from 18.4±5.4% to 74.0±4.9% of the control ( P n =37). The onset of inhibition occured 60 ms after the beginning of nucleus submedius stimulation and lasted about 100 ms, as determined by varying the conditioning-test time interval. Furthermore, ipsilateral lesions of the ventrolateral Orbital Cortex or bilateral lesions of the lateral or ventrolateral parts of periaqueductal gray eliminated the nucleus submedius-evoked inhibition of the jaw-opening reflex. These data suggest that the nucleus submedius plays an important role in modulation of orofacial nociception, and provide further support for a hypothesis that the antinociceptive effect of nucleus submedius stimulation is mediated by ventrolateral Orbital Cortex and activation of a descending inhibitory system in the periaqueductal gray.
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inhibitory effects of electrical stimulation of ventrolateral Orbital Cortex on the rat jaw opening reflex
Brain Research, 1998Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:In previous studies, we have shown that electrically or chemically evoked activation of the ventrolateral Orbital Cortex (VLO) depresses the rat tail-flick (TF) reflex, and this antinociceptive effect is mediated by the periaqueductal gray (PAG). The aim of the present study was to examine whether electrical stimulation of the VLO could inhibit the rat jaw-opening reflex (JOR), and to determine whether electrolytic lesions of the PAG could attenuate this VLO-evoked inhibition. Unilateral electrical stimulation of the VLO significantly depressed the JOR elicited by tooth pulp or facial skin stimuli, with a mean threshold of 30.5+/-2.3 microA (n=22). Increasing stimulation intensities from 30 to 80 microA resulted in greater reduction of the dEMG amplitude from 22.9+/-5.0% to 69.7+/-3.7% of the baseline value (P<0.01, n=22). The inhibitory effect appeared 50 ms after the beginning of VLO stimulation and lasted about 150 ms, as determined by varying the conditioning-test (C-T) time interval. Unilateral lateral or ventrolateral lesions of the PAG produced only a small attenuation of the VLO-evoked inhibition of the JOR, but bilateral lesions eliminated this inhibition. These findings suggest that the VLO plays an important role in modulation of orofacial nociceptive inputs, and provide further support for the hypothesis that the antinociceptive effect of VLO is mediated by PAG leading to activation of a brainstem descending inhibitory system and depression of nociceptive inputs at the trigeminal level. The role played by VLO in pain modulation is discussed in association with the proposed endogenous analgesic system consisting of medullary cord-Sm-VLO-PAG-medullary cord.
S Zhang - One of the best experts on this subject based on the ideXlab platform.
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electrically evoked inhibitory effects of the nucleus submedius on the jaw opening reflex are mediated by ventrolateral Orbital Cortex and periaqueductal gray matter in the rat
Neuroscience, 1999Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:Abstract In previous studies we have shown that electrical stimulation of the nucleus submedius inhibits the rat radiant heat-induced tail flick reflex, and that this antinociceptive effect is mediated by the ventrolateral Orbital Cortex and periaqueductal gray. The aim of the present study was to examine whether electrical stimulation of the nucleus submedius could inhibit the rat jaw-opening reflex, and to determine whether electrolytic lesions of the ventrolateral Orbital Cortex or the periaqueductal gray could attenuate the nucleus submedius-evoked inhibition. Experiments were performed on pentobarbital-anesthetized rats. The jaw-opening reflex elicited by electrical stimulation of the tooth pulp or the facial skin was monitored by recording the evoked digastric electromyogram. Conditioning stimulation was delivered unilaterally to the nucleus submedius 90 ms prior to each test stimulus to the tooth pulp. After that, electrolytic lesions were made in ventrolateral Orbital Cortex or periaqueductal gray, and the effect of nucleus submedius stimulation on the jaw-opening reflex was re-examined. Unilateral electrical stimulation of nucleus submedius was found to significantly depress the jaw-opening reflex (mean threshold of 28.0±1.4 μA, n =48), and the magnitude of inhibition increased linearly when the stimulus intensity was increased from 20 to 70 μA, resulting in depression of the digastric electromyogram amplitude from 18.4±5.4% to 74.0±4.9% of the control ( P n =37). The onset of inhibition occured 60 ms after the beginning of nucleus submedius stimulation and lasted about 100 ms, as determined by varying the conditioning-test time interval. Furthermore, ipsilateral lesions of the ventrolateral Orbital Cortex or bilateral lesions of the lateral or ventrolateral parts of periaqueductal gray eliminated the nucleus submedius-evoked inhibition of the jaw-opening reflex. These data suggest that the nucleus submedius plays an important role in modulation of orofacial nociception, and provide further support for a hypothesis that the antinociceptive effect of nucleus submedius stimulation is mediated by ventrolateral Orbital Cortex and activation of a descending inhibitory system in the periaqueductal gray.
