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Y F Xie

Publications and source records attributed to Y F Xie.

At least 19 recordsLinked to original sources

Involvement of glia in central sensitization in trigeminal subnucleus caudalis (medullary dorsal horn).

Central sensitization is a crucial mechanism underlying the increased excitability of nociceptive pathways following peripheral tissue injury and inflammation. We have previously demonstrated that the small-fiber excitant and inflammatory irritant mustard oil (MO) applied to the tooth pulp produces glutamatergic- and purinergic-dependent central sensitization in brainstem nociceptive neurons of trigeminal subnucleus caudalis (Vc). Recent studies have implicated both astrocytes and microglia in spinal nociceptive mechanisms, showing, for example, that inhibition of spinal astroglial metabolism or spinal microglial p38MAPK activation can attenuate hyperalgesia in inflammatory pain models but have not tested effects of glial inhibitors on central sensitization in functionally identified spinal nociceptive neurons. The aim of the present study was to determine whether glial cells are involved in the MO-induced central sensitization in Vc nociceptive neurons, by examining the effects of intrathecally applied SB203580 (SB), an inhibitor of p38MAPK, and fluoroacetate (FA), an inhibitor of the astroglial metabolic enzyme aconitase. During continuous superfusion of phosphate-buffered saline over Vc, MO application to the pulp-induced central sensitization in Vc nociceptive neurons reflected in significant increases in cutaneous mechanoreceptive field (RF) size and responses to noxious mechanical stimuli and a decrease in mechanical activation threshold. The i.t. application of SB or FA markedly attenuated the MO-induced increases in pinch RF size and responses to noxious stimuli and the decrease in activation threshold. Neither SB nor FA application significantly affected the baseline (i.e., pre-MO application) RF and response properties. These results suggest that glial metabolic processes are important in the development of Vc central sensitization.

Aconitate Hydratase↗

Central sensitization in thalamic nociceptive neurons induced by mustard oil application to rat molar tooth pulp.

We have recently demonstrated that application of mustard oil (MO), a small-fiber excitant and inflammatory irritant, to the rat maxillary molar tooth pulp induces central sensitization that is reflected in changes in spontaneous activity, mechanoreceptive field (RF) size, mechanical activation threshold, and responses to graded mechanical stimuli applied to the neuronal RF in trigeminal brainstem subnucleus caudalis and subnucleus oralis. The aim of this study was to test whether central sensitization can be induced in nociceptive neurons of the posterior thalamus by MO application to the pulp. Single unit neuronal activity was recorded in the ventroposterior medial nucleus (VPM) or posterior nuclear group (PO) of the thalamus in anesthetized rats, and nociceptive neurons were classified as wide dynamic range (WDR) or nociceptive-specific (NS). MO application to the pulp was studied in 47 thalamic nociceptive neurons and found to excite over 50% of the 35 VPM neurons tested and to produce significant long-lasting (over 40 min) increases in spontaneous activity, cutaneous pinch RF size and responses to graded mechanical stimuli, and a decrease in threshold in the 29 NS neurons tested; a smaller but statistically significant increase in mean spontaneous firing rate and decrease in activation threshold occurred following MO in the six WDR neurons tested. Vehicle application to the pulp did not produce any significant changes in six VPM NS neurons tested. MO application to the pulp produced pronounced increases in spontaneous activity, pinch RF size, and responses to mechanical stimuli, and a decrease in threshold in three of the six PO neurons. In conclusion, application of the inflammatory irritant MO to the tooth pulp results in central sensitization of thalamic nociceptive neurons and this neuronal hyperexcitability likely contributes to the behavioral consequences of peripheral inflammation manifesting as pain referral, hyperalgesia and allodynia.

Action Potentials↗

Endogenous ATP involvement in mustard-oil-induced central sensitization in trigeminal subnucleus caudalis (medullary dorsal horn).