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inhibitory effects of electrical stimulation of ventrolateral Orbital Cortex on the rat jaw opening reflex
Brain Research, 1998Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:In previous studies, we have shown that electrically or chemically evoked activation of the ventrolateral Orbital Cortex (VLO) depresses the rat tail-flick (TF) reflex, and this antinociceptive effect is mediated by the periaqueductal gray (PAG). The aim of the present study was to examine whether electrical stimulation of the VLO could inhibit the rat jaw-opening reflex (JOR), and to determine whether electrolytic lesions of the PAG could attenuate this VLO-evoked inhibition. Unilateral electrical stimulation of the VLO significantly depressed the JOR elicited by tooth pulp or facial skin stimuli, with a mean threshold of 30.5+/-2.3 microA (n=22). Increasing stimulation intensities from 30 to 80 microA resulted in greater reduction of the dEMG amplitude from 22.9+/-5.0% to 69.7+/-3.7% of the baseline value (P<0.01, n=22). The inhibitory effect appeared 50 ms after the beginning of VLO stimulation and lasted about 150 ms, as determined by varying the conditioning-test (C-T) time interval. Unilateral lateral or ventrolateral lesions of the PAG produced only a small attenuation of the VLO-evoked inhibition of the JOR, but bilateral lesions eliminated this inhibition. These findings suggest that the VLO plays an important role in modulation of orofacial nociceptive inputs, and provide further support for the hypothesis that the antinociceptive effect of VLO is mediated by PAG leading to activation of a brainstem descending inhibitory system and depression of nociceptive inputs at the trigeminal level. The role played by VLO in pain modulation is discussed in association with the proposed endogenous analgesic system consisting of medullary cord-Sm-VLO-PAG-medullary cord.
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inhibitory effects of glutamate induced activation of thalamic nucleus submedius are mediated by ventrolateral Orbital Cortex and periaqueductal gray in rats
European Journal of Pain, 1998Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:This study found that in lightly-anesthetized rats a unilateral micro-injection of glutamate (200 mm, 0.5 μ1) into the thalamic nucleus submedius (Sm) markedly depressed the radiant heat-evoked tail flick (TF) reflex. After injection, the mean TFL increased 25.6 ± 6.5% (n = 24) of the baseline at 5 min, up to a peak value (48.4 ± 7.2%) at 20 min, and recovered to the baseline level at 60 min. This inhibitory effect was dose-related and repeatable over a time interval of 1.0–1.5 h in the same animal. Furthermore, micro-injections of γ-aminobutyric acid (GABA) (100 mM) into the ipsilateral ventrolateral Orbital Cortex (VLO) (0.7μl), or bilaterally into the lateral or ventrolateral parts of the periaqueductal gray (PAG) (0.5 μ1 on each side), eliminated the Sm-evoked inhibition. After GABA was injected into VLO or PAG, the Sm applications of glutamate failed to produce any significant changes in TFL, with the TFL changes being similar to the saline control (p>0.05). These results confirmed our previous findings that electrical stimulation of Sm depressed the rat TF reflex and that this inhibitory effect was blocked by electrolytic lesion of the VLO or PAG. Therefore, the present study provides further support for the hypothesis that Sm plays an important role in modulation of nociception, and that its effects are mediated by the VLO-PAG pathway, leading to activation of the brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.
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involvement of the frontal ventrolateral Orbital Cortex in descending inhibition of nociception mediated by the periaqueductal gray in rats
Neuroscience Letters, 1997Co-Authors: S Zhang, Jingshi Tang, B Yuan, Hong JiaAbstract:Our previous findings which indicated that electrical stimulation of ventrolateral Orbital Cortex (VLO) can depress the rat tail flick (TF) reflex and that the VLO-evoked inhibitory effect is blocked by electrolytic lesions of periaqueductal gray (PAG) suggest a role of the VLO in the modulation of nociception. To further investigate the involvement of VLO in this nociceptive modulatory pathway, we tested the effects of microinjections of glutamate (200 mM, 0.7 μl) into the VLO on the TF reflex. An unilateral microinjection of glutamate into the VLO significantly depressed the TF reflex; and this effect was repeatable. Furthermore, bilateral microinjections of γ-aminobutyric acid (GABA; 100 mM, 0.5 μl on each side) into the ventrolateral parts of PAG could eliminate this VLO-evoked inhibition of the TF reflex. These results, along with our previous findings provide further support for a hypothesis that VLO, as a higher center in the frontal Cortex, plays an important role in modulation of nociception, and this role is mediated by PAG leading to activation of the brainstem descending inhibitory system which depresses the nociceptive information at the spinal level.