Central sensitization represents a sustained hypersensitive state of dorsal horn nociceptive neurons that can be evoked by peripheral inflammation or injury to nerves and tissues. It reflects neuroplastic changes such as increases in neuronal spontaneous activity, receptive field size, and responses to suprathreshold stimuli and a decrease in activation threshold. We recently demonstrated that purinergic receptor mechanisms in trigeminal subnucleus caudalis (Vc; medullary dorsal horn) are also involved in the initiation and maintenance of central sensitization in brain stem nociceptive neurons of trigeminal subnucleus oralis. The aim of the present study was to investigate whether endogenous ATP is involved in the development of central sensitization in Vc itself. The experiments were carried out on urethan/alpha-chloralose anesthetized and immobilized rats. Single neurons were recorded and identified as nociceptive-specific (NS) in the deep laminae of Vc. During continuous saline superfusion (0.6 ml/h it) over the caudal medulla, Vc neuronal central sensitization was readily induced by mustard oil application to the tooth pulp. However, this mustard-oil-induced central sensitization could be completely blocked by continuous intrathecal superfusion of the wide-spectrum P2X receptor antagonist pyridoxal-phosphate-6-azophenyl-2, 4-disulphonic acid tetra-sodium (33-100 microM) and by apyrase (an ectonucleotidase enzyme, 30 units/ml). Superfusion of the selective P2X1, P2X3 and P2X(2/3) receptor antagonist 2',3'-O-(2,4,6-trinitrophenyl) adenosine 5'-triphosphate (6-638 microM) partially blocked the Vc central sensitization. The two P2X receptor antagonists did not significantly affect the baseline nociceptive properties of the Vc neurons. These findings implicate endogenous ATP as an important mediator contributing to the development of central sensitization in nociceptive neurons of the deep laminae of the dorsal horn.

Action Potentials↗

Mu but not delta and kappa opioid receptor involvement in ventrolateral orbital cortex opioid-evoked antinociception in formalin test rats.

The present study was designed to investigate the roles of different subtypes of opioid receptors in ventrolateral orbital cortex (VLO) opioid-evoked antinociception in formalin test by using an automatic detection system for recording the nociceptive behavior (agitation) and a manual method for detecting the duration of licking the injected paw in the conscious rat. Formalin (5%, 50 microl) s.c. injected into the hindpaw produced a biphasic agitation response or lengthening duration of licking. Morphine (5 microg) microinjected unilaterally into VLO significantly inhibited the agitation response and the licking time, and these effects were blocked by pre-administration of the non-selective opioid receptor antagonist naloxone (1.0 microg) into the same site. Microinjection of endomorphin-1 (5 microg), a selective micro-receptor agonist, and [D-Ala2, D-Leu5]-enkephalin (DADLE, 10 microg), a delta-/micro-receptor agonist also inhibited the nociceptive behaviors, and both the effects were blocked by selective mu-receptor antagonist beta-funaltrexamine hydrochloride (beta-FNA; 3.75 microg), but the DADLE-evoked inhibition was not influenced by the selective delta-receptor antagonist naltrindole (5 microg). Microinjection of selective kappa-receptor agonist (+/-)-trans-U-50488 methanesulfonate salt (1.5 microg) failed to alter the nociceptive behaviors induced by formalin injection. The beta-FNA and naloxone applied into VLO and morphine into the adjacent regions ventral and dorsal to VLO had no effect on the formalin-evoked nociceptive behaviors. These results suggest that mu- but not delta- or kappa-opioid receptor is involved in the VLO opioid-evoked antinociception in formalin test rat.

Animals↗

[Cloning and analysis of a novel gene encoding N-terminal acetyltransferase subunit].

N-terminal acetylation is the most common modification in eukaryotic proteins, affecting stability and activity of proteins. NatA is one of the N-terminal acetytransferases in yeast. It is composed of two subunits, NAT1 and ARD1. Defect in one of them leads to loss of activity of NatA. Null mutant of NAT1 in yeast exhibits a variety of phenotypes, including depression of a silent mating type locus (HML), failing to enter G(0) in poor nutrient situations and chromosomes instability. Based on homology of NAT1 between yeast and other organisms, the full-length CDS (coding sequence) of HNAT1 was cloned and sequenced. Result of in situ hybridization in testis of rat showed that expression of NAT1 was high and its expression was different in different phases of spermatogenesis. The gene may play an important role in spermatogenesis.

Acetyltransferases↗

[Effect of nucleus raphe obscurus on myoelectric activity of sphincter of Oddi in rabbits].

The aim of the present study was to investigate the role of nucleus raphe obscurus (NRO) in regulating the motility of sphincter of Oddi (SO). After fasting about l8~24 h, the rabbits were anesthetized with urethane (1.0 g/kg), and the myoelectric signals of SO were induced by a pair of copper electrodes inserted into the subsera. The results of microinjection of various drugs into NRO are as follows. After glutamate (340 mmol/L, 0.1 microl) was injected, activity of SO was excited. With microinjection of GABA (1 mol/L,0.1 microl), the spike burst of SO was inhibited. Following microinjection of ketamine (180 mmol/L, 0.1 microl), a kind of N-methyl-D-aspartate (NMDA) receptor antagonist, SO motility was inhibited and the effect of glutamate was abolished. Injection of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (2 mmol/L, 0.1 microl), a non-NMDA receptor antagonist, also excited the myoelectric activity of SO, but did not inhibit the effect of glutamate. The effect of glutamate was abolished by intravenous injection of atropine (0.2 mg/kg) or bilateral vagotomy, but not by injection of phentolamine (1.5 mg/kg) or propronalol (1.5 mg/kg), or by transection of the spinal cord. The above results indicate that NRO mediation of SO activity is due to the effect of glutamate on the NMDA receptors in the nucleus, the output of which is sent through vagal nerve and peripheral M cholinergic receptor to exert excitation of gallbladder motility.

Animals↗

[Direct embryogenesis from protoplast of winter wheat].

Friable embryogenic calli were obtained on a modified N6 medium (NBD medium) from a winter wheat cultivar "Jinghua No. 1" (Triticum aestivum L. cv. Jinghua No. 1) and were transferred to a modified MS liquid medium (MSDL medium) to initiate embryogenic suspension cultures. Protoplasts were isolated from the suspensions and cultured on a modified MS medium (MSDP medium). The somatic embryoids were formed directly from the protoplasts and germinated into entire plants. The development of the somatic embryoids was very similar to that of zygotic embryos of wheat.

Protoplasts↗

[The establishment of two new evaluation criteria for cell state of plant cell suspension cultures].

An experiment on suspending rice cell cultures in sucrose solution and on optical density (OD) value in culture solution at 576 nm wave width was carried out, the result indicates that suspension rate (%) of suspensions, while suspending in 0.76 mol/L sucrose solution for 15 minutes at room temperature, can be employed as an judgment criterion of cell state. Suspending cell suspension in 0.76 mol/L sucrose solution is also a good approach on selecting cells from suspension cell mass, as a result, it is beneficial to establishing cell suspension. The browning of cell suspension is related to the necrosis degree of suspension cells. OD value of cell suspension liquid at 576 nm can be taken as a criterion with which the necrosis degree of cell suspension can be evaluated.

Cell Culture Techniques↗

Adenosine and opiate-like substances mediates antinociception at the spinal cord.

The effects of intrathecally administered naloxone or aminophylline on the antinociception produced by intrathecal NE, 5-HT, morphine or adenosine receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA) were observed in rats using the tail-flick test. The results show that: (1) the antinociception produced by NE with doses of 0.5 or 1.0 nmol could be completely blocked by both naloxone (240 nmol) and aminophylline (120 nmol); (2) neither naloxone (240 nmol) nor aminophylline (120 nmol) could alter the antinociception produced by 5-HT with doses of 60 or 120 nmol; and (3) the antinociception produced by morphine (0.5 nmol) could be blocked by both naloxone (240 nmol) and aminophylline (120 nmol), while the antinociception by NECA (0.5 nmol) could be blocked only by aminophylline (120 nmol), but not by naloxone (240 nmol). The results suggest that opiate-like substances (OLS) and adenosine are involved in the mediation of the NE-produced antinociception, but not in 5-HT-produced antinociception. Results also suggest that NE, OLS and adenosine may act in a sequential order in the performance of NE-induced antinociception at the spinal level.