Philippe Peigneux - One of the best experts on this subject based on the ideXlab platform.
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18f fludeoxyglucose positron emission tomography evidence for cerebral hypermetabolism in the awake state in narcolepsy and idiopathic hypersomnia
Frontiers in Neurology, 2017Co-Authors: Y Dauvilliers, Elisa Evangelista, Lucie Barateau, Delphine De Verbizier, Philippe PeigneuxAbstract:Background: Changes in structural and functional central nervous system have been reported in narcolepsy, with large discrepancies between studies. No study has investigated yet spontaneous brain activity at wake in idiopathic hypersomnia. We compared relative changes in regional brain metabolism in two central hypersomnia conditions with different clinical features, namely narcolepsy type 1 and idiopathic hypersomnia, and in healthy controls. Methods: Sixteen patients (12 males, median age 30 years [17–78]) with narcolepsy type 1, nine patients (2 males, median age 27 years [20–60]) with idiopathic hypersomnia and 19 healthy controls (16 males, median age 36 years [17–78]) were included. 18F-fludeoxyglucose positron emission tomography (PET) was performed in all drug-free subjects under similar conditions and instructions to stay in a wake resting state. Results: We found increased metabolism in the anterior and middle cingulate and the insula in the two pathological conditions as compared to healthy controls. The reverse contrast failed to evidence hypometabolism in patients vs. controls. Comparisons between patient groups were non significant. At sub-statistical threshold, we found higher right superior occipital gyrus glucose metabolism in narcolepsy and higher middle Orbital Cortex and supplementary motor area metabolism in idiopathic hypersomnia, findings that require further confirmation. Conclusions: There is significant hypermetabolism in narcolepsy and idiopathic hypersomnia in the wake resting state in a set of brain regions constitutive of the salience cortical network that may reflect a compensatory neurocircuitry activity secondary to sleepiness. Metabolic differences between the two disorders within the executive-control network may be a signature of abnormally functioning neural system leading to persistent drowsiness typical of idiopathic hypersomnia.
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[18F]Fludeoxyglucose-Positron Emission Tomography Evidence for Cerebral Hypermetabolism in the Awake State in Narcolepsy and Idiopathic Hypersomnia
Frontiers in Neurology, 2017Co-Authors: Y Dauvilliers, Elisa Evangelista, Lucie Barateau, Delphine De Verbizier, Philippe PeigneuxAbstract:BACKGROUND: Changes in structural and functional central nervous system have been reported in narcolepsy, with large discrepancies between studies. No study has investigated yet spontaneous brain activity at wake in idiopathic hypersomnia (IH). We compared relative changes in regional brain metabolism in two central hypersomnia conditions with different clinical features, namely narcolepsy type 1 (NT1) and IH, and in healthy controls. METHODS: Sixteen patients [12 males, median age 30 years (17-78)] with NT1, nine patients [2 males, median age 27 years (20-60)] with IH and 19 healthy controls [16 males, median age 36 years (17-78)] were included. 18F-fludeoxyglucose positron emission tomography (PET) was performed in all drug-free subjects under similar conditions and instructions to stay in a wake resting state. RESULTS: We found increased metabolism in the anterior and middle cingulate and the insula in the two pathological conditions as compared to healthy controls. The reverse contrast failed to evidence hypometabolism in patients vs. controls. Comparisons between patient groups were non-significant. At sub-statistical threshold, we found higher right superior occipital gyrus glucose metabolism in narcolepsy and higher middle Orbital Cortex and supplementary motor area metabolism in IH, findings that require further confirmation. CONCLUSION: There is significant hypermetabolism in narcolepsy and IH in the wake resting state in a set of brain regions constitutive of the salience cortical network that may reflect a compensatory neurocircuitry activity secondary to sleepiness. Metabolic differences between the two disorders within the executive-control network may be a signature of abnormally functioning neural system leading to persistent drowsiness typical of IH.