Adenosine↗

Interaction of serotonin and norepinephrine in spinal antinociception.

The interactions between different doses of serotonin (5-HT) and norepinephrine (NE) in in vivo experiments on rat spinal cord dorsal horn cells was investigated using the integrated electromyography (EMG) measurement of the nociceptive hindlimb flexor reflex (FR). The results indicate that (1) intrathecal (IT) administration of low doses of 5-HT (60 nmol) or NE (1.5 nmol) suppresses the nociceptive FR by 40% for 20 min, respectively; (2) administration of higher doses of 5-HT (240 nmol, IT) multiplies the suppression of the nociceptive FR by 80% for 40 min, and NE (15 nmol, IT) produces similar suppression of the nociceptive FR for 80 min; (3) concomitant administration of low doses of 5-HT (60 nmol, IT) and NE (1.5 nmol, IT) produces a summation of the nociceptive FR suppression both in amplitude and duration; (4) concomitant administration of the higher doses of 5-HT (240 nmol IT) with NE (15 nmol, IT) produces similar effect obtained as 5-HT given separately, and no summation was obtained as observed following the lower dosages; (5) serotonin (240 nmol, IT) given 40 min before NE (15 nmol, IT) attenuates the duration of the suppression induced by NE; (6) pretreatment with a selective 5-HT2 receptor antagonist ketanserin (60 nmol, IT) failed to abolish the 5-HT effects; (7) pretreatment with ketanserin prior to concomitant administration of the higher doses of 5-HT and NE prolongs the time duration of the nociceptive FR suppression.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Morphine and norepinephrine-induced antinociception at the spinal level is mediated by adenosine.

The purpose of this study was to examine whether adenosine or serotonin is involved in mediation of the antinociception produced by norepinephrine at the spinal cord level. Aminophylline, an adenosine receptor antagonist and naloxone given intrathecally (i.t.) were used to test the antinociception produced by i.t. norepinephrine, serotonin, morphine or the adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) by using the tail-flick assay in rats. It was observed that (1) aminophylline blocked the antinociception produced by norepinephrine, but exhibited no effect on the antinociception produced by serotonin, (2) aminophylline blocked the antinociception produced by morphine similarly to naloxone, (3) aminophylline blocked the antinociception produced by NECA and (4) naloxone failed to block the antinociception produced by NECA and serotonin. The results suggest that adenosine is involved in mediation of the norepinephrine-produced antinociception at the spinal level and that norepinephrine and adenosine may act in a sequential manner in norepinephrine-induced antinociception.

Adenosine↗

Norepinephrine and serotonin-induced antinociception are blocked by naloxone with different dosages.

The effects of intrathecally (IT) administered naloxone (Nal) on the antinociception produced by IT norepinephrine (NE), serotonin (5-HT), or morphine (Mor) were observed and compared in rats using the tail-flick (TF) assay. The results show that: a) NE, 5-HT, and Mor in doses of 1 nmol, 240 nmol, and 0.5 nmol, respectively, produce similar increases in amplitude and time in TF latency (TFL); b) Nal treatment of 240 and 360 nmol has no effects on TFL; c) the antinociception produced by NE (1 nmol) can be blocked by Nal (240 nmol); d) antinociception produced by Mor (0.5 nmol) can also be blocked by Nal (240 nmol); e) 240 nmol of Nal does not affect the 5-HT (120 nmol)-produced antinociception, while 360 nmol of Nal show a delayed blockade to the 5-HT (120 nmol)-produced antinociception. The results suggest that endogenous opiate-like substances may be involved in both NE- or 5-HT-produced antinociception at the spinal level, and these effects may be mediated through different types of opiate receptors.

Animals↗

Morphological evidence for the activation of descending modulatory control by nociceptive afferent pathways: an immunocytochemical study.

Immunocytochemical technique was used to compare the content of substance P (SP), Met-enkephalin (Met-Enk) and neurotensin (NT) on two sides of the lumbar dorsal horn of rats in which the unilateral dorsolateral funiculus was transected while formalin (0.2 ml, 5%) was injected equally into two hindpaws. The results showed that the SP-like immunoreactivity (SP-LI) and Met-Enk-LI were significantly higher and the NT-LI was significantly lower in the superficial laminae of dorsal horn on the side ipsilateral to the intact DLF than that on the opposite side, implying that peripheral noxious inputs can activate the supraspinal descending inhibitory systems which in turn modulate the transmission of noxious message at the spinal level by changing the activities of related peptidergic neurons.

Afferent Pathways↗

Serotonergic, noradrenergic and galaninergic projections to the nucleus parafascicularis.

Immunocytochemical staining for serotonin (5-HT), tyrosine hydroxylase (TH) and galanin (GAL) was combined with horseradish peroxidase (HRP) retrograde tract-tracing technique to analyze the localizations of 5-HT-, catecholamine (CA)- and GAL-containing neurons in the brainstem which project to the nucleus parafascicularis (PF) in rats. It is demonstrated that most of the retrogradely HRP-labeled neurons (70%) in bilateral periaqueductal gray (PAG) and raphe nuclei are positively immunostained by antiserum to 5-HT, and that most of the retrogradely HRP-labeled neurons (over 80%) in bilateral locus coeruleus (LC) are positively immunostained by antisera to both TH and GAL. The possible functions of these PF-petal serotonergic, catecholaminergic (actually noradrenergic) and galaninergic projections are discussed.

Animals↗

Effects of intrathecal monoamine antagonists and naloxone on the descending inhibition of the spinal transmission of noxious input in rats: study with a new experimental model.

An electrophysiological model has been developed to explore the transmitters and their relationships in the descending control of spinal transmission of noxious inputs. Nociceptive discharges were recorded extracellularly in parafascicular (Pf) neurons, and the caudal stump of longitudinally isolated dorsal half of the lower thoracic spinal cord was stimulated to simulate the descending volleys coming from the supraspinal structures. Nociceptive discharges in 34 Pf cells were markedly suppressed (83.2 +/- 13.9%) by the preceding spinal stimulation. Phentolamine, methysergide and naloxone were separately administered with random sequence in each of 25 cells by an intrathecal route to observe if the descending inhibition could be blocked by these drugs. The results suggested that in the dorsal spinal cord there exist at least two neurochemically different descending inhibitory fiber systems which comprise either the long descending adrenergic or serotonergic fibers and, most of the adrenergic fibers are succeeded by a propriospinal opioidergic neuron while a few of the serotonergic fibers have such a succession.

Animals↗

Effects of stimulation of superior colliculus on nociceptive unit discharges in parafascicular neurons and nocifensive reflex of hind limb in rat.

Effects of stimulation of the superior colliculus (SC) on the spontaneous and nociceptive discharges of parafascicular (PF) neurons were investigated in 43 urethane-anesthetized rats. Two groups of PF cells were sampled according to their responses to noxious stimuli: 59 of them were 'nociceptive-on' and 12 'nociceptive-off'. Following stimulation of the intermediate and deep layers of SC, the firing rate of nociceptive discharge of 'nociceptive-on' cells was inhibited significantly (-76 +/- 5%, P less than 0.01) in 75% cases tested, while the nociceptive response of 'nociceptive-off' cells was disinhibited markedly (79 +/- 9%, P less than 0.01) in 67% cases by the same stimulation. In 30 animals of this series the latency of hind limb withdrawal reflex elicited by noxious skin heating was compared before and after SC stimulation. In 24 cases in which the stimulating electrodes were positioned exactly in intermediate-deep layers of SC, SC stimulation lengthened the latency by 62 +/- 8% (P less than 0.01), while in 6 cases in which the electrodes drifted from these areas, the latency was not changed following the same stimulation.

Animals↗